Materiały źródłowe

• #1 Exercise-Induced Bronchoconstriction – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK557554/

  Exercise-induced bronchoconstriction (EIB) describes a transient airway narrowing occurring during physical exertion. […] It is caused by an acute large increase in the amount of air entering the airways that require heating and humidifying. In susceptible individuals, this results in inflammatory, neuronal, and vascular changes ultimately resulting in contraction of the bronchial smooth muscle and symptoms of dyspnea, cough, chest tightness, mucus production, and wheezing. […] Exercise-induced bronchoconstriction results from the alteration of normal lung physiology occurring with evaporative water loss, thermal changes, and irritant exposure induced by a large increase in minute ventilation and demand on the respiratory system to heat and humidify air with exercise-related hyperpnea.

• #2 Exercise-induced bronchoconstriction – UpToDate

  https://www.uptodate.com/contents/exercise-induced-bronchoconstriction

  Exercise-induced bronchoconstriction describes the acute onset of bronchoconstriction occurring during or, more frequently, minutes after exercise. […] However, this wording is potentially misleading because exercise is not an independent risk factor for asthma, but rather a trigger of bronchoconstriction in patients with underlying asthma. […] Thus, the term exercise-induced bronchoconstriction (EIB) is a more accurate reflection of the underlying pathophysiology and is generally preferred. […] EIB probably results from changes in airway physiology triggered by the large volume of relatively cool, dry air inhaled during vigorous activity. […] This is supported by the finding that EIB is attenuated when the inspired gas is more fully humidified and closer to body temperature. […] The effect of large-volume dry air inhalation on airway surface osmolality may be the primary stimulus responsible for bronchoconstriction.

• #3 Exercise-induced bronchoconstriction – UpToDate

  https://www.uptodate.com/contents/exercise-induced-bronchoconstriction

  Exercise-induced bronchoconstriction describes the acute onset of bronchoconstriction occurring during or, more frequently, minutes after exercise. […] However, this wording is potentially misleading because exercise is not an independent risk factor for asthma, but rather a trigger of bronchoconstriction in patients with underlying asthma. […] Thus, the term exercise-induced bronchoconstriction (EIB) is a more accurate reflection of the underlying pathophysiology and is generally preferred. […] EIB probably results from changes in airway physiology triggered by the large volume of relatively cool, dry air inhaled during vigorous activity. […] This is supported by the finding that EIB is attenuated when the inspired gas is more fully humidified and closer to body temperature. […] The effect of large-volume dry air inhalation on airway surface osmolality may be the primary stimulus responsible for bronchoconstriction.

• #4 Exercise-induced bronchoconstriction – Wikipedia

  https://en.wikipedia.org/wiki/Exercise-induced_bronchoconstriction

  Exercise-induced bronchoconstriction (EIB) occurs when the airways narrow as a result of exercise. This condition has been referred to as exercise-induced asthma (EIA); however, this term is no longer preferred. While exercise does not cause asthma, it is frequently an asthma trigger. […] While the potential triggering events for EIB are well recognized, the underlying pathogenesis is poorly understood. It usually occurs after at least several minutes of vigorous, aerobic activity, which increases oxygen demand to the point where breathing through the nose (nasal breathing) must be supplemented by mouth breathing. The resultant inhalation of air that has not been warmed and humidified by the nasal passages seems to generate increased blood flow to the linings of the bronchial tree, resulting in edema. Constriction of these small airways then follows, worsening the degree of obstruction to airflow. There is increasing evidence that the smooth muscle that lines the airways becomes progressively more sensitive to changes that occur as a result of injury to the airways from dehydration. The chemical mediators that provoke the muscle spasm appear to arise from mast cells.

• #5 Exercise-Induced Asthma: Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/1938228-overview

  Exercise-induced asthma is a condition of respiratory difficulty (bronchoconstriction) that is related to histamine release, is triggered by aerobic exercise, and lasts several minutes. Causes include medical conditions, environmental factors, and medications. […] EIA usually affects individuals who participate in sports that include an aerobic component. The condition can be seen in any sport, but EIA is much less common in predominantly anaerobic activities. This is likely due to the role of consistent and repetitive air movement through the airways (seen in aerobic sports), which affect airway humidity and temperature. EIA triggers an unknown biochemical and neurochemical pathway, resulting in the bronchospasm, which manifests as the symptoms of the disease. […] Although the exact mechanism of EIA is unknown, there are 2 predominant theories as to how the symptom complex is triggered. One is the airway humidity theory, which suggests that air movement through the airway results in relative drying of the airway. This, in turn, is believed to trigger a cascade of events that results in airway edema secondary to hyperemia and increased perfusion in an attempt to combat the drying. The result is bronchospasm.

• #6 Exercise-Induced Asthma: Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/1938228-overview

  The other theory is based on airway cooling and assumes that the air movement in the bronchial tree results in a decreased temperature of the bronchi, which may also trigger a hyperemic response in an effort to heat the airway. Again, the result is a spasm in the bronchi. […] Many authors believe there may be a combination of the above 2 theories that takes place, but the biochemical or physical pathways that mediate these responses are unclear. Evidence may even exist to support the idea that the resulting cascades are not the inflammatory pathways to which we attribute allergic asthma. […] Likewise, certain sports and their environments predispose individuals with asthma to experience EIA. Sports played in cold and dry environments usually result in more symptom manifestation for athletes with this condition. On the other hand, when the environment is warm and humid, the incidence and severity of EIA decrease.

• #7 The mechanism of exercise-induced asthma is . – PubMed

  https://pubmed.ncbi.nlm.nih.gov/10984363/

  Exercise-induced asthma (EIA) refers to the transient narrowing of the airways that follows vigorous exercise. The mechanism whereby EIA occurs is thought to relate to the consequences of heating and humidifying large volumes of air during exercise. […] In 1978 airway cooling was identified as an important stimulus for EIA; however, severe EIA also occurred when hot dry air was inspired, and there was no abnormal cooling of the airways. […] In 1986 the thermal hypothesis proposed that cooling of the airways needed to be followed by rapid rewarming and that these two events caused a vasoconstriction and a reactive hyperemia of the bronchial microcirculation, together with edema of the airway wall, causing the airways to narrow after exercise. […] The osmotic, or airway-drying, hypothesis developed from 1982-1992 because neither airway cooling nor rewarming appeared to be necessary for EIA to occur. As water is evaporated from the airway surface liquid, it becomes hyperosmolar and provides an osmotic stimulus for water to move from any cell nearby, resulting in cell volume loss. It is proposed that the regulatory volume increase, after cell shrinkage, is the key event resulting in release of inflammatory mediators that cause airway smooth muscle to contract and the airways of asthmatic subjects to narrow. This event may or may not be associated with airway edema. […] The osmotic and thermal theories come together by considering that inspiration of cold air not only cools the airways but also increases the numbers of airway generations becoming dehydrated in the humidifying process.

• #8 Exercise-induced bronchoconstriction: prevalence, pathophysiology, patient impact, diagnosis and management | npj Primary Care Respiratory Medicine

  https://www.nature.com/articles/s41533-018-0098-2

  Exercise-induced bronchoconstriction (EIB) can occur in individuals with and without asthma, and is prevalent among athletes of all levels. […] EIB can also prevent patients with asthma from participating in exercise and negatively impact their quality of life. […] EIB symptoms were improved by inhaling humid air at ambient temperatures and were completely prevented by inhaling fully saturated air, warmed to body temperature. These experiments formed the basis of the heat vs osmotic hypothesis to describe EIB pathophysiology. […] At present, the osmotic theory is widely accepted as the established underlying mechanism of EIB. The osmotic theory suggests that increased ventilation in the airways during periods of exercise leads to water loss from the airway surfaces by evaporation, thus dehydrating the airway surfaces and initiating the events that lead to the contraction of bronchial smooth muscle.

• #9 Exercise-induced bronchoconstriction: new evidence in pathogenesis, diagnosis and treatment | Asthma Research and Practice | Full Text

  https://asthmarp.biomedcentral.com/articles/10.1186/s40733-015-0004-4

  EIB was initially thought to be secondary to a mediator release from mast cells. […] Although mediator release does contribute to cause EIB, pathophysiologic changes induced by intense exercising are definitely more complex. At present, it is widely accepted that hyperventilation through the mouth associated with intense exercise causes the need for humidifying and heating large volumes of air during a short period of time. […] Elegant experiments performed by S.D. Anderson and coworkers show that the respiratory water loss and the increase in osmolarity of the airways surface liquid represent the major determinants of EIB (osmotic theory). […] The vasodilation associated with airways rewarming (thermal theory) may also play a role in inducing bronchial obstruction after exercise. […] However, in EIBwA, the epithelial damage of a large number of bronchial tree divisions down to peripheral airways represents the predominant pathogenic mechanism.

• #10 Exercise-Induced Bronchoconstriction – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK557554/

  Exercise-induced bronchoconstriction (EIB) describes a transient airway narrowing occurring during physical exertion. […] It is caused by an acute large increase in the amount of air entering the airways that require heating and humidifying. In susceptible individuals, this results in inflammatory, neuronal, and vascular changes ultimately resulting in contraction of the bronchial smooth muscle and symptoms of dyspnea, cough, chest tightness, mucus production, and wheezing. […] Exercise-induced bronchoconstriction results from the alteration of normal lung physiology occurring with evaporative water loss, thermal changes, and irritant exposure induced by a large increase in minute ventilation and demand on the respiratory system to heat and humidify air with exercise-related hyperpnea.

• #11 Exercise-Induced Bronchoconstriction – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK557554/

  As cells are dehydrated, there is an increase in osmolality, and the cells shrink in size, leading to an increase in cough, mucus, and loss of the physical barrier function of the epithelium. […] Decreased osmolality and increased electrolyte concentrations are thought to cause a regulatory increase in cell volume pulling fluid from the submucosal layer resulting in edema and release of inflammatory mediators, including histamine, leukotrienes, cysteine, tryptase, prostaglandins and mast cell degranulation. […] The osmotic theory is supported by evidence that EIB severity is directly related to the rate of water loss in the airways, EIB can be prevented by inhaling fully humidified air at body temperature, and bronchoconstriction can also be induced by inhalation of hyperosmolar saline. […] Long term exposure can lead to epithelial damage and shedding, with remodeling and inflammation resembling asthma. […] The process is partially reversible as studies have shown the lung damage and hyperresponsiveness improves over weeks to years when exposure and exercise are stopped.

• #12 Exercise-Induced Bronchoconstriction – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK557554/

  As cells are dehydrated, there is an increase in osmolality, and the cells shrink in size, leading to an increase in cough, mucus, and loss of the physical barrier function of the epithelium. […] Decreased osmolality and increased electrolyte concentrations are thought to cause a regulatory increase in cell volume pulling fluid from the submucosal layer resulting in edema and release of inflammatory mediators, including histamine, leukotrienes, cysteine, tryptase, prostaglandins and mast cell degranulation. […] The osmotic theory is supported by evidence that EIB severity is directly related to the rate of water loss in the airways, EIB can be prevented by inhaling fully humidified air at body temperature, and bronchoconstriction can also be induced by inhalation of hyperosmolar saline. […] Long term exposure can lead to epithelial damage and shedding, with remodeling and inflammation resembling asthma. […] The process is partially reversible as studies have shown the lung damage and hyperresponsiveness improves over weeks to years when exposure and exercise are stopped.

• #13 The mechanism of exercise-induced asthma is . – PubMed

  https://pubmed.ncbi.nlm.nih.gov/10984363/

  Exercise-induced asthma (EIA) refers to the transient narrowing of the airways that follows vigorous exercise. The mechanism whereby EIA occurs is thought to relate to the consequences of heating and humidifying large volumes of air during exercise. […] In 1978 airway cooling was identified as an important stimulus for EIA; however, severe EIA also occurred when hot dry air was inspired, and there was no abnormal cooling of the airways. […] In 1986 the thermal hypothesis proposed that cooling of the airways needed to be followed by rapid rewarming and that these two events caused a vasoconstriction and a reactive hyperemia of the bronchial microcirculation, together with edema of the airway wall, causing the airways to narrow after exercise. […] The osmotic, or airway-drying, hypothesis developed from 1982-1992 because neither airway cooling nor rewarming appeared to be necessary for EIA to occur. As water is evaporated from the airway surface liquid, it becomes hyperosmolar and provides an osmotic stimulus for water to move from any cell nearby, resulting in cell volume loss. It is proposed that the regulatory volume increase, after cell shrinkage, is the key event resulting in release of inflammatory mediators that cause airway smooth muscle to contract and the airways of asthmatic subjects to narrow. This event may or may not be associated with airway edema. […] The osmotic and thermal theories come together by considering that inspiration of cold air not only cools the airways but also increases the numbers of airway generations becoming dehydrated in the humidifying process.

• #14 Exercise-Induced Bronchoconstriction – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK557554/

  As cells are dehydrated, there is an increase in osmolality, and the cells shrink in size, leading to an increase in cough, mucus, and loss of the physical barrier function of the epithelium. […] Decreased osmolality and increased electrolyte concentrations are thought to cause a regulatory increase in cell volume pulling fluid from the submucosal layer resulting in edema and release of inflammatory mediators, including histamine, leukotrienes, cysteine, tryptase, prostaglandins and mast cell degranulation. […] The osmotic theory is supported by evidence that EIB severity is directly related to the rate of water loss in the airways, EIB can be prevented by inhaling fully humidified air at body temperature, and bronchoconstriction can also be induced by inhalation of hyperosmolar saline. […] Long term exposure can lead to epithelial damage and shedding, with remodeling and inflammation resembling asthma. […] The process is partially reversible as studies have shown the lung damage and hyperresponsiveness improves over weeks to years when exposure and exercise are stopped.

• #15 Exercise-induced bronchoconstriction: prevalence, pathophysiology, patient impact, diagnosis and management | npj Primary Care Respiratory Medicine

  https://www.nature.com/articles/s41533-018-0098-2

  During exercise-related hyperventilation, transient osmotic change at the airway surface occurs owing to reductions in epithelium liquid volume, which in turn triggers mast cell degranulation. […] Consequently, there is mast cell-mediated release of prostaglandins (prostaglandin D2), leukotrienes, histamine and tryptase. These signalling molecules are known to mediate airway smooth muscle contraction and increase mucus production and microvascular permeability and sensory nerve activation, and their release is thought to be the main stimulus for bronchoconstriction and airway oedema. […] In patients with EIB who do not have asthma, the mechanisms described by the osmotic theory are believed to be directly responsible for causing bronchoconstriction and associated symptoms. […] Intense ventilation of cold air can further increase dehydration of the airway surfaces and cause changes in bronchial blood flow, explaining why athletes performing in cold weather (e.g., ice hockey, Nordic skiing) demonstrate the highest rates of EIB. […] Epithelial injury that is caused by the inhalation of air pollutants and poorly conditioned air during exercise has also been hypothesised to be a contributing factor for the development of EIB in patients without asthma.

• #16 Exercise-induced Asthma and Bronchoconstriction | RT

  https://respiratory-therapy.com/disorders-diseases/chronic-pulmonary-disorders/asthma/exercise-induced-asthma-bronchoconstriction/

  Exercise-induced bronchoconstriction (EIB) and exercise-induced asthma (EIA) has been recognized in the medical community for a very long time. […] Why EIB/EIA occurs is not clear, but there are three commonly mentioned theories about the mechanism of these conditions. The first is described as the thermal theory. The mechanism here relates to the high volume of air moved in and out of the lung during exercise. This cools and dehydrates the airways, resulting in vasoconstriction, and stimulation of the cholinergic receptors that bring about bronchoconstriction and increased bronchial secretions. […] The second theory is described as the osmotic theory. The mechanism here relates to the bronchial dehydration that occurs with a large increase in minute ventilation. This dehydration causes a hyperosmotic environment in the airway walls, which activates the influx of eosinophils and mast cells. These cells cause the release of mediators such as leukotrienes, histamine, IL-8, tryptase, and prostaglandins. These mediators bring about smooth muscle fiber contraction and bronchoconstriction.

• #17 Exercise-Induced Bronchoconstriction – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK557554/

  As cells are dehydrated, there is an increase in osmolality, and the cells shrink in size, leading to an increase in cough, mucus, and loss of the physical barrier function of the epithelium. […] Decreased osmolality and increased electrolyte concentrations are thought to cause a regulatory increase in cell volume pulling fluid from the submucosal layer resulting in edema and release of inflammatory mediators, including histamine, leukotrienes, cysteine, tryptase, prostaglandins and mast cell degranulation. […] The osmotic theory is supported by evidence that EIB severity is directly related to the rate of water loss in the airways, EIB can be prevented by inhaling fully humidified air at body temperature, and bronchoconstriction can also be induced by inhalation of hyperosmolar saline. […] Long term exposure can lead to epithelial damage and shedding, with remodeling and inflammation resembling asthma. […] The process is partially reversible as studies have shown the lung damage and hyperresponsiveness improves over weeks to years when exposure and exercise are stopped.

• #18 Exercise-induced bronchoconstriction: prevalence, pathophysiology, patient impact, diagnosis and management | npj Primary Care Respiratory Medicine

  https://www.nature.com/articles/s41533-018-0098-2

  During exercise-related hyperventilation, transient osmotic change at the airway surface occurs owing to reductions in epithelium liquid volume, which in turn triggers mast cell degranulation. […] Consequently, there is mast cell-mediated release of prostaglandins (prostaglandin D2), leukotrienes, histamine and tryptase. These signalling molecules are known to mediate airway smooth muscle contraction and increase mucus production and microvascular permeability and sensory nerve activation, and their release is thought to be the main stimulus for bronchoconstriction and airway oedema. […] In patients with EIB who do not have asthma, the mechanisms described by the osmotic theory are believed to be directly responsible for causing bronchoconstriction and associated symptoms. […] Intense ventilation of cold air can further increase dehydration of the airway surfaces and cause changes in bronchial blood flow, explaining why athletes performing in cold weather (e.g., ice hockey, Nordic skiing) demonstrate the highest rates of EIB. […] Epithelial injury that is caused by the inhalation of air pollutants and poorly conditioned air during exercise has also been hypothesised to be a contributing factor for the development of EIB in patients without asthma.

• #19 Exercise-induced Asthma and Bronchoconstriction | RT

  https://respiratory-therapy.com/disorders-diseases/chronic-pulmonary-disorders/asthma/exercise-induced-asthma-bronchoconstriction/

  Exercise-induced bronchoconstriction (EIB) and exercise-induced asthma (EIA) has been recognized in the medical community for a very long time. […] Why EIB/EIA occurs is not clear, but there are three commonly mentioned theories about the mechanism of these conditions. The first is described as the thermal theory. The mechanism here relates to the high volume of air moved in and out of the lung during exercise. This cools and dehydrates the airways, resulting in vasoconstriction, and stimulation of the cholinergic receptors that bring about bronchoconstriction and increased bronchial secretions. […] The second theory is described as the osmotic theory. The mechanism here relates to the bronchial dehydration that occurs with a large increase in minute ventilation. This dehydration causes a hyperosmotic environment in the airway walls, which activates the influx of eosinophils and mast cells. These cells cause the release of mediators such as leukotrienes, histamine, IL-8, tryptase, and prostaglandins. These mediators bring about smooth muscle fiber contraction and bronchoconstriction.

• #20 Exercise-induced bronchoconstriction: prevalence, pathophysiology, patient impact, diagnosis and management | npj Primary Care Respiratory Medicine

  https://www.nature.com/articles/s41533-018-0098-2

  During exercise-related hyperventilation, transient osmotic change at the airway surface occurs owing to reductions in epithelium liquid volume, which in turn triggers mast cell degranulation. […] Consequently, there is mast cell-mediated release of prostaglandins (prostaglandin D2), leukotrienes, histamine and tryptase. These signalling molecules are known to mediate airway smooth muscle contraction and increase mucus production and microvascular permeability and sensory nerve activation, and their release is thought to be the main stimulus for bronchoconstriction and airway oedema. […] In patients with EIB who do not have asthma, the mechanisms described by the osmotic theory are believed to be directly responsible for causing bronchoconstriction and associated symptoms. […] Intense ventilation of cold air can further increase dehydration of the airway surfaces and cause changes in bronchial blood flow, explaining why athletes performing in cold weather (e.g., ice hockey, Nordic skiing) demonstrate the highest rates of EIB. […] Epithelial injury that is caused by the inhalation of air pollutants and poorly conditioned air during exercise has also been hypothesised to be a contributing factor for the development of EIB in patients without asthma.

• #21 Exercise-Induced Bronchoconstriction – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK557554/

  As cells are dehydrated, there is an increase in osmolality, and the cells shrink in size, leading to an increase in cough, mucus, and loss of the physical barrier function of the epithelium. […] Decreased osmolality and increased electrolyte concentrations are thought to cause a regulatory increase in cell volume pulling fluid from the submucosal layer resulting in edema and release of inflammatory mediators, including histamine, leukotrienes, cysteine, tryptase, prostaglandins and mast cell degranulation. […] The osmotic theory is supported by evidence that EIB severity is directly related to the rate of water loss in the airways, EIB can be prevented by inhaling fully humidified air at body temperature, and bronchoconstriction can also be induced by inhalation of hyperosmolar saline. […] Long term exposure can lead to epithelial damage and shedding, with remodeling and inflammation resembling asthma. […] The process is partially reversible as studies have shown the lung damage and hyperresponsiveness improves over weeks to years when exposure and exercise are stopped.

• #22 The mechanism of exercise-induced asthma is . – PubMed

  https://pubmed.ncbi.nlm.nih.gov/10984363/

  Exercise-induced asthma (EIA) refers to the transient narrowing of the airways that follows vigorous exercise. The mechanism whereby EIA occurs is thought to relate to the consequences of heating and humidifying large volumes of air during exercise. […] In 1978 airway cooling was identified as an important stimulus for EIA; however, severe EIA also occurred when hot dry air was inspired, and there was no abnormal cooling of the airways. […] In 1986 the thermal hypothesis proposed that cooling of the airways needed to be followed by rapid rewarming and that these two events caused a vasoconstriction and a reactive hyperemia of the bronchial microcirculation, together with edema of the airway wall, causing the airways to narrow after exercise. […] The osmotic, or airway-drying, hypothesis developed from 1982-1992 because neither airway cooling nor rewarming appeared to be necessary for EIA to occur. As water is evaporated from the airway surface liquid, it becomes hyperosmolar and provides an osmotic stimulus for water to move from any cell nearby, resulting in cell volume loss. It is proposed that the regulatory volume increase, after cell shrinkage, is the key event resulting in release of inflammatory mediators that cause airway smooth muscle to contract and the airways of asthmatic subjects to narrow. This event may or may not be associated with airway edema. […] The osmotic and thermal theories come together by considering that inspiration of cold air not only cools the airways but also increases the numbers of airway generations becoming dehydrated in the humidifying process.

• #23 Exercise-induced bronchoconstriction: new evidence in pathogenesis, diagnosis and treatment | Asthma Research and Practice | Full Text

  https://asthmarp.biomedcentral.com/articles/10.1186/s40733-015-0004-4

  EIB was initially thought to be secondary to a mediator release from mast cells. […] Although mediator release does contribute to cause EIB, pathophysiologic changes induced by intense exercising are definitely more complex. At present, it is widely accepted that hyperventilation through the mouth associated with intense exercise causes the need for humidifying and heating large volumes of air during a short period of time. […] Elegant experiments performed by S.D. Anderson and coworkers show that the respiratory water loss and the increase in osmolarity of the airways surface liquid represent the major determinants of EIB (osmotic theory). […] The vasodilation associated with airways rewarming (thermal theory) may also play a role in inducing bronchial obstruction after exercise. […] However, in EIBwA, the epithelial damage of a large number of bronchial tree divisions down to peripheral airways represents the predominant pathogenic mechanism.

• #24 The mechanism of exercise-induced asthma is . – PubMed

  https://pubmed.ncbi.nlm.nih.gov/10984363/

  Exercise-induced asthma (EIA) refers to the transient narrowing of the airways that follows vigorous exercise. The mechanism whereby EIA occurs is thought to relate to the consequences of heating and humidifying large volumes of air during exercise. […] In 1978 airway cooling was identified as an important stimulus for EIA; however, severe EIA also occurred when hot dry air was inspired, and there was no abnormal cooling of the airways. […] In 1986 the thermal hypothesis proposed that cooling of the airways needed to be followed by rapid rewarming and that these two events caused a vasoconstriction and a reactive hyperemia of the bronchial microcirculation, together with edema of the airway wall, causing the airways to narrow after exercise. […] The osmotic, or airway-drying, hypothesis developed from 1982-1992 because neither airway cooling nor rewarming appeared to be necessary for EIA to occur. As water is evaporated from the airway surface liquid, it becomes hyperosmolar and provides an osmotic stimulus for water to move from any cell nearby, resulting in cell volume loss. It is proposed that the regulatory volume increase, after cell shrinkage, is the key event resulting in release of inflammatory mediators that cause airway smooth muscle to contract and the airways of asthmatic subjects to narrow. This event may or may not be associated with airway edema. […] The osmotic and thermal theories come together by considering that inspiration of cold air not only cools the airways but also increases the numbers of airway generations becoming dehydrated in the humidifying process.

• #25 Exercise-induced Asthma and Bronchoconstriction | RT

  https://respiratory-therapy.com/disorders-diseases/chronic-pulmonary-disorders/asthma/exercise-induced-asthma-bronchoconstriction/

  Exercise-induced bronchoconstriction (EIB) and exercise-induced asthma (EIA) has been recognized in the medical community for a very long time. […] Why EIB/EIA occurs is not clear, but there are three commonly mentioned theories about the mechanism of these conditions. The first is described as the thermal theory. The mechanism here relates to the high volume of air moved in and out of the lung during exercise. This cools and dehydrates the airways, resulting in vasoconstriction, and stimulation of the cholinergic receptors that bring about bronchoconstriction and increased bronchial secretions. […] The second theory is described as the osmotic theory. The mechanism here relates to the bronchial dehydration that occurs with a large increase in minute ventilation. This dehydration causes a hyperosmotic environment in the airway walls, which activates the influx of eosinophils and mast cells. These cells cause the release of mediators such as leukotrienes, histamine, IL-8, tryptase, and prostaglandins. These mediators bring about smooth muscle fiber contraction and bronchoconstriction.

• #26 The mechanism of exercise-induced asthma is . – PubMed

  https://pubmed.ncbi.nlm.nih.gov/10984363/

  Exercise-induced asthma (EIA) refers to the transient narrowing of the airways that follows vigorous exercise. The mechanism whereby EIA occurs is thought to relate to the consequences of heating and humidifying large volumes of air during exercise. […] In 1978 airway cooling was identified as an important stimulus for EIA; however, severe EIA also occurred when hot dry air was inspired, and there was no abnormal cooling of the airways. […] In 1986 the thermal hypothesis proposed that cooling of the airways needed to be followed by rapid rewarming and that these two events caused a vasoconstriction and a reactive hyperemia of the bronchial microcirculation, together with edema of the airway wall, causing the airways to narrow after exercise. […] The osmotic, or airway-drying, hypothesis developed from 1982-1992 because neither airway cooling nor rewarming appeared to be necessary for EIA to occur. As water is evaporated from the airway surface liquid, it becomes hyperosmolar and provides an osmotic stimulus for water to move from any cell nearby, resulting in cell volume loss. It is proposed that the regulatory volume increase, after cell shrinkage, is the key event resulting in release of inflammatory mediators that cause airway smooth muscle to contract and the airways of asthmatic subjects to narrow. This event may or may not be associated with airway edema. […] The osmotic and thermal theories come together by considering that inspiration of cold air not only cools the airways but also increases the numbers of airway generations becoming dehydrated in the humidifying process.

• #27

  https://www.jci.org/articles/view/112549

  To determine if postexercise thermal events play a role in exercise-induced asthma (EIA), nine normal and eight asthmatic subjects on three occasions exercised while they inhaled frigid air. […] These data demonstrate that the severity of EIA is dependent not only on airway cooling but also upon the rapidity and magnitude of airway rewarming postchallenge.

• #28 Exercise-induced bronchoconstriction: new evidence in pathogenesis, diagnosis and treatment | Asthma Research and Practice | Full Text

  https://asthmarp.biomedcentral.com/articles/10.1186/s40733-015-0004-4

  EIB was initially thought to be secondary to a mediator release from mast cells. […] Although mediator release does contribute to cause EIB, pathophysiologic changes induced by intense exercising are definitely more complex. At present, it is widely accepted that hyperventilation through the mouth associated with intense exercise causes the need for humidifying and heating large volumes of air during a short period of time. […] Elegant experiments performed by S.D. Anderson and coworkers show that the respiratory water loss and the increase in osmolarity of the airways surface liquid represent the major determinants of EIB (osmotic theory). […] The vasodilation associated with airways rewarming (thermal theory) may also play a role in inducing bronchial obstruction after exercise. […] However, in EIBwA, the epithelial damage of a large number of bronchial tree divisions down to peripheral airways represents the predominant pathogenic mechanism.

• #29 Section 5: Exercise-Induced Asthma

  https://www.txhealthsteps.com/static/warehouse/1076-2011-Feb-1-3d1m08v5m6t78987cr9s/section_5.html

  The underlying mechanism in exercise-induced asthma involves the delivery of cold, dry air to the lower airways. With strenuous exercise, hyperventilation causes a bypass of the hydrating and warming functions of the nose and upper airway. The loss of heat and fluid from the airways results in a hyperosmolar lining fluid, which stimulates mediator release that results in epithelial and mast cell activation. Additionally, cooling of the airways is thought to be followed by vascular congestion and dilation of the bronchial circulation on rewarming after exercise. The resultant mucosal swelling and edema can produce airway narrowing. […] An inward sloping of the expiratory flow volume loop and a reduction in the expiratory flows [at least a 10 to 12 percent decrease in the Forced Expiratory Volume in 1 second (FEV1)] after exercise is considered diagnostic for EIA. Additionally, changes in the inspiratory portion of the flow volume loop can be seen that may be diagnostic of vocal cord dysfunction. […] Treatment for EIA can be divided between non-pharmacologic and pharmacologic therapies.

• #30

  https://www.jci.org/articles/view/112549

  To determine if postexercise thermal events play a role in exercise-induced asthma (EIA), nine normal and eight asthmatic subjects on three occasions exercised while they inhaled frigid air. […] These data demonstrate that the severity of EIA is dependent not only on airway cooling but also upon the rapidity and magnitude of airway rewarming postchallenge.

• #31

  https://www.jci.org/articles/view/109492

  Recent data demonstrate that the magnitude of the heat loss that occurs from the respiratory tract during exercise correlates with the degree of post-exertional obstruction that develops in asthmatics. […] Because it has been shown that inhaling 100% oxygen during exercise blunts the obstructive response, we wondered if this effect could be accounted for by differing values of heat exchange with air and oxygen breathing. […] Under all inspired gas conditions, oxygen breathing produced significantly less obstruction than air. […] As the latter fell, so did the magnitude of the postexercise obstruction. […] Thus, the effects of hyperoxia on exercise-induced asthma can be accounted for solely by alterations in heat exchange.

• #32 The mechanism of exercise-induced asthma is . – PubMed

  https://pubmed.ncbi.nlm.nih.gov/10984363/

  Exercise-induced asthma (EIA) refers to the transient narrowing of the airways that follows vigorous exercise. The mechanism whereby EIA occurs is thought to relate to the consequences of heating and humidifying large volumes of air during exercise. […] In 1978 airway cooling was identified as an important stimulus for EIA; however, severe EIA also occurred when hot dry air was inspired, and there was no abnormal cooling of the airways. […] In 1986 the thermal hypothesis proposed that cooling of the airways needed to be followed by rapid rewarming and that these two events caused a vasoconstriction and a reactive hyperemia of the bronchial microcirculation, together with edema of the airway wall, causing the airways to narrow after exercise. […] The osmotic, or airway-drying, hypothesis developed from 1982-1992 because neither airway cooling nor rewarming appeared to be necessary for EIA to occur. As water is evaporated from the airway surface liquid, it becomes hyperosmolar and provides an osmotic stimulus for water to move from any cell nearby, resulting in cell volume loss. It is proposed that the regulatory volume increase, after cell shrinkage, is the key event resulting in release of inflammatory mediators that cause airway smooth muscle to contract and the airways of asthmatic subjects to narrow. This event may or may not be associated with airway edema. […] The osmotic and thermal theories come together by considering that inspiration of cold air not only cools the airways but also increases the numbers of airway generations becoming dehydrated in the humidifying process.

• #33 Exercise-induced bronchoconstriction: new evidence in pathogenesis, diagnosis and treatment | Asthma Research and Practice | Full Text

  https://asthmarp.biomedcentral.com/articles/10.1186/s40733-015-0004-4

  EIB was initially thought to be secondary to a mediator release from mast cells. […] Although mediator release does contribute to cause EIB, pathophysiologic changes induced by intense exercising are definitely more complex. At present, it is widely accepted that hyperventilation through the mouth associated with intense exercise causes the need for humidifying and heating large volumes of air during a short period of time. […] Elegant experiments performed by S.D. Anderson and coworkers show that the respiratory water loss and the increase in osmolarity of the airways surface liquid represent the major determinants of EIB (osmotic theory). […] The vasodilation associated with airways rewarming (thermal theory) may also play a role in inducing bronchial obstruction after exercise. […] However, in EIBwA, the epithelial damage of a large number of bronchial tree divisions down to peripheral airways represents the predominant pathogenic mechanism.

• #34 The mechanism of exercise-induced asthma is . – PubMed

  https://pubmed.ncbi.nlm.nih.gov/10984363/

  Exercise-induced asthma (EIA) refers to the transient narrowing of the airways that follows vigorous exercise. The mechanism whereby EIA occurs is thought to relate to the consequences of heating and humidifying large volumes of air during exercise. […] In 1978 airway cooling was identified as an important stimulus for EIA; however, severe EIA also occurred when hot dry air was inspired, and there was no abnormal cooling of the airways. […] In 1986 the thermal hypothesis proposed that cooling of the airways needed to be followed by rapid rewarming and that these two events caused a vasoconstriction and a reactive hyperemia of the bronchial microcirculation, together with edema of the airway wall, causing the airways to narrow after exercise. […] The osmotic, or airway-drying, hypothesis developed from 1982-1992 because neither airway cooling nor rewarming appeared to be necessary for EIA to occur. As water is evaporated from the airway surface liquid, it becomes hyperosmolar and provides an osmotic stimulus for water to move from any cell nearby, resulting in cell volume loss. It is proposed that the regulatory volume increase, after cell shrinkage, is the key event resulting in release of inflammatory mediators that cause airway smooth muscle to contract and the airways of asthmatic subjects to narrow. This event may or may not be associated with airway edema. […] The osmotic and thermal theories come together by considering that inspiration of cold air not only cools the airways but also increases the numbers of airway generations becoming dehydrated in the humidifying process.

• #35 Exercise-induced bronchoconstriction: prevalence, pathophysiology, patient impact, diagnosis and management | npj Primary Care Respiratory Medicine

  https://www.nature.com/articles/s41533-018-0098-2

  During exercise-related hyperventilation, transient osmotic change at the airway surface occurs owing to reductions in epithelium liquid volume, which in turn triggers mast cell degranulation. […] Consequently, there is mast cell-mediated release of prostaglandins (prostaglandin D2), leukotrienes, histamine and tryptase. These signalling molecules are known to mediate airway smooth muscle contraction and increase mucus production and microvascular permeability and sensory nerve activation, and their release is thought to be the main stimulus for bronchoconstriction and airway oedema. […] In patients with EIB who do not have asthma, the mechanisms described by the osmotic theory are believed to be directly responsible for causing bronchoconstriction and associated symptoms. […] Intense ventilation of cold air can further increase dehydration of the airway surfaces and cause changes in bronchial blood flow, explaining why athletes performing in cold weather (e.g., ice hockey, Nordic skiing) demonstrate the highest rates of EIB. […] Epithelial injury that is caused by the inhalation of air pollutants and poorly conditioned air during exercise has also been hypothesised to be a contributing factor for the development of EIB in patients without asthma.

• #36 Exercise-Induced Bronchoconstriction – a Short Review with Practical Recommendations

  https://www.germanjournalsportsmedicine.com/archive/archive-2012/heft-10/exercise-induced-bronchoconstriction-a-short-review-with-practical-recommendations/

  The classic early onset pattern reflects the signs of allergic asthma characterized by atopy, eosinophilic airway inflammation and positive methacholine responsiveness with a rapid onset of symptoms at exercise initiation. The divergent pattern comprises a late onset phenotype during a sports career and therefore with more phases of high ventilation. […] Problematic environmental conditions during the activity such as cold ambient temperatures for winter sports or organic chlorine products from indoor swimming pools clearly enhance the effect of intensive physical activity on both conditions.

• #37 Exercise-induced Asthma and Bronchoconstriction | RT

  https://respiratory-therapy.com/disorders-diseases/chronic-pulmonary-disorders/asthma/exercise-induced-asthma-bronchoconstriction/

  The third theory is described as the theory of epithelium microtrauma. The mechanism here relates to small airway epithelium dehydration combined with exposure to shear stress caused increased airflow and increased transepithelial pressure gradient. […] With repeated damage and repair, bronchial hyperreactivity and airway remodeling occurs.

• #38 Exercise-Induced Bronchoconstriction – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK557554/

  As cells are dehydrated, there is an increase in osmolality, and the cells shrink in size, leading to an increase in cough, mucus, and loss of the physical barrier function of the epithelium. […] Decreased osmolality and increased electrolyte concentrations are thought to cause a regulatory increase in cell volume pulling fluid from the submucosal layer resulting in edema and release of inflammatory mediators, including histamine, leukotrienes, cysteine, tryptase, prostaglandins and mast cell degranulation. […] The osmotic theory is supported by evidence that EIB severity is directly related to the rate of water loss in the airways, EIB can be prevented by inhaling fully humidified air at body temperature, and bronchoconstriction can also be induced by inhalation of hyperosmolar saline. […] Long term exposure can lead to epithelial damage and shedding, with remodeling and inflammation resembling asthma. […] The process is partially reversible as studies have shown the lung damage and hyperresponsiveness improves over weeks to years when exposure and exercise are stopped.

• #39 Exercise-induced bronchoconstriction: prevalence, pathophysiology, patient impact, diagnosis and management | npj Primary Care Respiratory Medicine

  https://www.nature.com/articles/s41533-018-0098-2

  During exercise-related hyperventilation, transient osmotic change at the airway surface occurs owing to reductions in epithelium liquid volume, which in turn triggers mast cell degranulation. […] Consequently, there is mast cell-mediated release of prostaglandins (prostaglandin D2), leukotrienes, histamine and tryptase. These signalling molecules are known to mediate airway smooth muscle contraction and increase mucus production and microvascular permeability and sensory nerve activation, and their release is thought to be the main stimulus for bronchoconstriction and airway oedema. […] In patients with EIB who do not have asthma, the mechanisms described by the osmotic theory are believed to be directly responsible for causing bronchoconstriction and associated symptoms. […] Intense ventilation of cold air can further increase dehydration of the airway surfaces and cause changes in bronchial blood flow, explaining why athletes performing in cold weather (e.g., ice hockey, Nordic skiing) demonstrate the highest rates of EIB. […] Epithelial injury that is caused by the inhalation of air pollutants and poorly conditioned air during exercise has also been hypothesised to be a contributing factor for the development of EIB in patients without asthma.

• #40 Exercise-Induced Bronchoconstriction – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK557554/

  As cells are dehydrated, there is an increase in osmolality, and the cells shrink in size, leading to an increase in cough, mucus, and loss of the physical barrier function of the epithelium. […] Decreased osmolality and increased electrolyte concentrations are thought to cause a regulatory increase in cell volume pulling fluid from the submucosal layer resulting in edema and release of inflammatory mediators, including histamine, leukotrienes, cysteine, tryptase, prostaglandins and mast cell degranulation. […] The osmotic theory is supported by evidence that EIB severity is directly related to the rate of water loss in the airways, EIB can be prevented by inhaling fully humidified air at body temperature, and bronchoconstriction can also be induced by inhalation of hyperosmolar saline. […] Long term exposure can lead to epithelial damage and shedding, with remodeling and inflammation resembling asthma. […] The process is partially reversible as studies have shown the lung damage and hyperresponsiveness improves over weeks to years when exposure and exercise are stopped.

• #41

  https://journals.lww.com/acsm-csmr/fulltext/2016/05000/exercise_induced_bronchoconstriction.5.aspx

  Transient immunosuppression also may develop in athletes during periods of intense training, with increased susceptibility to respiratory infections (especially viral), which may increase airway response to exercise acutely and affect overall asthma control (1,2). […] The key stimulus is airway dehydration due to increased ventilation, resulting in a loss of heat, drying of the airways, as well as increased intracellular osmolarity. This triggers the release of inflammatory mediators, leading to airway smooth muscle contraction and airway edema (1,2). […] Mechanical stress/injury to airway epithelium plays a role in the acute response to exercise as well as in the development of airway remodeling in athletes through their effects on smooth muscle contractile properties causing hypersensitivity leading to bronchoconstriction (1,2).

• #42 Exercise-induced Asthma and Bronchoconstriction | RT

  https://respiratory-therapy.com/disorders-diseases/chronic-pulmonary-disorders/asthma/exercise-induced-asthma-bronchoconstriction/

  The third theory is described as the theory of epithelium microtrauma. The mechanism here relates to small airway epithelium dehydration combined with exposure to shear stress caused increased airflow and increased transepithelial pressure gradient. […] With repeated damage and repair, bronchial hyperreactivity and airway remodeling occurs.

• #43 Exercise-induced Asthma and Bronchoconstriction | RT

  https://respiratory-therapy.com/disorders-diseases/chronic-pulmonary-disorders/asthma/exercise-induced-asthma-bronchoconstriction/

  The third theory is described as the theory of epithelium microtrauma. The mechanism here relates to small airway epithelium dehydration combined with exposure to shear stress caused increased airflow and increased transepithelial pressure gradient. […] With repeated damage and repair, bronchial hyperreactivity and airway remodeling occurs.

• #44 Exercise-Induced Bronchoconstriction – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK557554/

  As cells are dehydrated, there is an increase in osmolality, and the cells shrink in size, leading to an increase in cough, mucus, and loss of the physical barrier function of the epithelium. […] Decreased osmolality and increased electrolyte concentrations are thought to cause a regulatory increase in cell volume pulling fluid from the submucosal layer resulting in edema and release of inflammatory mediators, including histamine, leukotrienes, cysteine, tryptase, prostaglandins and mast cell degranulation. […] The osmotic theory is supported by evidence that EIB severity is directly related to the rate of water loss in the airways, EIB can be prevented by inhaling fully humidified air at body temperature, and bronchoconstriction can also be induced by inhalation of hyperosmolar saline. […] Long term exposure can lead to epithelial damage and shedding, with remodeling and inflammation resembling asthma. […] The process is partially reversible as studies have shown the lung damage and hyperresponsiveness improves over weeks to years when exposure and exercise are stopped.

• #45 Exercise-induced asthma in asthmatic children. Predisposing factors | Allergologia et Immunopathologia

  https://www.elsevier.es/es-revista-allergologia-et-immunopathologia-105-articulo-exercise-induced-asthma-in-asthmatic-children–S0301054608725357

  It is recognized that airway inflammation plays a central role in the pathogenesis of asthma, but how it relates to exercise-induced bronchoconstriction (EIB) is not completely understood. Various studies have investigated the relationship between EIB and baseline concentrations of inflammatory markers in exhaled condensated breath and induced sputum. The baseline concentrations of inflammatory markers are higher in asthmatic children with EIB. […] The exposure to indoor allergens may favour the development of EIB. Exercise-induced bronchoconstriction has been associated with eosinophilic airway inflammation, bronchial hyper responsiveness (BHR), atopy and airway obstruction. […] The results of the multivariable logistic regression analysis confirmed indoor allergen sensitization as a risk factor to EIB and the immunotherapy treatment as a protector factor in the development of EIB.

• #46

  https://www.termedia.pl/Asthma-and-exercise-induced-respiratory-disorders-r-nin-athletes-The-position-paper-of-the-Polish-Society-r-nof-Allergology-and-Polish-Society-of-Sports-Medicine,123,36304,1,0.html

  Asthma is a heterogeneous disease typically associated with a chronic respiratory inflammation which is defined as a syndrome of such respiratory symptoms as wheezing, dyspnoea, chest tightening and coughing which differ in time and intensity and are connected with variable airways obstruction. Currently discussed pathogenic mechanisms potentially responsible for exercise-induced bronchoconstriction in people who practice high-intensity exercise on a regular basis include: osmotic and thermal changes in airways mucosa caused by exercise-induced hyperventilation (osmotic and thermal hypothesis); damage to respiratory epithelium; increasing severity of the airway inflammation; neural activation. Osmotic and thermal changes to bronchial mucosa are the rationale behind the osmotic and thermal hypotheses which are considered as classical ones in the attempts to explain the pathogenesis of EIB in athletes. Increased water evaporation from the mucosa during exercise leads to the increase in the osmolarity of the fluid covering the respiratory epithelium. The changes to osmotic relations result in the lysis of the cells and the release of the mediators including cysteinyl leukotrienes which have strong bronchoconstrictive properties. Furthermore, the airway cooling activates cholinergic receptors, which causes increased tension of bronchial smooth muscles and enhanced fluid secretion in airways. Directly after exercise completion the respiratory tract warming commences and leads to secondary hyperaemia and increased capillary permeability in the bronchial wall. A rise in the number of inflammatory cells (eosinophils, neutrophils, epithelial cells) has been observed in the respiratory tract of athletes. A large body of evidence has already proven that damage to respiratory epithelium during exercise (particularly in adverse environmental conditions) significantly increases susceptibility to EIB. The conclusions mentioned above were drawn from the analyses of the markers of respiratory epithelium damage (e.g. protein CC16). Unfavourable and harmful environmental conditions for exercise can also contribute to respiratory tract damage and increased susceptibility to EIB. The most spectacular associations were found in the relations between exposure to chlorine compounds (trichloramine) while swimming and the increase in bronchial hyperreactivity (BHR). Exposure to dry and cold air while practicing endurance winter sports can be another factor which increases the risk of EIB. Some other studies, however, do not provide results which are compelling enough to significantly associate exercise in adverse conditions with predisposition to EIB. It is suggested that damage to respiratory epithelium occurs only in the presence of BHR symptoms or exercise-induced bronchoconstriction. Consequently, mutual causation and the sequence of the described phenomena are still open to discussion. The innervation of the respiratory tract is mainly composed of parasympathetic fibres. Stimulation of parasympathetic cholinergic fibres results in bronchoconstriction. In the light of the recent research, high-intensity exercise is thought to magnify para-sympathomimetic activity, thereby increasing the tension of bronchial smooth muscles and, consequently, increasing the probability of EIB. The relationship between BHR and some autonomic nervous system-dependent responses, e.g. perspiration, tearing, saliva production, have been reported. However, although chronically enhanced parasympathomimetic nervous system activity is observed there are data which do not confirm the correlation between BHR and dysfunctional autonomic regulation. Some authors suggest that autonomic modulation may be involved in BHR development but only when accompanied by the risk of inspiring harmful components of the air. Neurogenic inflammation is also considered in the investigation of EIB pathogenesis. High-intensity exercise elevates the concentration of substance P which is one of the key mediators of neurogenic inflammation. Acetylcholine and nerve growth factor (NGF) have also been put forward as potentially involved in the development of the EIB-provoking inflammation. Since none of the aforementioned mechanisms fully explains the pathogenesis of EIB, potential interaction of several mechanisms should be taken into account while assessing individual predisposition to exercise-induced respiratory symptoms. The identification of the athletes susceptible to EIB appears to be the key issue here as it may contribute to the improvement of preventive measures. The observations made within the last 20-30 years indicate that the asthma rate is higher in athletes, especially those practicing endurance sports. The risk of asthma in the athletes with atopy symptoms is several times higher than in healthy population.

• #47 Exercise induced asthma &bronchospasm | PPT

  https://www.slideshare.net/slideshow/exercise-induced-asthma-bronchospasm/16736403

  Exercise-induced asthma (EIA) and bronchospasm are triggered by exercise in patients with or without chronic asthma. EIA is diagnosed when exercise causes a 15% decrease in lung function and symptoms start after exercise and resolve within 60 minutes. It is common, affecting 10-20% of the general population and up to 90% of asthmatics. […] There are 2 theories for EIA pathogenesis: thermal osmotic Thermal hypothesis, there is no role for biochemical mediators. Osmotic theory has been gaining a wider acceptance in recent years. […] Several studies have noted an increase in the concentration of cysteinyl leukotrienes (CysLTs) in the airways of patients with EIB. A recent study found that the fraction of exhaled nitric oxide (FENO) is elevated in asthmatic patients with EIB, Angiopoetin 2, a mediator that enhances microvascular permeability, is increased in the airways in EIB Mast cell infiltration of the airways has also been implicated in EIB. […] Symptoms begin during or after exercise and usually worsen 5-20 minutes after stopping activity. Some people experience a late-phase reaction 4-12 hours after exercising. Symptoms usually less severe.

• #48 MECHANISM OF EXERCISE INDUCED ASTHMA | Pediatric Research

  https://www.nature.com/articles/pr19771273

  There is uncertainty regarding the relative importance of chemical mediator release (humoral) and direct physical stimulation of epithelial irritant receptors (neurogenic) in producing exercise induced asthma (EIA). […] We conclude that EIA is due to the release of chemical mediators from bronchial mast cells, rather than by a direct physical effect on the irritant receptors. Moreover, the results with steam imply that the stimulus for this release is the cooling and/or drying effect of the inspired air as a result of the hyperventilation occurring during exercise. Once released these mediators, particularly histamine, then presumably induce bronchoconstriction by activating epithelial irritant receptors.

• #49 Exercise induced asthma &bronchospasm | PPT

  https://www.slideshare.net/slideshow/exercise-induced-asthma-bronchospasm/16736403

  Exercise-induced asthma (EIA) and bronchospasm are triggered by exercise in patients with or without chronic asthma. EIA is diagnosed when exercise causes a 15% decrease in lung function and symptoms start after exercise and resolve within 60 minutes. It is common, affecting 10-20% of the general population and up to 90% of asthmatics. […] There are 2 theories for EIA pathogenesis: thermal osmotic Thermal hypothesis, there is no role for biochemical mediators. Osmotic theory has been gaining a wider acceptance in recent years. […] Several studies have noted an increase in the concentration of cysteinyl leukotrienes (CysLTs) in the airways of patients with EIB. A recent study found that the fraction of exhaled nitric oxide (FENO) is elevated in asthmatic patients with EIB, Angiopoetin 2, a mediator that enhances microvascular permeability, is increased in the airways in EIB Mast cell infiltration of the airways has also been implicated in EIB. […] Symptoms begin during or after exercise and usually worsen 5-20 minutes after stopping activity. Some people experience a late-phase reaction 4-12 hours after exercising. Symptoms usually less severe.

• #50 Exercise induced asthma &bronchospasm | PPT

  https://www.slideshare.net/slideshow/exercise-induced-asthma-bronchospasm/16736403

  Exercise-induced asthma (EIA) and bronchospasm are triggered by exercise in patients with or without chronic asthma. EIA is diagnosed when exercise causes a 15% decrease in lung function and symptoms start after exercise and resolve within 60 minutes. It is common, affecting 10-20% of the general population and up to 90% of asthmatics. […] There are 2 theories for EIA pathogenesis: thermal osmotic Thermal hypothesis, there is no role for biochemical mediators. Osmotic theory has been gaining a wider acceptance in recent years. […] Several studies have noted an increase in the concentration of cysteinyl leukotrienes (CysLTs) in the airways of patients with EIB. A recent study found that the fraction of exhaled nitric oxide (FENO) is elevated in asthmatic patients with EIB, Angiopoetin 2, a mediator that enhances microvascular permeability, is increased in the airways in EIB Mast cell infiltration of the airways has also been implicated in EIB. […] Symptoms begin during or after exercise and usually worsen 5-20 minutes after stopping activity. Some people experience a late-phase reaction 4-12 hours after exercising. Symptoms usually less severe.

• #51 Exercise induced asthma &bronchospasm | PPT

  https://www.slideshare.net/slideshow/exercise-induced-asthma-bronchospasm/16736403

  Exercise-induced asthma (EIA) and bronchospasm are triggered by exercise in patients with or without chronic asthma. EIA is diagnosed when exercise causes a 15% decrease in lung function and symptoms start after exercise and resolve within 60 minutes. It is common, affecting 10-20% of the general population and up to 90% of asthmatics. […] There are 2 theories for EIA pathogenesis: thermal osmotic Thermal hypothesis, there is no role for biochemical mediators. Osmotic theory has been gaining a wider acceptance in recent years. […] Several studies have noted an increase in the concentration of cysteinyl leukotrienes (CysLTs) in the airways of patients with EIB. A recent study found that the fraction of exhaled nitric oxide (FENO) is elevated in asthmatic patients with EIB, Angiopoetin 2, a mediator that enhances microvascular permeability, is increased in the airways in EIB Mast cell infiltration of the airways has also been implicated in EIB. […] Symptoms begin during or after exercise and usually worsen 5-20 minutes after stopping activity. Some people experience a late-phase reaction 4-12 hours after exercising. Symptoms usually less severe.

• #52

  https://www.termedia.pl/Asthma-and-exercise-induced-respiratory-disorders-r-nin-athletes-The-position-paper-of-the-Polish-Society-r-nof-Allergology-and-Polish-Society-of-Sports-Medicine,123,36304,1,0.html

  Asthma is a heterogeneous disease typically associated with a chronic respiratory inflammation which is defined as a syndrome of such respiratory symptoms as wheezing, dyspnoea, chest tightening and coughing which differ in time and intensity and are connected with variable airways obstruction. Currently discussed pathogenic mechanisms potentially responsible for exercise-induced bronchoconstriction in people who practice high-intensity exercise on a regular basis include: osmotic and thermal changes in airways mucosa caused by exercise-induced hyperventilation (osmotic and thermal hypothesis); damage to respiratory epithelium; increasing severity of the airway inflammation; neural activation. Osmotic and thermal changes to bronchial mucosa are the rationale behind the osmotic and thermal hypotheses which are considered as classical ones in the attempts to explain the pathogenesis of EIB in athletes. Increased water evaporation from the mucosa during exercise leads to the increase in the osmolarity of the fluid covering the respiratory epithelium. The changes to osmotic relations result in the lysis of the cells and the release of the mediators including cysteinyl leukotrienes which have strong bronchoconstrictive properties. Furthermore, the airway cooling activates cholinergic receptors, which causes increased tension of bronchial smooth muscles and enhanced fluid secretion in airways. Directly after exercise completion the respiratory tract warming commences and leads to secondary hyperaemia and increased capillary permeability in the bronchial wall. A rise in the number of inflammatory cells (eosinophils, neutrophils, epithelial cells) has been observed in the respiratory tract of athletes. A large body of evidence has already proven that damage to respiratory epithelium during exercise (particularly in adverse environmental conditions) significantly increases susceptibility to EIB. The conclusions mentioned above were drawn from the analyses of the markers of respiratory epithelium damage (e.g. protein CC16). Unfavourable and harmful environmental conditions for exercise can also contribute to respiratory tract damage and increased susceptibility to EIB. The most spectacular associations were found in the relations between exposure to chlorine compounds (trichloramine) while swimming and the increase in bronchial hyperreactivity (BHR). Exposure to dry and cold air while practicing endurance winter sports can be another factor which increases the risk of EIB. Some other studies, however, do not provide results which are compelling enough to significantly associate exercise in adverse conditions with predisposition to EIB. It is suggested that damage to respiratory epithelium occurs only in the presence of BHR symptoms or exercise-induced bronchoconstriction. Consequently, mutual causation and the sequence of the described phenomena are still open to discussion. The innervation of the respiratory tract is mainly composed of parasympathetic fibres. Stimulation of parasympathetic cholinergic fibres results in bronchoconstriction. In the light of the recent research, high-intensity exercise is thought to magnify para-sympathomimetic activity, thereby increasing the tension of bronchial smooth muscles and, consequently, increasing the probability of EIB. The relationship between BHR and some autonomic nervous system-dependent responses, e.g. perspiration, tearing, saliva production, have been reported. However, although chronically enhanced parasympathomimetic nervous system activity is observed there are data which do not confirm the correlation between BHR and dysfunctional autonomic regulation. Some authors suggest that autonomic modulation may be involved in BHR development but only when accompanied by the risk of inspiring harmful components of the air. Neurogenic inflammation is also considered in the investigation of EIB pathogenesis. High-intensity exercise elevates the concentration of substance P which is one of the key mediators of neurogenic inflammation. Acetylcholine and nerve growth factor (NGF) have also been put forward as potentially involved in the development of the EIB-provoking inflammation. Since none of the aforementioned mechanisms fully explains the pathogenesis of EIB, potential interaction of several mechanisms should be taken into account while assessing individual predisposition to exercise-induced respiratory symptoms. The identification of the athletes susceptible to EIB appears to be the key issue here as it may contribute to the improvement of preventive measures. The observations made within the last 20-30 years indicate that the asthma rate is higher in athletes, especially those practicing endurance sports. The risk of asthma in the athletes with atopy symptoms is several times higher than in healthy population.

• #53

  https://www.termedia.pl/Asthma-and-exercise-induced-respiratory-disorders-r-nin-athletes-The-position-paper-of-the-Polish-Society-r-nof-Allergology-and-Polish-Society-of-Sports-Medicine,123,36304,1,0.html

  Asthma is a heterogeneous disease typically associated with a chronic respiratory inflammation which is defined as a syndrome of such respiratory symptoms as wheezing, dyspnoea, chest tightening and coughing which differ in time and intensity and are connected with variable airways obstruction. Currently discussed pathogenic mechanisms potentially responsible for exercise-induced bronchoconstriction in people who practice high-intensity exercise on a regular basis include: osmotic and thermal changes in airways mucosa caused by exercise-induced hyperventilation (osmotic and thermal hypothesis); damage to respiratory epithelium; increasing severity of the airway inflammation; neural activation. Osmotic and thermal changes to bronchial mucosa are the rationale behind the osmotic and thermal hypotheses which are considered as classical ones in the attempts to explain the pathogenesis of EIB in athletes. Increased water evaporation from the mucosa during exercise leads to the increase in the osmolarity of the fluid covering the respiratory epithelium. The changes to osmotic relations result in the lysis of the cells and the release of the mediators including cysteinyl leukotrienes which have strong bronchoconstrictive properties. Furthermore, the airway cooling activates cholinergic receptors, which causes increased tension of bronchial smooth muscles and enhanced fluid secretion in airways. Directly after exercise completion the respiratory tract warming commences and leads to secondary hyperaemia and increased capillary permeability in the bronchial wall. A rise in the number of inflammatory cells (eosinophils, neutrophils, epithelial cells) has been observed in the respiratory tract of athletes. A large body of evidence has already proven that damage to respiratory epithelium during exercise (particularly in adverse environmental conditions) significantly increases susceptibility to EIB. The conclusions mentioned above were drawn from the analyses of the markers of respiratory epithelium damage (e.g. protein CC16). Unfavourable and harmful environmental conditions for exercise can also contribute to respiratory tract damage and increased susceptibility to EIB. The most spectacular associations were found in the relations between exposure to chlorine compounds (trichloramine) while swimming and the increase in bronchial hyperreactivity (BHR). Exposure to dry and cold air while practicing endurance winter sports can be another factor which increases the risk of EIB. Some other studies, however, do not provide results which are compelling enough to significantly associate exercise in adverse conditions with predisposition to EIB. It is suggested that damage to respiratory epithelium occurs only in the presence of BHR symptoms or exercise-induced bronchoconstriction. Consequently, mutual causation and the sequence of the described phenomena are still open to discussion. The innervation of the respiratory tract is mainly composed of parasympathetic fibres. Stimulation of parasympathetic cholinergic fibres results in bronchoconstriction. In the light of the recent research, high-intensity exercise is thought to magnify para-sympathomimetic activity, thereby increasing the tension of bronchial smooth muscles and, consequently, increasing the probability of EIB. The relationship between BHR and some autonomic nervous system-dependent responses, e.g. perspiration, tearing, saliva production, have been reported. However, although chronically enhanced parasympathomimetic nervous system activity is observed there are data which do not confirm the correlation between BHR and dysfunctional autonomic regulation. Some authors suggest that autonomic modulation may be involved in BHR development but only when accompanied by the risk of inspiring harmful components of the air. Neurogenic inflammation is also considered in the investigation of EIB pathogenesis. High-intensity exercise elevates the concentration of substance P which is one of the key mediators of neurogenic inflammation. Acetylcholine and nerve growth factor (NGF) have also been put forward as potentially involved in the development of the EIB-provoking inflammation. Since none of the aforementioned mechanisms fully explains the pathogenesis of EIB, potential interaction of several mechanisms should be taken into account while assessing individual predisposition to exercise-induced respiratory symptoms. The identification of the athletes susceptible to EIB appears to be the key issue here as it may contribute to the improvement of preventive measures. The observations made within the last 20-30 years indicate that the asthma rate is higher in athletes, especially those practicing endurance sports. The risk of asthma in the athletes with atopy symptoms is several times higher than in healthy population.

• #54 Exercise-induced bronchoconstriction: new evidence in pathogenesis, diagnosis and treatment | Asthma Research and Practice | Full Text

  https://asthmarp.biomedcentral.com/articles/10.1186/s40733-015-0004-4

  A direct effect of viral infections, occupational agents and exercise may in fact represent a causal mechanism of bronchoconstriction, alternative to the classic eosinophilic mast cell-dependent pathway occurring in allergic asthma. […] The role of epithelial damage and of substances released by the epithelium and found in sputum, such as interleukin-8 and leukotrienes, and in serum or urines, such as Nerve Growth Factor (NGF) and the Clara cell protein CC16, may also explain the heterogeneous inflammatory response reported in EIBwA. […] The importance of aquaporin, expressed by the subepithelial glandular cells, in regulating the water transport through the epithelium, as well as the increased mucus production, as shown by the increased expression of MUC5AC in induced sputum, may be also relevant in EIBwA. […] At last, autonomic dysregulation may also have a role in causing bronchial obstruction in EIBwA, both through the basal increased parasympathetic tone shown in athletes and through reflex mechanisms induced by exercise.

• #55 Exercise-induced asthma in asthmatic children. Predisposing factors | Allergologia et Immunopathologia

  https://www.elsevier.es/es-revista-allergologia-et-immunopathologia-105-articulo-exercise-induced-asthma-in-asthmatic-children–S0301054608725357

  It is recognized that airway inflammation plays a central role in the pathogenesis of asthma, but how it relates to exercise-induced bronchoconstriction (EIB) is not completely understood. Various studies have investigated the relationship between EIB and baseline concentrations of inflammatory markers in exhaled condensated breath and induced sputum. The baseline concentrations of inflammatory markers are higher in asthmatic children with EIB. […] The exposure to indoor allergens may favour the development of EIB. Exercise-induced bronchoconstriction has been associated with eosinophilic airway inflammation, bronchial hyper responsiveness (BHR), atopy and airway obstruction. […] The results of the multivariable logistic regression analysis confirmed indoor allergen sensitization as a risk factor to EIB and the immunotherapy treatment as a protector factor in the development of EIB.

• #56 Exercise-induced bronchoconstriction: prevalence, pathophysiology, patient impact, diagnosis and management | npj Primary Care Respiratory Medicine

  https://www.nature.com/articles/s41533-018-0098-2

  During exercise-related hyperventilation, transient osmotic change at the airway surface occurs owing to reductions in epithelium liquid volume, which in turn triggers mast cell degranulation. […] Consequently, there is mast cell-mediated release of prostaglandins (prostaglandin D2), leukotrienes, histamine and tryptase. These signalling molecules are known to mediate airway smooth muscle contraction and increase mucus production and microvascular permeability and sensory nerve activation, and their release is thought to be the main stimulus for bronchoconstriction and airway oedema. […] In patients with EIB who do not have asthma, the mechanisms described by the osmotic theory are believed to be directly responsible for causing bronchoconstriction and associated symptoms. […] Intense ventilation of cold air can further increase dehydration of the airway surfaces and cause changes in bronchial blood flow, explaining why athletes performing in cold weather (e.g., ice hockey, Nordic skiing) demonstrate the highest rates of EIB. […] Epithelial injury that is caused by the inhalation of air pollutants and poorly conditioned air during exercise has also been hypothesised to be a contributing factor for the development of EIB in patients without asthma.

• #57 Exercise-induced bronchoconstriction: new evidence in pathogenesis, diagnosis and treatment | Asthma Research and Practice | Full Text

  https://asthmarp.biomedcentral.com/articles/10.1186/s40733-015-0004-4

  A direct effect of viral infections, occupational agents and exercise may in fact represent a causal mechanism of bronchoconstriction, alternative to the classic eosinophilic mast cell-dependent pathway occurring in allergic asthma. […] The role of epithelial damage and of substances released by the epithelium and found in sputum, such as interleukin-8 and leukotrienes, and in serum or urines, such as Nerve Growth Factor (NGF) and the Clara cell protein CC16, may also explain the heterogeneous inflammatory response reported in EIBwA. […] The importance of aquaporin, expressed by the subepithelial glandular cells, in regulating the water transport through the epithelium, as well as the increased mucus production, as shown by the increased expression of MUC5AC in induced sputum, may be also relevant in EIBwA. […] At last, autonomic dysregulation may also have a role in causing bronchial obstruction in EIBwA, both through the basal increased parasympathetic tone shown in athletes and through reflex mechanisms induced by exercise.

• #58

  https://www.termedia.pl/Asthma-and-exercise-induced-respiratory-disorders-r-nin-athletes-The-position-paper-of-the-Polish-Society-r-nof-Allergology-and-Polish-Society-of-Sports-Medicine,123,36304,1,0.html

  Asthma is a heterogeneous disease typically associated with a chronic respiratory inflammation which is defined as a syndrome of such respiratory symptoms as wheezing, dyspnoea, chest tightening and coughing which differ in time and intensity and are connected with variable airways obstruction. Currently discussed pathogenic mechanisms potentially responsible for exercise-induced bronchoconstriction in people who practice high-intensity exercise on a regular basis include: osmotic and thermal changes in airways mucosa caused by exercise-induced hyperventilation (osmotic and thermal hypothesis); damage to respiratory epithelium; increasing severity of the airway inflammation; neural activation. Osmotic and thermal changes to bronchial mucosa are the rationale behind the osmotic and thermal hypotheses which are considered as classical ones in the attempts to explain the pathogenesis of EIB in athletes. Increased water evaporation from the mucosa during exercise leads to the increase in the osmolarity of the fluid covering the respiratory epithelium. The changes to osmotic relations result in the lysis of the cells and the release of the mediators including cysteinyl leukotrienes which have strong bronchoconstrictive properties. Furthermore, the airway cooling activates cholinergic receptors, which causes increased tension of bronchial smooth muscles and enhanced fluid secretion in airways. Directly after exercise completion the respiratory tract warming commences and leads to secondary hyperaemia and increased capillary permeability in the bronchial wall. A rise in the number of inflammatory cells (eosinophils, neutrophils, epithelial cells) has been observed in the respiratory tract of athletes. A large body of evidence has already proven that damage to respiratory epithelium during exercise (particularly in adverse environmental conditions) significantly increases susceptibility to EIB. The conclusions mentioned above were drawn from the analyses of the markers of respiratory epithelium damage (e.g. protein CC16). Unfavourable and harmful environmental conditions for exercise can also contribute to respiratory tract damage and increased susceptibility to EIB. The most spectacular associations were found in the relations between exposure to chlorine compounds (trichloramine) while swimming and the increase in bronchial hyperreactivity (BHR). Exposure to dry and cold air while practicing endurance winter sports can be another factor which increases the risk of EIB. Some other studies, however, do not provide results which are compelling enough to significantly associate exercise in adverse conditions with predisposition to EIB. It is suggested that damage to respiratory epithelium occurs only in the presence of BHR symptoms or exercise-induced bronchoconstriction. Consequently, mutual causation and the sequence of the described phenomena are still open to discussion. The innervation of the respiratory tract is mainly composed of parasympathetic fibres. Stimulation of parasympathetic cholinergic fibres results in bronchoconstriction. In the light of the recent research, high-intensity exercise is thought to magnify para-sympathomimetic activity, thereby increasing the tension of bronchial smooth muscles and, consequently, increasing the probability of EIB. The relationship between BHR and some autonomic nervous system-dependent responses, e.g. perspiration, tearing, saliva production, have been reported. However, although chronically enhanced parasympathomimetic nervous system activity is observed there are data which do not confirm the correlation between BHR and dysfunctional autonomic regulation. Some authors suggest that autonomic modulation may be involved in BHR development but only when accompanied by the risk of inspiring harmful components of the air. Neurogenic inflammation is also considered in the investigation of EIB pathogenesis. High-intensity exercise elevates the concentration of substance P which is one of the key mediators of neurogenic inflammation. Acetylcholine and nerve growth factor (NGF) have also been put forward as potentially involved in the development of the EIB-provoking inflammation. Since none of the aforementioned mechanisms fully explains the pathogenesis of EIB, potential interaction of several mechanisms should be taken into account while assessing individual predisposition to exercise-induced respiratory symptoms. The identification of the athletes susceptible to EIB appears to be the key issue here as it may contribute to the improvement of preventive measures. The observations made within the last 20-30 years indicate that the asthma rate is higher in athletes, especially those practicing endurance sports. The risk of asthma in the athletes with atopy symptoms is several times higher than in healthy population.

• #59

  https://www.termedia.pl/Asthma-and-exercise-induced-respiratory-disorders-r-nin-athletes-The-position-paper-of-the-Polish-Society-r-nof-Allergology-and-Polish-Society-of-Sports-Medicine,123,36304,1,0.html

  Asthma is a heterogeneous disease typically associated with a chronic respiratory inflammation which is defined as a syndrome of such respiratory symptoms as wheezing, dyspnoea, chest tightening and coughing which differ in time and intensity and are connected with variable airways obstruction. Currently discussed pathogenic mechanisms potentially responsible for exercise-induced bronchoconstriction in people who practice high-intensity exercise on a regular basis include: osmotic and thermal changes in airways mucosa caused by exercise-induced hyperventilation (osmotic and thermal hypothesis); damage to respiratory epithelium; increasing severity of the airway inflammation; neural activation. Osmotic and thermal changes to bronchial mucosa are the rationale behind the osmotic and thermal hypotheses which are considered as classical ones in the attempts to explain the pathogenesis of EIB in athletes. Increased water evaporation from the mucosa during exercise leads to the increase in the osmolarity of the fluid covering the respiratory epithelium. The changes to osmotic relations result in the lysis of the cells and the release of the mediators including cysteinyl leukotrienes which have strong bronchoconstrictive properties. Furthermore, the airway cooling activates cholinergic receptors, which causes increased tension of bronchial smooth muscles and enhanced fluid secretion in airways. Directly after exercise completion the respiratory tract warming commences and leads to secondary hyperaemia and increased capillary permeability in the bronchial wall. A rise in the number of inflammatory cells (eosinophils, neutrophils, epithelial cells) has been observed in the respiratory tract of athletes. A large body of evidence has already proven that damage to respiratory epithelium during exercise (particularly in adverse environmental conditions) significantly increases susceptibility to EIB. The conclusions mentioned above were drawn from the analyses of the markers of respiratory epithelium damage (e.g. protein CC16). Unfavourable and harmful environmental conditions for exercise can also contribute to respiratory tract damage and increased susceptibility to EIB. The most spectacular associations were found in the relations between exposure to chlorine compounds (trichloramine) while swimming and the increase in bronchial hyperreactivity (BHR). Exposure to dry and cold air while practicing endurance winter sports can be another factor which increases the risk of EIB. Some other studies, however, do not provide results which are compelling enough to significantly associate exercise in adverse conditions with predisposition to EIB. It is suggested that damage to respiratory epithelium occurs only in the presence of BHR symptoms or exercise-induced bronchoconstriction. Consequently, mutual causation and the sequence of the described phenomena are still open to discussion. The innervation of the respiratory tract is mainly composed of parasympathetic fibres. Stimulation of parasympathetic cholinergic fibres results in bronchoconstriction. In the light of the recent research, high-intensity exercise is thought to magnify para-sympathomimetic activity, thereby increasing the tension of bronchial smooth muscles and, consequently, increasing the probability of EIB. The relationship between BHR and some autonomic nervous system-dependent responses, e.g. perspiration, tearing, saliva production, have been reported. However, although chronically enhanced parasympathomimetic nervous system activity is observed there are data which do not confirm the correlation between BHR and dysfunctional autonomic regulation. Some authors suggest that autonomic modulation may be involved in BHR development but only when accompanied by the risk of inspiring harmful components of the air. Neurogenic inflammation is also considered in the investigation of EIB pathogenesis. High-intensity exercise elevates the concentration of substance P which is one of the key mediators of neurogenic inflammation. Acetylcholine and nerve growth factor (NGF) have also been put forward as potentially involved in the development of the EIB-provoking inflammation. Since none of the aforementioned mechanisms fully explains the pathogenesis of EIB, potential interaction of several mechanisms should be taken into account while assessing individual predisposition to exercise-induced respiratory symptoms. The identification of the athletes susceptible to EIB appears to be the key issue here as it may contribute to the improvement of preventive measures. The observations made within the last 20-30 years indicate that the asthma rate is higher in athletes, especially those practicing endurance sports. The risk of asthma in the athletes with atopy symptoms is several times higher than in healthy population.

• #60

  https://www.termedia.pl/Asthma-and-exercise-induced-respiratory-disorders-r-nin-athletes-The-position-paper-of-the-Polish-Society-r-nof-Allergology-and-Polish-Society-of-Sports-Medicine,123,36304,1,0.html

  Asthma is a heterogeneous disease typically associated with a chronic respiratory inflammation which is defined as a syndrome of such respiratory symptoms as wheezing, dyspnoea, chest tightening and coughing which differ in time and intensity and are connected with variable airways obstruction. Currently discussed pathogenic mechanisms potentially responsible for exercise-induced bronchoconstriction in people who practice high-intensity exercise on a regular basis include: osmotic and thermal changes in airways mucosa caused by exercise-induced hyperventilation (osmotic and thermal hypothesis); damage to respiratory epithelium; increasing severity of the airway inflammation; neural activation. Osmotic and thermal changes to bronchial mucosa are the rationale behind the osmotic and thermal hypotheses which are considered as classical ones in the attempts to explain the pathogenesis of EIB in athletes. Increased water evaporation from the mucosa during exercise leads to the increase in the osmolarity of the fluid covering the respiratory epithelium. The changes to osmotic relations result in the lysis of the cells and the release of the mediators including cysteinyl leukotrienes which have strong bronchoconstrictive properties. Furthermore, the airway cooling activates cholinergic receptors, which causes increased tension of bronchial smooth muscles and enhanced fluid secretion in airways. Directly after exercise completion the respiratory tract warming commences and leads to secondary hyperaemia and increased capillary permeability in the bronchial wall. A rise in the number of inflammatory cells (eosinophils, neutrophils, epithelial cells) has been observed in the respiratory tract of athletes. A large body of evidence has already proven that damage to respiratory epithelium during exercise (particularly in adverse environmental conditions) significantly increases susceptibility to EIB. The conclusions mentioned above were drawn from the analyses of the markers of respiratory epithelium damage (e.g. protein CC16). Unfavourable and harmful environmental conditions for exercise can also contribute to respiratory tract damage and increased susceptibility to EIB. The most spectacular associations were found in the relations between exposure to chlorine compounds (trichloramine) while swimming and the increase in bronchial hyperreactivity (BHR). Exposure to dry and cold air while practicing endurance winter sports can be another factor which increases the risk of EIB. Some other studies, however, do not provide results which are compelling enough to significantly associate exercise in adverse conditions with predisposition to EIB. It is suggested that damage to respiratory epithelium occurs only in the presence of BHR symptoms or exercise-induced bronchoconstriction. Consequently, mutual causation and the sequence of the described phenomena are still open to discussion. The innervation of the respiratory tract is mainly composed of parasympathetic fibres. Stimulation of parasympathetic cholinergic fibres results in bronchoconstriction. In the light of the recent research, high-intensity exercise is thought to magnify para-sympathomimetic activity, thereby increasing the tension of bronchial smooth muscles and, consequently, increasing the probability of EIB. The relationship between BHR and some autonomic nervous system-dependent responses, e.g. perspiration, tearing, saliva production, have been reported. However, although chronically enhanced parasympathomimetic nervous system activity is observed there are data which do not confirm the correlation between BHR and dysfunctional autonomic regulation. Some authors suggest that autonomic modulation may be involved in BHR development but only when accompanied by the risk of inspiring harmful components of the air. Neurogenic inflammation is also considered in the investigation of EIB pathogenesis. High-intensity exercise elevates the concentration of substance P which is one of the key mediators of neurogenic inflammation. Acetylcholine and nerve growth factor (NGF) have also been put forward as potentially involved in the development of the EIB-provoking inflammation. Since none of the aforementioned mechanisms fully explains the pathogenesis of EIB, potential interaction of several mechanisms should be taken into account while assessing individual predisposition to exercise-induced respiratory symptoms. The identification of the athletes susceptible to EIB appears to be the key issue here as it may contribute to the improvement of preventive measures. The observations made within the last 20-30 years indicate that the asthma rate is higher in athletes, especially those practicing endurance sports. The risk of asthma in the athletes with atopy symptoms is several times higher than in healthy population.

• #61

  https://www.termedia.pl/Asthma-and-exercise-induced-respiratory-disorders-r-nin-athletes-The-position-paper-of-the-Polish-Society-r-nof-Allergology-and-Polish-Society-of-Sports-Medicine,123,36304,1,0.html

  Asthma is a heterogeneous disease typically associated with a chronic respiratory inflammation which is defined as a syndrome of such respiratory symptoms as wheezing, dyspnoea, chest tightening and coughing which differ in time and intensity and are connected with variable airways obstruction. Currently discussed pathogenic mechanisms potentially responsible for exercise-induced bronchoconstriction in people who practice high-intensity exercise on a regular basis include: osmotic and thermal changes in airways mucosa caused by exercise-induced hyperventilation (osmotic and thermal hypothesis); damage to respiratory epithelium; increasing severity of the airway inflammation; neural activation. Osmotic and thermal changes to bronchial mucosa are the rationale behind the osmotic and thermal hypotheses which are considered as classical ones in the attempts to explain the pathogenesis of EIB in athletes. Increased water evaporation from the mucosa during exercise leads to the increase in the osmolarity of the fluid covering the respiratory epithelium. The changes to osmotic relations result in the lysis of the cells and the release of the mediators including cysteinyl leukotrienes which have strong bronchoconstrictive properties. Furthermore, the airway cooling activates cholinergic receptors, which causes increased tension of bronchial smooth muscles and enhanced fluid secretion in airways. Directly after exercise completion the respiratory tract warming commences and leads to secondary hyperaemia and increased capillary permeability in the bronchial wall. A rise in the number of inflammatory cells (eosinophils, neutrophils, epithelial cells) has been observed in the respiratory tract of athletes. A large body of evidence has already proven that damage to respiratory epithelium during exercise (particularly in adverse environmental conditions) significantly increases susceptibility to EIB. The conclusions mentioned above were drawn from the analyses of the markers of respiratory epithelium damage (e.g. protein CC16). Unfavourable and harmful environmental conditions for exercise can also contribute to respiratory tract damage and increased susceptibility to EIB. The most spectacular associations were found in the relations between exposure to chlorine compounds (trichloramine) while swimming and the increase in bronchial hyperreactivity (BHR). Exposure to dry and cold air while practicing endurance winter sports can be another factor which increases the risk of EIB. Some other studies, however, do not provide results which are compelling enough to significantly associate exercise in adverse conditions with predisposition to EIB. It is suggested that damage to respiratory epithelium occurs only in the presence of BHR symptoms or exercise-induced bronchoconstriction. Consequently, mutual causation and the sequence of the described phenomena are still open to discussion. The innervation of the respiratory tract is mainly composed of parasympathetic fibres. Stimulation of parasympathetic cholinergic fibres results in bronchoconstriction. In the light of the recent research, high-intensity exercise is thought to magnify para-sympathomimetic activity, thereby increasing the tension of bronchial smooth muscles and, consequently, increasing the probability of EIB. The relationship between BHR and some autonomic nervous system-dependent responses, e.g. perspiration, tearing, saliva production, have been reported. However, although chronically enhanced parasympathomimetic nervous system activity is observed there are data which do not confirm the correlation between BHR and dysfunctional autonomic regulation. Some authors suggest that autonomic modulation may be involved in BHR development but only when accompanied by the risk of inspiring harmful components of the air. Neurogenic inflammation is also considered in the investigation of EIB pathogenesis. High-intensity exercise elevates the concentration of substance P which is one of the key mediators of neurogenic inflammation. Acetylcholine and nerve growth factor (NGF) have also been put forward as potentially involved in the development of the EIB-provoking inflammation. Since none of the aforementioned mechanisms fully explains the pathogenesis of EIB, potential interaction of several mechanisms should be taken into account while assessing individual predisposition to exercise-induced respiratory symptoms. The identification of the athletes susceptible to EIB appears to be the key issue here as it may contribute to the improvement of preventive measures. The observations made within the last 20-30 years indicate that the asthma rate is higher in athletes, especially those practicing endurance sports. The risk of asthma in the athletes with atopy symptoms is several times higher than in healthy population.

• #62 Exercise-induced bronchoconstriction in children: Delphi study and consensus document about definition and epidemiology, diagnostic work-up, treatment, and follow-up | Respiratory Research | Full Text

  https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-024-03078-5

  The underlying mechanisms responsible for EIB are complex and not fully understood. Osmotic and thermal theories have been proposed. Environmental factors, such as low temperature, low humidity, exposure to allergens and pollution, and individual factors like atopy and airway inflammation play a role in triggering EIB.

• #63 Exercise-Induced Asthma: Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/1938228-overview

  The other theory is based on airway cooling and assumes that the air movement in the bronchial tree results in a decreased temperature of the bronchi, which may also trigger a hyperemic response in an effort to heat the airway. Again, the result is a spasm in the bronchi. […] Many authors believe there may be a combination of the above 2 theories that takes place, but the biochemical or physical pathways that mediate these responses are unclear. Evidence may even exist to support the idea that the resulting cascades are not the inflammatory pathways to which we attribute allergic asthma. […] Likewise, certain sports and their environments predispose individuals with asthma to experience EIA. Sports played in cold and dry environments usually result in more symptom manifestation for athletes with this condition. On the other hand, when the environment is warm and humid, the incidence and severity of EIA decrease.

• #64 Exercise-induced bronchoconstriction: prevalence, pathophysiology, patient impact, diagnosis and management | npj Primary Care Respiratory Medicine

  https://www.nature.com/articles/s41533-018-0098-2

  During exercise-related hyperventilation, transient osmotic change at the airway surface occurs owing to reductions in epithelium liquid volume, which in turn triggers mast cell degranulation. […] Consequently, there is mast cell-mediated release of prostaglandins (prostaglandin D2), leukotrienes, histamine and tryptase. These signalling molecules are known to mediate airway smooth muscle contraction and increase mucus production and microvascular permeability and sensory nerve activation, and their release is thought to be the main stimulus for bronchoconstriction and airway oedema. […] In patients with EIB who do not have asthma, the mechanisms described by the osmotic theory are believed to be directly responsible for causing bronchoconstriction and associated symptoms. […] Intense ventilation of cold air can further increase dehydration of the airway surfaces and cause changes in bronchial blood flow, explaining why athletes performing in cold weather (e.g., ice hockey, Nordic skiing) demonstrate the highest rates of EIB. […] Epithelial injury that is caused by the inhalation of air pollutants and poorly conditioned air during exercise has also been hypothesised to be a contributing factor for the development of EIB in patients without asthma.

• #65 Exercise-Induced Asthma: Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/1938228-overview

  The other theory is based on airway cooling and assumes that the air movement in the bronchial tree results in a decreased temperature of the bronchi, which may also trigger a hyperemic response in an effort to heat the airway. Again, the result is a spasm in the bronchi. […] Many authors believe there may be a combination of the above 2 theories that takes place, but the biochemical or physical pathways that mediate these responses are unclear. Evidence may even exist to support the idea that the resulting cascades are not the inflammatory pathways to which we attribute allergic asthma. […] Likewise, certain sports and their environments predispose individuals with asthma to experience EIA. Sports played in cold and dry environments usually result in more symptom manifestation for athletes with this condition. On the other hand, when the environment is warm and humid, the incidence and severity of EIA decrease.

• #66 What Is Exercise Induced Asthma? | AAFA.org

  https://aafa.org/asthma/asthma-triggers-causes/exercise-induced-asthma/

  Everyone needs to exercise, even people with asthma! A strong, healthy body is one of your best defenses against disease. But some people have asthma episodes during exercise. This is called exercise-induced bronchoconstriction. By taking steps to control your asthma, you should be able to exercise free of symptoms. […] If you have asthma symptoms during exercise or physical activity, you may have exercise-induced bronchoconstriction (EIB). In the past, it was called exercise-induced asthma. But that name wrongly suggests that exercise causes asthma. […] Anyone can have shortness of breath during exercise. If you have EIB, your airways become tight, narrowed, and inflamed during physical activity. This happens because you breathe dry air during exercise, causing you to lose heat, water, or both from your airways. Dryness of the air, rather than the temperature, seems to be the most likely trigger.

• #67 Exercise-Induced Bronchospasm: Cause and Treatment | Mount Sinai Today

  https://health.mountsinai.org/blog/exercise-induced-bronchospasm-cause-and-treatment/

  The mechanism is related to cooling and drying of the airways; hence, running in cold, dry air is worse than warm, humid air. The underlying state of the airways might make it worse, too. For example, some asthmatics only have problems with EIB during their pollen allergy seasons, after an upper respiratory infection, or when they have been previously exposed to a cat or other irritant. Irritants also can come into play when exercise is performed on days with poor air quality due to pollution. […] Typically, the airways dilate during exercise. About 5 to 10 minutes post-exercise is when the airways narrow and bronchospasm occurs. It will usually spontaneously resolve in 30 minutes or so. […] EIB can occur without exercise, too. Anything that results in breathing in and out rapidly can trigger it, particularly in the asthmatic.

• #68

  https://www.termedia.pl/Asthma-and-exercise-induced-respiratory-disorders-r-nin-athletes-The-position-paper-of-the-Polish-Society-r-nof-Allergology-and-Polish-Society-of-Sports-Medicine,123,36304,1,0.html

  Asthma is a heterogeneous disease typically associated with a chronic respiratory inflammation which is defined as a syndrome of such respiratory symptoms as wheezing, dyspnoea, chest tightening and coughing which differ in time and intensity and are connected with variable airways obstruction. Currently discussed pathogenic mechanisms potentially responsible for exercise-induced bronchoconstriction in people who practice high-intensity exercise on a regular basis include: osmotic and thermal changes in airways mucosa caused by exercise-induced hyperventilation (osmotic and thermal hypothesis); damage to respiratory epithelium; increasing severity of the airway inflammation; neural activation. Osmotic and thermal changes to bronchial mucosa are the rationale behind the osmotic and thermal hypotheses which are considered as classical ones in the attempts to explain the pathogenesis of EIB in athletes. Increased water evaporation from the mucosa during exercise leads to the increase in the osmolarity of the fluid covering the respiratory epithelium. The changes to osmotic relations result in the lysis of the cells and the release of the mediators including cysteinyl leukotrienes which have strong bronchoconstrictive properties. Furthermore, the airway cooling activates cholinergic receptors, which causes increased tension of bronchial smooth muscles and enhanced fluid secretion in airways. Directly after exercise completion the respiratory tract warming commences and leads to secondary hyperaemia and increased capillary permeability in the bronchial wall. A rise in the number of inflammatory cells (eosinophils, neutrophils, epithelial cells) has been observed in the respiratory tract of athletes. A large body of evidence has already proven that damage to respiratory epithelium during exercise (particularly in adverse environmental conditions) significantly increases susceptibility to EIB. The conclusions mentioned above were drawn from the analyses of the markers of respiratory epithelium damage (e.g. protein CC16). Unfavourable and harmful environmental conditions for exercise can also contribute to respiratory tract damage and increased susceptibility to EIB. The most spectacular associations were found in the relations between exposure to chlorine compounds (trichloramine) while swimming and the increase in bronchial hyperreactivity (BHR). Exposure to dry and cold air while practicing endurance winter sports can be another factor which increases the risk of EIB. Some other studies, however, do not provide results which are compelling enough to significantly associate exercise in adverse conditions with predisposition to EIB. It is suggested that damage to respiratory epithelium occurs only in the presence of BHR symptoms or exercise-induced bronchoconstriction. Consequently, mutual causation and the sequence of the described phenomena are still open to discussion. The innervation of the respiratory tract is mainly composed of parasympathetic fibres. Stimulation of parasympathetic cholinergic fibres results in bronchoconstriction. In the light of the recent research, high-intensity exercise is thought to magnify para-sympathomimetic activity, thereby increasing the tension of bronchial smooth muscles and, consequently, increasing the probability of EIB. The relationship between BHR and some autonomic nervous system-dependent responses, e.g. perspiration, tearing, saliva production, have been reported. However, although chronically enhanced parasympathomimetic nervous system activity is observed there are data which do not confirm the correlation between BHR and dysfunctional autonomic regulation. Some authors suggest that autonomic modulation may be involved in BHR development but only when accompanied by the risk of inspiring harmful components of the air. Neurogenic inflammation is also considered in the investigation of EIB pathogenesis. High-intensity exercise elevates the concentration of substance P which is one of the key mediators of neurogenic inflammation. Acetylcholine and nerve growth factor (NGF) have also been put forward as potentially involved in the development of the EIB-provoking inflammation. Since none of the aforementioned mechanisms fully explains the pathogenesis of EIB, potential interaction of several mechanisms should be taken into account while assessing individual predisposition to exercise-induced respiratory symptoms. The identification of the athletes susceptible to EIB appears to be the key issue here as it may contribute to the improvement of preventive measures. The observations made within the last 20-30 years indicate that the asthma rate is higher in athletes, especially those practicing endurance sports. The risk of asthma in the athletes with atopy symptoms is several times higher than in healthy population.

• #69 Exercise-Induced Bronchoconstriction – a Short Review with Practical Recommendations

  https://www.germanjournalsportsmedicine.com/archive/archive-2012/heft-10/exercise-induced-bronchoconstriction-a-short-review-with-practical-recommendations/

  The classic early onset pattern reflects the signs of allergic asthma characterized by atopy, eosinophilic airway inflammation and positive methacholine responsiveness with a rapid onset of symptoms at exercise initiation. The divergent pattern comprises a late onset phenotype during a sports career and therefore with more phases of high ventilation. […] Problematic environmental conditions during the activity such as cold ambient temperatures for winter sports or organic chlorine products from indoor swimming pools clearly enhance the effect of intensive physical activity on both conditions.

• #70 Exercise-induced asthma in asthmatic children. Predisposing factors | Allergologia et Immunopathologia

  https://www.elsevier.es/es-revista-allergologia-et-immunopathologia-105-articulo-exercise-induced-asthma-in-asthmatic-children–S0301054608725357

  It is recognized that airway inflammation plays a central role in the pathogenesis of asthma, but how it relates to exercise-induced bronchoconstriction (EIB) is not completely understood. Various studies have investigated the relationship between EIB and baseline concentrations of inflammatory markers in exhaled condensated breath and induced sputum. The baseline concentrations of inflammatory markers are higher in asthmatic children with EIB. […] The exposure to indoor allergens may favour the development of EIB. Exercise-induced bronchoconstriction has been associated with eosinophilic airway inflammation, bronchial hyper responsiveness (BHR), atopy and airway obstruction. […] The results of the multivariable logistic regression analysis confirmed indoor allergen sensitization as a risk factor to EIB and the immunotherapy treatment as a protector factor in the development of EIB.

• #71 Exercise-Induced Asthma: Managing Respiratory Issues in Athletes

  https://www.mdpi.com/2411-5142/9/1/15

  Airway Hyper-Responsiveness: Athletes with EIBA often display heightened airway sensitivity, resulting in increased reactivity to various triggers. This heightened sensitivity can result from a combination of genetic factors and ongoing exposure to irritants, allergens, or environmental pollutants. […] Environmental Factors: Environmental conditions significantly impact EIBA in athletes, with factors such as cold dry air, allergens, pollutants, and temperature fluctuations exacerbating the symptoms. […] The diagnosis of EIB holds paramount significance for athletes due to its profound medical implications for their performance and overall health. However, arriving at an accurate diagnosis can often pose a significant challenge, primarily because athletes may exhibit lung function parameters, which appear to be within normal ranges.

• #72 Exercise-induced asthma – Symptoms & causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/exercise-induced-asthma/symptoms-causes/syc-20372300

  Exercise-induced bronchoconstriction is more likely to occur in: People with asthma. About 90% of people with asthma have exercise-induced bronchoconstriction. However, the condition also can occur in people without asthma. […] If not treated, exercise-induced bronchoconstriction can result in: Serious or life-threatening breathing difficulties, particularly among people with poorly managed asthma.

• #73

  https://www.termedia.pl/Asthma-and-exercise-induced-respiratory-disorders-r-nin-athletes-The-position-paper-of-the-Polish-Society-r-nof-Allergology-and-Polish-Society-of-Sports-Medicine,123,36304,1,0.html

  Asthma is a heterogeneous disease typically associated with a chronic respiratory inflammation which is defined as a syndrome of such respiratory symptoms as wheezing, dyspnoea, chest tightening and coughing which differ in time and intensity and are connected with variable airways obstruction. Currently discussed pathogenic mechanisms potentially responsible for exercise-induced bronchoconstriction in people who practice high-intensity exercise on a regular basis include: osmotic and thermal changes in airways mucosa caused by exercise-induced hyperventilation (osmotic and thermal hypothesis); damage to respiratory epithelium; increasing severity of the airway inflammation; neural activation. Osmotic and thermal changes to bronchial mucosa are the rationale behind the osmotic and thermal hypotheses which are considered as classical ones in the attempts to explain the pathogenesis of EIB in athletes. Increased water evaporation from the mucosa during exercise leads to the increase in the osmolarity of the fluid covering the respiratory epithelium. The changes to osmotic relations result in the lysis of the cells and the release of the mediators including cysteinyl leukotrienes which have strong bronchoconstrictive properties. Furthermore, the airway cooling activates cholinergic receptors, which causes increased tension of bronchial smooth muscles and enhanced fluid secretion in airways. Directly after exercise completion the respiratory tract warming commences and leads to secondary hyperaemia and increased capillary permeability in the bronchial wall. A rise in the number of inflammatory cells (eosinophils, neutrophils, epithelial cells) has been observed in the respiratory tract of athletes. A large body of evidence has already proven that damage to respiratory epithelium during exercise (particularly in adverse environmental conditions) significantly increases susceptibility to EIB. The conclusions mentioned above were drawn from the analyses of the markers of respiratory epithelium damage (e.g. protein CC16). Unfavourable and harmful environmental conditions for exercise can also contribute to respiratory tract damage and increased susceptibility to EIB. The most spectacular associations were found in the relations between exposure to chlorine compounds (trichloramine) while swimming and the increase in bronchial hyperreactivity (BHR). Exposure to dry and cold air while practicing endurance winter sports can be another factor which increases the risk of EIB. Some other studies, however, do not provide results which are compelling enough to significantly associate exercise in adverse conditions with predisposition to EIB. It is suggested that damage to respiratory epithelium occurs only in the presence of BHR symptoms or exercise-induced bronchoconstriction. Consequently, mutual causation and the sequence of the described phenomena are still open to discussion. The innervation of the respiratory tract is mainly composed of parasympathetic fibres. Stimulation of parasympathetic cholinergic fibres results in bronchoconstriction. In the light of the recent research, high-intensity exercise is thought to magnify para-sympathomimetic activity, thereby increasing the tension of bronchial smooth muscles and, consequently, increasing the probability of EIB. The relationship between BHR and some autonomic nervous system-dependent responses, e.g. perspiration, tearing, saliva production, have been reported. However, although chronically enhanced parasympathomimetic nervous system activity is observed there are data which do not confirm the correlation between BHR and dysfunctional autonomic regulation. Some authors suggest that autonomic modulation may be involved in BHR development but only when accompanied by the risk of inspiring harmful components of the air. Neurogenic inflammation is also considered in the investigation of EIB pathogenesis. High-intensity exercise elevates the concentration of substance P which is one of the key mediators of neurogenic inflammation. Acetylcholine and nerve growth factor (NGF) have also been put forward as potentially involved in the development of the EIB-provoking inflammation. Since none of the aforementioned mechanisms fully explains the pathogenesis of EIB, potential interaction of several mechanisms should be taken into account while assessing individual predisposition to exercise-induced respiratory symptoms. The identification of the athletes susceptible to EIB appears to be the key issue here as it may contribute to the improvement of preventive measures. The observations made within the last 20-30 years indicate that the asthma rate is higher in athletes, especially those practicing endurance sports. The risk of asthma in the athletes with atopy symptoms is several times higher than in healthy population.

• #74 Exercise-induced asthma in asthmatic children. Predisposing factors | Allergologia et Immunopathologia

  https://www.elsevier.es/es-revista-allergologia-et-immunopathologia-105-articulo-exercise-induced-asthma-in-asthmatic-children–S0301054608725357

  It is recognized that airway inflammation plays a central role in the pathogenesis of asthma, but how it relates to exercise-induced bronchoconstriction (EIB) is not completely understood. Various studies have investigated the relationship between EIB and baseline concentrations of inflammatory markers in exhaled condensated breath and induced sputum. The baseline concentrations of inflammatory markers are higher in asthmatic children with EIB. […] The exposure to indoor allergens may favour the development of EIB. Exercise-induced bronchoconstriction has been associated with eosinophilic airway inflammation, bronchial hyper responsiveness (BHR), atopy and airway obstruction. […] The results of the multivariable logistic regression analysis confirmed indoor allergen sensitization as a risk factor to EIB and the immunotherapy treatment as a protector factor in the development of EIB.

• #75

  https://journals.lww.com/acsm-csmr/fulltext/2016/05000/exercise_induced_bronchoconstriction.5.aspx

  Transient immunosuppression also may develop in athletes during periods of intense training, with increased susceptibility to respiratory infections (especially viral), which may increase airway response to exercise acutely and affect overall asthma control (1,2). […] The key stimulus is airway dehydration due to increased ventilation, resulting in a loss of heat, drying of the airways, as well as increased intracellular osmolarity. This triggers the release of inflammatory mediators, leading to airway smooth muscle contraction and airway edema (1,2). […] Mechanical stress/injury to airway epithelium plays a role in the acute response to exercise as well as in the development of airway remodeling in athletes through their effects on smooth muscle contractile properties causing hypersensitivity leading to bronchoconstriction (1,2).

• #76 Pulmonary Issues in the Athlete/Exercise Induced Bronchoconstriction | PM&R KnowledgeNow

  https://now.aapmr.org/pulmonary-issues-in-the-athleteexercise-induced-asthma/

  The re-warming hypothesis has some supporting evidence, but is mostly overlooked for the above hypertonicity mechanism. […] The majority of guidelines are based on studies in patients with both EIB and asthma, and limited data exists on athletes with EIB as their only diagnosis of airway hyperresponsiveness. Optimal treatments may be different in those with EIB and underlying asthma versus those with EIB alone. Additionally, the method used to detect EIB can greatly affect the estimates of prevalence as routine diagnostic strategies may not be appropriate for elite athletes. For this reason, sport-specific protocols performed in provocative environments need to be established. […] In respect to better understanding pathogenesis, new cytokine and genetic markers are being investigated to assess their contributions to the development of EIB. Several genetic alterations have been discovered which may protect or predispose athletes to EIB, but further studies are needed to better delineate the role of genetic susceptibility in EIB.

• #77 Exercise-induced bronchoconstriction – Wikipedia

  https://en.wikipedia.org/wiki/Exercise-induced_bronchoconstriction

  Mouth breathing as a result of decreased nasal breathing also increases lung surface exposure to irritants, pollutants, and allergens, causing neutrophilic inflammation in response to reactive oxygen species formation; research has found that individuals with genetically hindered glutathione counteraction of this oxidative stress are likely at a higher risk of developing EIB.

• #78 Exercise-Induced Asthma: Practice Essentials, Background, Anatomy

  https://emedicine.medscape.com/article/1938228-overview

  Exercise-induced asthma is a condition of respiratory difficulty (bronchoconstriction) that is related to histamine release, is triggered by aerobic exercise, and lasts several minutes. Causes include medical conditions, environmental factors, and medications. […] EIA usually affects individuals who participate in sports that include an aerobic component. The condition can be seen in any sport, but EIA is much less common in predominantly anaerobic activities. This is likely due to the role of consistent and repetitive air movement through the airways (seen in aerobic sports), which affect airway humidity and temperature. EIA triggers an unknown biochemical and neurochemical pathway, resulting in the bronchospasm, which manifests as the symptoms of the disease. […] Although the exact mechanism of EIA is unknown, there are 2 predominant theories as to how the symptom complex is triggered. One is the airway humidity theory, which suggests that air movement through the airway results in relative drying of the airway. This, in turn, is believed to trigger a cascade of events that results in airway edema secondary to hyperemia and increased perfusion in an attempt to combat the drying. The result is bronchospasm.

• #79 Exercise-Induced Bronchoconstriction – a Short Review with Practical Recommendations

  https://www.germanjournalsportsmedicine.com/archive/archive-2012/heft-10/exercise-induced-bronchoconstriction-a-short-review-with-practical-recommendations/

  Fragestellung: Übersichtsdarstellung der aktuellen Literatur zum Thema belastungsinduzierter Ventilationstörungen (exercise-induced asthma (EIA); exerciseinduced bronchoconstriktion (EIB)) mit kurzer Zusammenfassung der Pathogenese, Diagnose und Behandlung. […] Zusammenfassung: Die Termini EIA und EIB beschreiben einerseits belastungsinduzierte Symptome im Sinne asthmatischer Beschwerden wie Atemnot, Husten, Giemen mit thorakale Enge andererseits eine exspiratorische obstruktive Ventilationsstörung nach einer definierten Belastung. Pathophysiologisch kommt es bei beiden Ereignissen durch Abkühlen und Feuchtigkeitsverlust der Atemwege zu einem relevanten Anstieg von Mediatoren sowie zur Aktivierung von Entzündungszellen bis hin zu Ausbildung einer chronischen Entzündungsreaktion. […] Pathogenesis The mechanism for development of EIA and EIB in athletes includes two hypotheses. Both relate to the increased ventilation of up to >200L/min in elite athletes during exercise, resulting in an increased loss of water from the respiratory tract and cooling of the airways. This results in vasoconstriction of bronchial vessels followed by secondary reactive hyperemia, edema and airway narrowing. Furthermore, a relevant release of mediators from mast cells and other inflammatory cells of the airways, by changing the osmolarity of the periciliary fluid lining the respiratory mucosal membranes, can be measured. These mechanisms affect the course of EIA/EIB significantly, especially by inducing a chronically inflammatory response of the bronchial airways.

• #80 Exercise-Induced Bronchospasm: Cause and Treatment | Mount Sinai Today

  https://health.mountsinai.org/blog/exercise-induced-bronchospasm-cause-and-treatment/

  In the summer, we are outdoors—and hopefully exercising—more often. About 10% of people who exercise will get exercise-induced bronchospasm (EIB). Symptoms may include wheezing, excessive shortness of breath, chest tightness, or just coughing beginning 5 to 10 minutes after exercise. EIB occurs most frequently in persons with asthma, particularly those whose asthma is not well controlled. Various studies show that up to 90% of people with asthma have EIB. But it can also occur in isolation—in a person without asthma. […] When we exercise, we need more air to keep our muscles oxygenated and working properly. This requires more rapid breathing. In susceptible folks, this triggers release of chemicals from mast cells (allergy cells) that cause narrowing of the airways in the lungs (bronchospasm). The more rapid the breathing, the more severe the attack might be. Thus, running is more likely to provoke an attack than jogging, and jogging more so than walking.

• #81 Exercise-induced bronchoconstriction – Wikipedia

  https://en.wikipedia.org/wiki/Exercise-induced_bronchoconstriction

  Exercise-induced bronchoconstriction (EIB) occurs when the airways narrow as a result of exercise. This condition has been referred to as exercise-induced asthma (EIA); however, this term is no longer preferred. While exercise does not cause asthma, it is frequently an asthma trigger. […] While the potential triggering events for EIB are well recognized, the underlying pathogenesis is poorly understood. It usually occurs after at least several minutes of vigorous, aerobic activity, which increases oxygen demand to the point where breathing through the nose (nasal breathing) must be supplemented by mouth breathing. The resultant inhalation of air that has not been warmed and humidified by the nasal passages seems to generate increased blood flow to the linings of the bronchial tree, resulting in edema. Constriction of these small airways then follows, worsening the degree of obstruction to airflow. There is increasing evidence that the smooth muscle that lines the airways becomes progressively more sensitive to changes that occur as a result of injury to the airways from dehydration. The chemical mediators that provoke the muscle spasm appear to arise from mast cells.

• #82 Section 5: Exercise-Induced Asthma

  https://www.txhealthsteps.com/static/warehouse/1076-2011-Feb-1-3d1m08v5m6t78987cr9s/section_5.html

  The underlying mechanism in exercise-induced asthma involves the delivery of cold, dry air to the lower airways. With strenuous exercise, hyperventilation causes a bypass of the hydrating and warming functions of the nose and upper airway. The loss of heat and fluid from the airways results in a hyperosmolar lining fluid, which stimulates mediator release that results in epithelial and mast cell activation. Additionally, cooling of the airways is thought to be followed by vascular congestion and dilation of the bronchial circulation on rewarming after exercise. The resultant mucosal swelling and edema can produce airway narrowing. […] An inward sloping of the expiratory flow volume loop and a reduction in the expiratory flows [at least a 10 to 12 percent decrease in the Forced Expiratory Volume in 1 second (FEV1)] after exercise is considered diagnostic for EIA. Additionally, changes in the inspiratory portion of the flow volume loop can be seen that may be diagnostic of vocal cord dysfunction. […] Treatment for EIA can be divided between non-pharmacologic and pharmacologic therapies.

• #83 Exercise-Induced Asthma Clinical Presentation: History, Physical Examination, Phases of EIA

  https://emedicine.medscape.com/article/1938228-clinical

  Patients with exercise-induced asthma (EIA) usually present complaining of exercise-related respiratory symptoms. […] The mechanism is unknown but is believed to involve the following possibilities: depletion of mast cell mediators, release of endogenous catecholamines, and release of endogenous protective prostaglandins. […] This phase occurs 3-9 hours after the initial exercise challenge, and unlike the refractory phase, the late phase manifests as an increase in symptoms, with cough, wheezing, or shortness of breath.

• #84 Exercise induced asthma &bronchospasm | PPT

  https://www.slideshare.net/slideshow/exercise-induced-asthma-bronchospasm/16736403

  Exercise-induced asthma (EIA) and bronchospasm are triggered by exercise in patients with or without chronic asthma. EIA is diagnosed when exercise causes a 15% decrease in lung function and symptoms start after exercise and resolve within 60 minutes. It is common, affecting 10-20% of the general population and up to 90% of asthmatics. […] There are 2 theories for EIA pathogenesis: thermal osmotic Thermal hypothesis, there is no role for biochemical mediators. Osmotic theory has been gaining a wider acceptance in recent years. […] Several studies have noted an increase in the concentration of cysteinyl leukotrienes (CysLTs) in the airways of patients with EIB. A recent study found that the fraction of exhaled nitric oxide (FENO) is elevated in asthmatic patients with EIB, Angiopoetin 2, a mediator that enhances microvascular permeability, is increased in the airways in EIB Mast cell infiltration of the airways has also been implicated in EIB. […] Symptoms begin during or after exercise and usually worsen 5-20 minutes after stopping activity. Some people experience a late-phase reaction 4-12 hours after exercising. Symptoms usually less severe.

• #85 Exercise-Induced Bronchospasm: Cause and Treatment | Mount Sinai Today

  https://health.mountsinai.org/blog/exercise-induced-bronchospasm-cause-and-treatment/

  The mechanism is related to cooling and drying of the airways; hence, running in cold, dry air is worse than warm, humid air. The underlying state of the airways might make it worse, too. For example, some asthmatics only have problems with EIB during their pollen allergy seasons, after an upper respiratory infection, or when they have been previously exposed to a cat or other irritant. Irritants also can come into play when exercise is performed on days with poor air quality due to pollution. […] Typically, the airways dilate during exercise. About 5 to 10 minutes post-exercise is when the airways narrow and bronchospasm occurs. It will usually spontaneously resolve in 30 minutes or so. […] EIB can occur without exercise, too. Anything that results in breathing in and out rapidly can trigger it, particularly in the asthmatic.

• #86 Exercise-Induced Asthma Clinical Presentation: History, Physical Examination, Phases of EIA

  https://emedicine.medscape.com/article/1938228-clinical

  Patients with exercise-induced asthma (EIA) usually present complaining of exercise-related respiratory symptoms. […] The mechanism is unknown but is believed to involve the following possibilities: depletion of mast cell mediators, release of endogenous catecholamines, and release of endogenous protective prostaglandins. […] This phase occurs 3-9 hours after the initial exercise challenge, and unlike the refractory phase, the late phase manifests as an increase in symptoms, with cough, wheezing, or shortness of breath.

• #87 Exercise-Induced Asthma Clinical Presentation: History, Physical Examination, Phases of EIA

  https://emedicine.medscape.com/article/1938228-clinical

  Patients with exercise-induced asthma (EIA) usually present complaining of exercise-related respiratory symptoms. […] The mechanism is unknown but is believed to involve the following possibilities: depletion of mast cell mediators, release of endogenous catecholamines, and release of endogenous protective prostaglandins. […] This phase occurs 3-9 hours after the initial exercise challenge, and unlike the refractory phase, the late phase manifests as an increase in symptoms, with cough, wheezing, or shortness of breath.

• #88 Exercise-Induced Asthma Clinical Presentation: History, Physical Examination, Phases of EIA

  https://emedicine.medscape.com/article/1938228-clinical

  Patients with exercise-induced asthma (EIA) usually present complaining of exercise-related respiratory symptoms. […] The mechanism is unknown but is believed to involve the following possibilities: depletion of mast cell mediators, release of endogenous catecholamines, and release of endogenous protective prostaglandins. […] This phase occurs 3-9 hours after the initial exercise challenge, and unlike the refractory phase, the late phase manifests as an increase in symptoms, with cough, wheezing, or shortness of breath.

• #89 Exercise-Induced Asthma Clinical Presentation: History, Physical Examination, Phases of EIA

  https://emedicine.medscape.com/article/1938228-clinical

  Patients with exercise-induced asthma (EIA) usually present complaining of exercise-related respiratory symptoms. […] The mechanism is unknown but is believed to involve the following possibilities: depletion of mast cell mediators, release of endogenous catecholamines, and release of endogenous protective prostaglandins. […] This phase occurs 3-9 hours after the initial exercise challenge, and unlike the refractory phase, the late phase manifests as an increase in symptoms, with cough, wheezing, or shortness of breath.

• #90 Cross refractoriness between sodium metabisulphite and exercise induced asthma. | Thorax

  https://thorax.bmj.com/content/49/3/245

  BACKGROUND–Exercise and inhaled sodium metabisulphite are thought to cause bronchoconstriction in asthma through different mechanisms. […] The mechanism of refractoriness is unclear, although depletion of mast cell derived mediators or neurotransmitters has been suggested. […] Recent studies suggest a common mechanism involving release of inhibitory prostaglandins. […] This study shows some cross refractoriness between exercise and sodium metabisulphite induced bronchoconstriction, in keeping with a partially shared mechanism of refractoriness.

• #91 Exercise-Induced Asthma Clinical Presentation: History, Physical Examination, Phases of EIA

  https://emedicine.medscape.com/article/1938228-clinical

  Patients with exercise-induced asthma (EIA) usually present complaining of exercise-related respiratory symptoms. […] The mechanism is unknown but is believed to involve the following possibilities: depletion of mast cell mediators, release of endogenous catecholamines, and release of endogenous protective prostaglandins. […] This phase occurs 3-9 hours after the initial exercise challenge, and unlike the refractory phase, the late phase manifests as an increase in symptoms, with cough, wheezing, or shortness of breath.

• #92 Exercise induced asthma &bronchospasm | PPT

  https://www.slideshare.net/slideshow/exercise-induced-asthma-bronchospasm/16736403

  Exercise-induced asthma (EIA) and bronchospasm are triggered by exercise in patients with or without chronic asthma. EIA is diagnosed when exercise causes a 15% decrease in lung function and symptoms start after exercise and resolve within 60 minutes. It is common, affecting 10-20% of the general population and up to 90% of asthmatics. […] There are 2 theories for EIA pathogenesis: thermal osmotic Thermal hypothesis, there is no role for biochemical mediators. Osmotic theory has been gaining a wider acceptance in recent years. […] Several studies have noted an increase in the concentration of cysteinyl leukotrienes (CysLTs) in the airways of patients with EIB. A recent study found that the fraction of exhaled nitric oxide (FENO) is elevated in asthmatic patients with EIB, Angiopoetin 2, a mediator that enhances microvascular permeability, is increased in the airways in EIB Mast cell infiltration of the airways has also been implicated in EIB. […] Symptoms begin during or after exercise and usually worsen 5-20 minutes after stopping activity. Some people experience a late-phase reaction 4-12 hours after exercising. Symptoms usually less severe.

• #93 Exercise-induced bronchoconstriction: prevalence, pathophysiology, patient impact, diagnosis and management | npj Primary Care Respiratory Medicine

  https://www.nature.com/articles/s41533-018-0098-2

  During exercise-related hyperventilation, transient osmotic change at the airway surface occurs owing to reductions in epithelium liquid volume, which in turn triggers mast cell degranulation. […] Consequently, there is mast cell-mediated release of prostaglandins (prostaglandin D2), leukotrienes, histamine and tryptase. These signalling molecules are known to mediate airway smooth muscle contraction and increase mucus production and microvascular permeability and sensory nerve activation, and their release is thought to be the main stimulus for bronchoconstriction and airway oedema. […] In patients with EIB who do not have asthma, the mechanisms described by the osmotic theory are believed to be directly responsible for causing bronchoconstriction and associated symptoms. […] Intense ventilation of cold air can further increase dehydration of the airway surfaces and cause changes in bronchial blood flow, explaining why athletes performing in cold weather (e.g., ice hockey, Nordic skiing) demonstrate the highest rates of EIB. […] Epithelial injury that is caused by the inhalation of air pollutants and poorly conditioned air during exercise has also been hypothesised to be a contributing factor for the development of EIB in patients without asthma.

• #94 Exercise-induced bronchoconstriction: new evidence in pathogenesis, diagnosis and treatment | Asthma Research and Practice | Full Text

  https://asthmarp.biomedcentral.com/articles/10.1186/s40733-015-0004-4

  EIB was initially thought to be secondary to a mediator release from mast cells. […] Although mediator release does contribute to cause EIB, pathophysiologic changes induced by intense exercising are definitely more complex. At present, it is widely accepted that hyperventilation through the mouth associated with intense exercise causes the need for humidifying and heating large volumes of air during a short period of time. […] Elegant experiments performed by S.D. Anderson and coworkers show that the respiratory water loss and the increase in osmolarity of the airways surface liquid represent the major determinants of EIB (osmotic theory). […] The vasodilation associated with airways rewarming (thermal theory) may also play a role in inducing bronchial obstruction after exercise. […] However, in EIBwA, the epithelial damage of a large number of bronchial tree divisions down to peripheral airways represents the predominant pathogenic mechanism.

• #95 Exercise-induced asthma – Symptoms & causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/exercise-induced-asthma/symptoms-causes/syc-20372300

  Exercise-induced bronchoconstriction is more likely to occur in: People with asthma. About 90% of people with asthma have exercise-induced bronchoconstriction. However, the condition also can occur in people without asthma. […] If not treated, exercise-induced bronchoconstriction can result in: Serious or life-threatening breathing difficulties, particularly among people with poorly managed asthma.

• #96 Exercise-Induced Bronchoconstriction – a Short Review with Practical Recommendations

  https://www.germanjournalsportsmedicine.com/archive/archive-2012/heft-10/exercise-induced-bronchoconstriction-a-short-review-with-practical-recommendations/

  The classic early onset pattern reflects the signs of allergic asthma characterized by atopy, eosinophilic airway inflammation and positive methacholine responsiveness with a rapid onset of symptoms at exercise initiation. The divergent pattern comprises a late onset phenotype during a sports career and therefore with more phases of high ventilation. […] Problematic environmental conditions during the activity such as cold ambient temperatures for winter sports or organic chlorine products from indoor swimming pools clearly enhance the effect of intensive physical activity on both conditions.

• #97 Exercise-Induced Bronchoconstriction – a Short Review with Practical Recommendations

  https://www.germanjournalsportsmedicine.com/archive/archive-2012/heft-10/exercise-induced-bronchoconstriction-a-short-review-with-practical-recommendations/

  The classic early onset pattern reflects the signs of allergic asthma characterized by atopy, eosinophilic airway inflammation and positive methacholine responsiveness with a rapid onset of symptoms at exercise initiation. The divergent pattern comprises a late onset phenotype during a sports career and therefore with more phases of high ventilation. […] Problematic environmental conditions during the activity such as cold ambient temperatures for winter sports or organic chlorine products from indoor swimming pools clearly enhance the effect of intensive physical activity on both conditions.

• #98 Exercise-Induced Bronchoconstriction – a Short Review with Practical Recommendations

  https://www.germanjournalsportsmedicine.com/archive/archive-2012/heft-10/exercise-induced-bronchoconstriction-a-short-review-with-practical-recommendations/

  The classic early onset pattern reflects the signs of allergic asthma characterized by atopy, eosinophilic airway inflammation and positive methacholine responsiveness with a rapid onset of symptoms at exercise initiation. The divergent pattern comprises a late onset phenotype during a sports career and therefore with more phases of high ventilation. […] Problematic environmental conditions during the activity such as cold ambient temperatures for winter sports or organic chlorine products from indoor swimming pools clearly enhance the effect of intensive physical activity on both conditions.

• #99 Exercise-Induced Asthma: Managing Respiratory Issues in Athletes

  https://www.mdpi.com/2411-5142/9/1/15

  The principles for diagnosing EIBA in athletes closely align with those used in the general population, primarily centering on demonstrating airflow limitation. […] The overall management of EIB, whether with or without underlying asthma, should align with similar principles for both athletes and non-athletes. Therefore, the general guidelines for symptom control, prevention of exacerbations, avoidance of airflow limitation, and reducing the risk of asthma-related complications should be followed diligently. […] Inhaled corticosteroids (ICS) are the cornerstone of asthma therapy in athletes. Short-acting beta agonists (SABA) are discouraged as sole treatments. […] The pharmacological therapy for EIB in individuals with asthma follows the same principles as the general therapy for asthma, with the approach being based on the severity and frequency of symptoms. The primary long-term goal is to reduce airway inflammation and prevent bronchoconstriction.

• #100 Exercise-induced bronchoconstriction: prevalence, pathophysiology, patient impact, diagnosis and management | npj Primary Care Respiratory Medicine

  https://www.nature.com/articles/s41533-018-0098-2

  During exercise-related hyperventilation, transient osmotic change at the airway surface occurs owing to reductions in epithelium liquid volume, which in turn triggers mast cell degranulation. […] Consequently, there is mast cell-mediated release of prostaglandins (prostaglandin D2), leukotrienes, histamine and tryptase. These signalling molecules are known to mediate airway smooth muscle contraction and increase mucus production and microvascular permeability and sensory nerve activation, and their release is thought to be the main stimulus for bronchoconstriction and airway oedema. […] In patients with EIB who do not have asthma, the mechanisms described by the osmotic theory are believed to be directly responsible for causing bronchoconstriction and associated symptoms. […] Intense ventilation of cold air can further increase dehydration of the airway surfaces and cause changes in bronchial blood flow, explaining why athletes performing in cold weather (e.g., ice hockey, Nordic skiing) demonstrate the highest rates of EIB. […] Epithelial injury that is caused by the inhalation of air pollutants and poorly conditioned air during exercise has also been hypothesised to be a contributing factor for the development of EIB in patients without asthma.

• #101 Pulmonary Issues in the Athlete/Exercise Induced Bronchoconstriction | PM&R KnowledgeNow

  https://now.aapmr.org/pulmonary-issues-in-the-athleteexercise-induced-asthma/

  Exercise-induced bronchoconstriction (EIB) is defined as the transient airway narrowing that occurs following exercise without regards to the presence or absence of asthma. While the term exercise-induced asthma (EIA) has been used, the term is misleading as exercise is not an independent risk factor for asthma, but, instead, a trigger for bronchoconstriction in some asthmatics. EIB may be present in patients with or without underlying asthma and can affect athletes of all levels. […] EIB occurs following high-intensity exercise when high minute ventilation dehydrates the airways and ultimately results in the release of inflammatory mediators. This occurs more frequently in cold/dry environmental conditions. The sustained high-level ventilation reached during exercise and the water content of inspired air are the two most important factors of EIB.

• #102 Exercise-Induced Bronchoconstriction – a Short Review with Practical Recommendations

  https://www.germanjournalsportsmedicine.com/archive/archive-2012/heft-10/exercise-induced-bronchoconstriction-a-short-review-with-practical-recommendations/

  The classic early onset pattern reflects the signs of allergic asthma characterized by atopy, eosinophilic airway inflammation and positive methacholine responsiveness with a rapid onset of symptoms at exercise initiation. The divergent pattern comprises a late onset phenotype during a sports career and therefore with more phases of high ventilation. […] Problematic environmental conditions during the activity such as cold ambient temperatures for winter sports or organic chlorine products from indoor swimming pools clearly enhance the effect of intensive physical activity on both conditions.

• #103 Exercise-induced bronchoconstriction: prevalence, pathophysiology, patient impact, diagnosis and management | npj Primary Care Respiratory Medicine

  https://www.nature.com/articles/s41533-018-0098-2

  During exercise-related hyperventilation, transient osmotic change at the airway surface occurs owing to reductions in epithelium liquid volume, which in turn triggers mast cell degranulation. […] Consequently, there is mast cell-mediated release of prostaglandins (prostaglandin D2), leukotrienes, histamine and tryptase. These signalling molecules are known to mediate airway smooth muscle contraction and increase mucus production and microvascular permeability and sensory nerve activation, and their release is thought to be the main stimulus for bronchoconstriction and airway oedema. […] In patients with EIB who do not have asthma, the mechanisms described by the osmotic theory are believed to be directly responsible for causing bronchoconstriction and associated symptoms. […] Intense ventilation of cold air can further increase dehydration of the airway surfaces and cause changes in bronchial blood flow, explaining why athletes performing in cold weather (e.g., ice hockey, Nordic skiing) demonstrate the highest rates of EIB. […] Epithelial injury that is caused by the inhalation of air pollutants and poorly conditioned air during exercise has also been hypothesised to be a contributing factor for the development of EIB in patients without asthma.

• #104 Exercise-induced bronchoconstriction: new evidence in pathogenesis, diagnosis and treatment | Asthma Research and Practice | Full Text

  https://asthmarp.biomedcentral.com/articles/10.1186/s40733-015-0004-4

  EIB was initially thought to be secondary to a mediator release from mast cells. […] Although mediator release does contribute to cause EIB, pathophysiologic changes induced by intense exercising are definitely more complex. At present, it is widely accepted that hyperventilation through the mouth associated with intense exercise causes the need for humidifying and heating large volumes of air during a short period of time. […] Elegant experiments performed by S.D. Anderson and coworkers show that the respiratory water loss and the increase in osmolarity of the airways surface liquid represent the major determinants of EIB (osmotic theory). […] The vasodilation associated with airways rewarming (thermal theory) may also play a role in inducing bronchial obstruction after exercise. […] However, in EIBwA, the epithelial damage of a large number of bronchial tree divisions down to peripheral airways represents the predominant pathogenic mechanism.

• #105 Exercise-induced bronchoconstriction: new evidence in pathogenesis, diagnosis and treatment | Asthma Research and Practice | Full Text

  https://asthmarp.biomedcentral.com/articles/10.1186/s40733-015-0004-4

  A direct effect of viral infections, occupational agents and exercise may in fact represent a causal mechanism of bronchoconstriction, alternative to the classic eosinophilic mast cell-dependent pathway occurring in allergic asthma. […] The role of epithelial damage and of substances released by the epithelium and found in sputum, such as interleukin-8 and leukotrienes, and in serum or urines, such as Nerve Growth Factor (NGF) and the Clara cell protein CC16, may also explain the heterogeneous inflammatory response reported in EIBwA. […] The importance of aquaporin, expressed by the subepithelial glandular cells, in regulating the water transport through the epithelium, as well as the increased mucus production, as shown by the increased expression of MUC5AC in induced sputum, may be also relevant in EIBwA. […] At last, autonomic dysregulation may also have a role in causing bronchial obstruction in EIBwA, both through the basal increased parasympathetic tone shown in athletes and through reflex mechanisms induced by exercise.

• #106 Exercise-induced bronchoconstriction: new evidence in pathogenesis, diagnosis and treatment | Asthma Research and Practice | Full Text

  https://asthmarp.biomedcentral.com/articles/10.1186/s40733-015-0004-4

  A direct effect of viral infections, occupational agents and exercise may in fact represent a causal mechanism of bronchoconstriction, alternative to the classic eosinophilic mast cell-dependent pathway occurring in allergic asthma. […] The role of epithelial damage and of substances released by the epithelium and found in sputum, such as interleukin-8 and leukotrienes, and in serum or urines, such as Nerve Growth Factor (NGF) and the Clara cell protein CC16, may also explain the heterogeneous inflammatory response reported in EIBwA. […] The importance of aquaporin, expressed by the subepithelial glandular cells, in regulating the water transport through the epithelium, as well as the increased mucus production, as shown by the increased expression of MUC5AC in induced sputum, may be also relevant in EIBwA. […] At last, autonomic dysregulation may also have a role in causing bronchial obstruction in EIBwA, both through the basal increased parasympathetic tone shown in athletes and through reflex mechanisms induced by exercise.

• #107 Exercise-induced bronchoconstriction: new evidence in pathogenesis, diagnosis and treatment | Asthma Research and Practice | Full Text

  https://asthmarp.biomedcentral.com/articles/10.1186/s40733-015-0004-4

  A direct effect of viral infections, occupational agents and exercise may in fact represent a causal mechanism of bronchoconstriction, alternative to the classic eosinophilic mast cell-dependent pathway occurring in allergic asthma. […] The role of epithelial damage and of substances released by the epithelium and found in sputum, such as interleukin-8 and leukotrienes, and in serum or urines, such as Nerve Growth Factor (NGF) and the Clara cell protein CC16, may also explain the heterogeneous inflammatory response reported in EIBwA. […] The importance of aquaporin, expressed by the subepithelial glandular cells, in regulating the water transport through the epithelium, as well as the increased mucus production, as shown by the increased expression of MUC5AC in induced sputum, may be also relevant in EIBwA. […] At last, autonomic dysregulation may also have a role in causing bronchial obstruction in EIBwA, both through the basal increased parasympathetic tone shown in athletes and through reflex mechanisms induced by exercise.

• #108 Exercise-Induced Asthma: Managing Respiratory Issues in Athletes

  https://www.mdpi.com/2411-5142/9/1/15

  The paradox of asthma in sports lies in the fact that while exercise can trigger asthma symptoms, it is still recommended, and asthma should not deter individuals from participating in sports because sport reduces the minute ventilation required for a given level of exercise and decreases the stimulus for bronchoconstriction.

• #109 Exercise-Induced Asthma: Managing Respiratory Issues in Athletes

  https://www.mdpi.com/2411-5142/9/1/15

  The paradox of asthma in sports lies in the fact that while exercise can trigger asthma symptoms, it is still recommended, and asthma should not deter individuals from participating in sports because sport reduces the minute ventilation required for a given level of exercise and decreases the stimulus for bronchoconstriction.

• #110 What Is Exercise Induced Asthma? | AAFA.org

  https://aafa.org/asthma/asthma-triggers-causes/exercise-induced-asthma/

  The dry and/or cold air is the main asthma trigger for airway narrowing (bronchoconstriction) and inflammation seen in EIB. Exercise that exposes you to cold, dry air is more likely to cause asthma symptoms than exercise involving warm, humid air. […] When you exercise, your body demands more oxygen so you breathe faster and deeper. You usually breathe in through your mouth during exercise. Air that you breathe in from your mouth is dryer and cooler than when you breathe through your nose. […] Good general health, physical conditioning, and medical treatment can prevent EIB in most people. If you have EIB, your doctor will prescribe asthma medicine for you to take to help you manage your symptoms. […] Exercise benefits your entire body. While exercise cannot cure your asthma, some of its health benefits can help keep your asthma well-controlled.

• #111 Managing Exercise-Induced Bronchoconstriction

  https://www.uspharmacist.com/article/managing-exerciseinduced-bronchoconstriction

  Exercise-induced bronchoconstriction (EIB) is a common condition that affects many individuals, especially those with asthma. It is characterized by the narrowing of the airways in response to physical activity or exercise, leading to symptoms such as coughing, wheezing, shortness of breath, and chest tightness. […] To properly advise patients on pharmacologic therapy, pharmacists must have a thorough understanding of the mechanism and symptoms of EIB. […] The mechanism of action of EIB must be understood to guarantee that the appropriate treatment option is prescribed. The two mechanisms proposed to cause EIB are drying of the airway and mucosal cooling. When the airway surface liquid in the lungs dries up from excessive breathing brought on by exercise, it results in increased coughing and mucus production. This loss in water produces a hyperosmolar environment, shifting water out of the cell, thereby shrinking it. Inflammatory mediators such histamines, prostaglandins, and leukotrienes are released as a result. Additionally, as mucus cools from breathing, cholinergic airway receptors are stimulated, leading to an increase in mucus output and smooth muscle tone. These dual mechanisms feed into each other, causing bronchoconstriction when people exercise.

• #112 Exercise-Induced Asthma: Managing Respiratory Issues in Athletes

  https://www.mdpi.com/2411-5142/9/1/15

  The principles for diagnosing EIBA in athletes closely align with those used in the general population, primarily centering on demonstrating airflow limitation. […] The overall management of EIB, whether with or without underlying asthma, should align with similar principles for both athletes and non-athletes. Therefore, the general guidelines for symptom control, prevention of exacerbations, avoidance of airflow limitation, and reducing the risk of asthma-related complications should be followed diligently. […] Inhaled corticosteroids (ICS) are the cornerstone of asthma therapy in athletes. Short-acting beta agonists (SABA) are discouraged as sole treatments. […] The pharmacological therapy for EIB in individuals with asthma follows the same principles as the general therapy for asthma, with the approach being based on the severity and frequency of symptoms. The primary long-term goal is to reduce airway inflammation and prevent bronchoconstriction.

• #113 Exercise-Induced Asthma: Managing Respiratory Issues in Athletes

  https://www.mdpi.com/2411-5142/9/1/15

  The principles for diagnosing EIBA in athletes closely align with those used in the general population, primarily centering on demonstrating airflow limitation. […] The overall management of EIB, whether with or without underlying asthma, should align with similar principles for both athletes and non-athletes. Therefore, the general guidelines for symptom control, prevention of exacerbations, avoidance of airflow limitation, and reducing the risk of asthma-related complications should be followed diligently. […] Inhaled corticosteroids (ICS) are the cornerstone of asthma therapy in athletes. Short-acting beta agonists (SABA) are discouraged as sole treatments. […] The pharmacological therapy for EIB in individuals with asthma follows the same principles as the general therapy for asthma, with the approach being based on the severity and frequency of symptoms. The primary long-term goal is to reduce airway inflammation and prevent bronchoconstriction.

• #114 Exercise-Induced Asthma: Managing Respiratory Issues in Athletes

  https://www.mdpi.com/2411-5142/9/1/15

  The principles for diagnosing EIBA in athletes closely align with those used in the general population, primarily centering on demonstrating airflow limitation. […] The overall management of EIB, whether with or without underlying asthma, should align with similar principles for both athletes and non-athletes. Therefore, the general guidelines for symptom control, prevention of exacerbations, avoidance of airflow limitation, and reducing the risk of asthma-related complications should be followed diligently. […] Inhaled corticosteroids (ICS) are the cornerstone of asthma therapy in athletes. Short-acting beta agonists (SABA) are discouraged as sole treatments. […] The pharmacological therapy for EIB in individuals with asthma follows the same principles as the general therapy for asthma, with the approach being based on the severity and frequency of symptoms. The primary long-term goal is to reduce airway inflammation and prevent bronchoconstriction.

• #115 Exercise-Induced Bronchospasm: Cause and Treatment | Mount Sinai Today

  https://health.mountsinai.org/blog/exercise-induced-bronchospasm-cause-and-treatment/

  The treatment, which involves prevention, is fairly simple. We tell all asthmatics to use a short-acting beta agonist (the rescue inhaler), such as albuterol, 15 minutes prior to exercise. But you should check with the doctor that prescribed this, as there might be other issues she or he will want to discuss with you about exercise. […] If there is underlying asthma, it should be maintained in tip-top shape with other controller medications, as well. But even with adequate medications, in some patients in certain situations, such as extreme exercise in frigid air, EIB can be difficult to control.

• #116 Montelukast (Singulair): Uses, Side Effects, Interactions, Pictures, Warnings & Dosing – WebMD

  https://www.webmd.com/drugs/2/drug-6478-8277/montelukast-oral/montelukast-oral/details

  Montelukast is commonly used for the long-term treatment of asthma and to prevent symptoms of exercise-induced asthma. […] Montelukast helps improve asthma symptoms by blocking substances in the body called leukotrienes that cause inflammation and swelling. […] If you are taking montelukast to prevent exercise-induced asthma, take your dose at least 2 hours before exercise. Always have your rescue inhaler with you.

• #117 Asthma: pathogenesis and novel drugs for treatment | The BMJ

  https://www.bmj.com/content/349/bmj.g5517/rapid-responses

  Vitamin C is involved in the metabolism of histamine and prostaglandins, which are involved in bronchoconstriction. […] In asthmatics, vitamin C decreased post-exercise nitric oxide and cysteinyl leukotrienes. […] There is strong evidence indicating that, in some conditions, vitamin C can reduce bronchoconstriction. […] Three RCTs assessed the effect of vitamin C on asthmatics who suffered from exercise-induced bronchoconstriction (EIB), and found that vitamin C reduced postexercise FEV1 decline by 48%. […] A cough after a marathon run can as well originate from non-viral irritation of the airways, such as with an EIB-kind of etiology. […] Thus, in eight RCTs with subjects under physical stress, vitamin C decreased both objective pulmonary function outcomes and subjective respiratory symptoms.

• #118 Asthma: pathogenesis and novel drugs for treatment | The BMJ

  https://www.bmj.com/content/349/bmj.g5517/rapid-responses

  Even if vitamin C may not be effective for patients with permanent stable asthma, it may beneficially influence pulmonary functions of some asthmatics under certain forms of acute stress, such as when they endure heavy physical activity or suffer from a viral respiratory tract infection. […] Evidently, vitamin C should also be included in the list of potential asthma drugs that should be examined in much more detail.

• #119

  https://link.springer.com/article/10.1007/s11882-005-0084-y

  There is still active debate on the acute mechanism of exercise-induced bronchoconstriction (EIB). […] it is likely that this vasculature enhances the airway response to dehydration and contributes to the pathogenesis of EIB, particularly in elite athletes. […] Accumulating evidence suggests that airway smooth muscle (ASM) becomes more sensitive as a result of repeated exposure to bulk plasma in response to airway injury from dehydration. […] Recent evidence also demonstrates sufficient concentrations of mediators that could affect ASM. […] Paradoxically, mediator release from mast cells may be enhanced and their contractile effects greater when 2-receptor agonists are taken daily. […] The effect of drugs that have the potential to reduce microvascular leak and reduce or inhibit release or action of these mediators needs to be investigated in elite athletes.

• #120

  https://link.springer.com/article/10.1007/s11882-005-0084-y

  There is still active debate on the acute mechanism of exercise-induced bronchoconstriction (EIB). […] it is likely that this vasculature enhances the airway response to dehydration and contributes to the pathogenesis of EIB, particularly in elite athletes. […] Accumulating evidence suggests that airway smooth muscle (ASM) becomes more sensitive as a result of repeated exposure to bulk plasma in response to airway injury from dehydration. […] Recent evidence also demonstrates sufficient concentrations of mediators that could affect ASM. […] Paradoxically, mediator release from mast cells may be enhanced and their contractile effects greater when 2-receptor agonists are taken daily. […] The effect of drugs that have the potential to reduce microvascular leak and reduce or inhibit release or action of these mediators needs to be investigated in elite athletes.

• #121 Exercise-Induced Bronchospasm vs. Exercise-Induced Asthma | AAFP

  https://www.aafp.org/pubs/afp/issues/2004/0215/p808.html

  Although the difference between them has not been fully elucidated, EIB is a bronchospastic disorder, and EIA is an inflammatory condition. […] Studies on EIB are lacking. Two studies examined subjects after exercise and were unable to document increased inflammation on bronchoalveolar lavage or in blood histamine levels. This evidence suggests that EIB may not have an inflammatory base. […] Currently, there are several theories that attempt to explain the mechanism of EIB. The two with the most consensus are the thermal and osmolarity theories. The thermal theory is based on the assumption that hyperventilation during exercise causes loss of heat and drying of the airways that in turn causes a transient bronchoconstrictive response. The osmolarity theory suggests that it is the heat lost during exercise and the rapid rewarming of the airways after exercise that causes a reactive hyperemia of the microvasculature and edema of the airways that sets up an osmotic gradient, which stimulates the release of proinflammatory substances from mast cell and other inflammatory cells. This therapy could possibly explain why steroids and other anti-inflammatory agents have been shown to improve symptoms in patients with EIB. […] As Dr. Hermansen has noted, more research is needed to elucidate the pathophysiology of EIB.

• #122 Pulmonary Issues in the Athlete/Exercise Induced Bronchoconstriction | PM&R KnowledgeNow

  https://now.aapmr.org/pulmonary-issues-in-the-athleteexercise-induced-asthma/

  The re-warming hypothesis has some supporting evidence, but is mostly overlooked for the above hypertonicity mechanism. […] The majority of guidelines are based on studies in patients with both EIB and asthma, and limited data exists on athletes with EIB as their only diagnosis of airway hyperresponsiveness. Optimal treatments may be different in those with EIB and underlying asthma versus those with EIB alone. Additionally, the method used to detect EIB can greatly affect the estimates of prevalence as routine diagnostic strategies may not be appropriate for elite athletes. For this reason, sport-specific protocols performed in provocative environments need to be established. […] In respect to better understanding pathogenesis, new cytokine and genetic markers are being investigated to assess their contributions to the development of EIB. Several genetic alterations have been discovered which may protect or predispose athletes to EIB, but further studies are needed to better delineate the role of genetic susceptibility in EIB.

• #123 Pulmonary Issues in the Athlete/Exercise Induced Bronchoconstriction | PM&R KnowledgeNow

  https://now.aapmr.org/pulmonary-issues-in-the-athleteexercise-induced-asthma/

  The re-warming hypothesis has some supporting evidence, but is mostly overlooked for the above hypertonicity mechanism. […] The majority of guidelines are based on studies in patients with both EIB and asthma, and limited data exists on athletes with EIB as their only diagnosis of airway hyperresponsiveness. Optimal treatments may be different in those with EIB and underlying asthma versus those with EIB alone. Additionally, the method used to detect EIB can greatly affect the estimates of prevalence as routine diagnostic strategies may not be appropriate for elite athletes. For this reason, sport-specific protocols performed in provocative environments need to be established. […] In respect to better understanding pathogenesis, new cytokine and genetic markers are being investigated to assess their contributions to the development of EIB. Several genetic alterations have been discovered which may protect or predispose athletes to EIB, but further studies are needed to better delineate the role of genetic susceptibility in EIB.

• #124 Pulmonary Issues in the Athlete/Exercise Induced Bronchoconstriction | PM&R KnowledgeNow

  https://now.aapmr.org/pulmonary-issues-in-the-athleteexercise-induced-asthma/

  The re-warming hypothesis has some supporting evidence, but is mostly overlooked for the above hypertonicity mechanism. […] The majority of guidelines are based on studies in patients with both EIB and asthma, and limited data exists on athletes with EIB as their only diagnosis of airway hyperresponsiveness. Optimal treatments may be different in those with EIB and underlying asthma versus those with EIB alone. Additionally, the method used to detect EIB can greatly affect the estimates of prevalence as routine diagnostic strategies may not be appropriate for elite athletes. For this reason, sport-specific protocols performed in provocative environments need to be established. […] In respect to better understanding pathogenesis, new cytokine and genetic markers are being investigated to assess their contributions to the development of EIB. Several genetic alterations have been discovered which may protect or predispose athletes to EIB, but further studies are needed to better delineate the role of genetic susceptibility in EIB.

• #125 Pulmonary Issues in the Athlete/Exercise Induced Bronchoconstriction | PM&R KnowledgeNow

  https://now.aapmr.org/pulmonary-issues-in-the-athleteexercise-induced-asthma/

  The re-warming hypothesis has some supporting evidence, but is mostly overlooked for the above hypertonicity mechanism. […] The majority of guidelines are based on studies in patients with both EIB and asthma, and limited data exists on athletes with EIB as their only diagnosis of airway hyperresponsiveness. Optimal treatments may be different in those with EIB and underlying asthma versus those with EIB alone. Additionally, the method used to detect EIB can greatly affect the estimates of prevalence as routine diagnostic strategies may not be appropriate for elite athletes. For this reason, sport-specific protocols performed in provocative environments need to be established. […] In respect to better understanding pathogenesis, new cytokine and genetic markers are being investigated to assess their contributions to the development of EIB. Several genetic alterations have been discovered which may protect or predispose athletes to EIB, but further studies are needed to better delineate the role of genetic susceptibility in EIB.

• #126

  https://www-.grantome.com/grant/NIH/R01-HL033791-09

  The long-term objective of this proposal is to determine the mechanism by which exercise produces airway obstruction in asthmatics. […] Thus, if one could unravel the manner in which exercise produces airway obstruction, it may be possible to gain great insights into the pathophysiology of asthma in general and ultimately into mechanisms for its control. […] The proposed studies are designed to: (1) to examine, in greater depth, the role of the bronchial microvasculature in the development of EIA; (2) to determine if mediators of immediate hypersensitivity are released with thermal challenges and if they play a role in producing the obstructive response; (3) to further explore the mechanism for the refractory period; and (4) to examine the relationship between the airway obstruction produced by ultrasonic aerosols and thermal challenges.

• #127

  https://www-.grantome.com/grant/NIH/R01-HL033791-09

  The long-term objective of this proposal is to determine the mechanism by which exercise produces airway obstruction in asthmatics. […] Thus, if one could unravel the manner in which exercise produces airway obstruction, it may be possible to gain great insights into the pathophysiology of asthma in general and ultimately into mechanisms for its control. […] The proposed studies are designed to: (1) to examine, in greater depth, the role of the bronchial microvasculature in the development of EIA; (2) to determine if mediators of immediate hypersensitivity are released with thermal challenges and if they play a role in producing the obstructive response; (3) to further explore the mechanism for the refractory period; and (4) to examine the relationship between the airway obstruction produced by ultrasonic aerosols and thermal challenges.

• #128

  https://www-.grantome.com/grant/NIH/R01-HL033791-09

  The long-term objective of this proposal is to determine the mechanism by which exercise produces airway obstruction in asthmatics. […] Thus, if one could unravel the manner in which exercise produces airway obstruction, it may be possible to gain great insights into the pathophysiology of asthma in general and ultimately into mechanisms for its control. […] The proposed studies are designed to: (1) to examine, in greater depth, the role of the bronchial microvasculature in the development of EIA; (2) to determine if mediators of immediate hypersensitivity are released with thermal challenges and if they play a role in producing the obstructive response; (3) to further explore the mechanism for the refractory period; and (4) to examine the relationship between the airway obstruction produced by ultrasonic aerosols and thermal challenges.

• #129

  https://www-.grantome.com/grant/NIH/R01-HL033791-09

  These data will permit a systemation evaluation of the variables that are believed to be important in the pathogenesis of EIA. […] The third goal will be obtained by determining if repetitive exercise slows the rate of airway rewarming and if this phenomenon can be offset by increasing the end-challenge thermal gradient. […] The final aim will be accomplished by having asthmatics undergo an exercise bronchoprovocation while airstream temperatures are recorded.

• #130 Exercise-induced asthma (EIA) — Pathogenesis

  https://scholar.sun.ac.za/handle/10019.1/85352

  Exercise-induced asthma (EIA) is defined as ‘the condition in which exercise induces symptoms of asthma in patients who have asthma’. The question is whether EIA is a distinct phenotype of asthma or whether it is just another trigger of symptoms in asthmatic patients.

• #131 Pulmonary Issues in the Athlete/Exercise Induced Bronchoconstriction | PM&R KnowledgeNow

  https://now.aapmr.org/pulmonary-issues-in-the-athleteexercise-induced-asthma/

  The mechanism of EIB is likely multifactorial and not entirely understood, with several theories existing to explain the pathophysiology. The osmotic theory is the most universally accepted. It infers that large volumes of cool, dry air inhaled during exercise lead to changes in the osmolarity of the airway surfaces. A hyperosmolar environment results, triggering a mast cell-mediated release of mediators (i.e. histamine, leukotrienes, prostaglandins) from inflammatory cells, which cause bronchial smooth muscle constriction and edema. Uncontrolled underlying airway inflammation may exacerbate this response. These osmotic and mechanical stresses due to repeated heavy ventilation may also contribute to airway remodeling in the long-term through effects on epithelial cells. Over time this process alters smooth muscle contractile properties, leading to increased bronchial hyper-responsiveness.

• #132 Exercise-induced bronchoconstriction in children: Delphi study and consensus document about definition and epidemiology, diagnostic work-up, treatment, and follow-up | Respiratory Research | Full Text

  https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-024-03078-5

  Exercise-induced bronchoconstriction (EIB) is common in children with asthma but can be present also in children without asthma, especially athletes. […] The mechanisms involved in EIB are complex and not yet fully understood. Two main theories have been proposed: the osmotic theory and the thermal or vascular theory. Both theories might work together and are based on bronchoconstriction and airway edema occurring during exercise. According to the osmotic theory, bronchoconstriction is induced by hyperosmolarity of airway cells, caused by water loss through evaporation when airways need to warm and humidify the cold and dry air inspired into the airways during the hyperventilation of exercise. The hyperosmolarity resulting from drying and cooling of the airways causes hyperflux and degranulation of eosinophils and mast cells with release of inflammatory mediators (histamine, interleukins, tryptase, leukotrienes and prostaglandins) responsible for smooth muscle contraction and mucus production in the bronchial tree.

• #133 Exercise-induced bronchoconstriction: prevalence, pathophysiology, patient impact, diagnosis and management | npj Primary Care Respiratory Medicine

  https://www.nature.com/articles/s41533-018-0098-2

  Exercise-induced bronchoconstriction (EIB) can occur in individuals with and without asthma, and is prevalent among athletes of all levels. […] EIB can also prevent patients with asthma from participating in exercise and negatively impact their quality of life. […] EIB symptoms were improved by inhaling humid air at ambient temperatures and were completely prevented by inhaling fully saturated air, warmed to body temperature. These experiments formed the basis of the heat vs osmotic hypothesis to describe EIB pathophysiology. […] At present, the osmotic theory is widely accepted as the established underlying mechanism of EIB. The osmotic theory suggests that increased ventilation in the airways during periods of exercise leads to water loss from the airway surfaces by evaporation, thus dehydrating the airway surfaces and initiating the events that lead to the contraction of bronchial smooth muscle.

• #134 Exercise-induced Asthma and Bronchoconstriction | RT

  https://respiratory-therapy.com/disorders-diseases/chronic-pulmonary-disorders/asthma/exercise-induced-asthma-bronchoconstriction/

  Exercise-induced bronchoconstriction (EIB) and exercise-induced asthma (EIA) has been recognized in the medical community for a very long time. […] Why EIB/EIA occurs is not clear, but there are three commonly mentioned theories about the mechanism of these conditions. The first is described as the thermal theory. The mechanism here relates to the high volume of air moved in and out of the lung during exercise. This cools and dehydrates the airways, resulting in vasoconstriction, and stimulation of the cholinergic receptors that bring about bronchoconstriction and increased bronchial secretions. […] The second theory is described as the osmotic theory. The mechanism here relates to the bronchial dehydration that occurs with a large increase in minute ventilation. This dehydration causes a hyperosmotic environment in the airway walls, which activates the influx of eosinophils and mast cells. These cells cause the release of mediators such as leukotrienes, histamine, IL-8, tryptase, and prostaglandins. These mediators bring about smooth muscle fiber contraction and bronchoconstriction.

• #135 Exercise-induced bronchoconstriction: new evidence in pathogenesis, diagnosis and treatment | Asthma Research and Practice | Full Text

  https://asthmarp.biomedcentral.com/articles/10.1186/s40733-015-0004-4

  EIB was initially thought to be secondary to a mediator release from mast cells. […] Although mediator release does contribute to cause EIB, pathophysiologic changes induced by intense exercising are definitely more complex. At present, it is widely accepted that hyperventilation through the mouth associated with intense exercise causes the need for humidifying and heating large volumes of air during a short period of time. […] Elegant experiments performed by S.D. Anderson and coworkers show that the respiratory water loss and the increase in osmolarity of the airways surface liquid represent the major determinants of EIB (osmotic theory). […] The vasodilation associated with airways rewarming (thermal theory) may also play a role in inducing bronchial obstruction after exercise. […] However, in EIBwA, the epithelial damage of a large number of bronchial tree divisions down to peripheral airways represents the predominant pathogenic mechanism.

• #136 Exercise-Induced Bronchospasm vs. Exercise-Induced Asthma | AAFP

  https://www.aafp.org/pubs/afp/issues/2004/0215/p808.html

  Although the difference between them has not been fully elucidated, EIB is a bronchospastic disorder, and EIA is an inflammatory condition. […] Studies on EIB are lacking. Two studies examined subjects after exercise and were unable to document increased inflammation on bronchoalveolar lavage or in blood histamine levels. This evidence suggests that EIB may not have an inflammatory base. […] Currently, there are several theories that attempt to explain the mechanism of EIB. The two with the most consensus are the thermal and osmolarity theories. The thermal theory is based on the assumption that hyperventilation during exercise causes loss of heat and drying of the airways that in turn causes a transient bronchoconstrictive response. The osmolarity theory suggests that it is the heat lost during exercise and the rapid rewarming of the airways after exercise that causes a reactive hyperemia of the microvasculature and edema of the airways that sets up an osmotic gradient, which stimulates the release of proinflammatory substances from mast cell and other inflammatory cells. This therapy could possibly explain why steroids and other anti-inflammatory agents have been shown to improve symptoms in patients with EIB. […] As Dr. Hermansen has noted, more research is needed to elucidate the pathophysiology of EIB.

• #137 Exercise-induced Asthma and Bronchoconstriction | RT

  https://respiratory-therapy.com/disorders-diseases/chronic-pulmonary-disorders/asthma/exercise-induced-asthma-bronchoconstriction/

  The third theory is described as the theory of epithelium microtrauma. The mechanism here relates to small airway epithelium dehydration combined with exposure to shear stress caused increased airflow and increased transepithelial pressure gradient. […] With repeated damage and repair, bronchial hyperreactivity and airway remodeling occurs.

• #138

  https://journals.lww.com/acsm-csmr/fulltext/2016/05000/exercise_induced_bronchoconstriction.5.aspx

  Transient immunosuppression also may develop in athletes during periods of intense training, with increased susceptibility to respiratory infections (especially viral), which may increase airway response to exercise acutely and affect overall asthma control (1,2). […] The key stimulus is airway dehydration due to increased ventilation, resulting in a loss of heat, drying of the airways, as well as increased intracellular osmolarity. This triggers the release of inflammatory mediators, leading to airway smooth muscle contraction and airway edema (1,2). […] Mechanical stress/injury to airway epithelium plays a role in the acute response to exercise as well as in the development of airway remodeling in athletes through their effects on smooth muscle contractile properties causing hypersensitivity leading to bronchoconstriction (1,2).

• #139 Exercise-induced asthma in asthmatic children. Predisposing factors | Allergologia et Immunopathologia

  https://www.elsevier.es/es-revista-allergologia-et-immunopathologia-105-articulo-exercise-induced-asthma-in-asthmatic-children–S0301054608725357

  Exercise-induced bronchoconstriction (EIB) has a high prevalence in children with asthma, and this is a common problem, even in case of controlled asthma, because of the high levels of physical activity in the childhood. […] The mechanisms of EIB have not fully been elucidated. While exercise may provide multiple stimuli for induce bronchoconstriction, hyperpnoea is the dominant stimulus for inducing EIB. Cooling and drying, and possibly re-warming affect airways resulting in the release of multiple local inflammatory mediators of which histamine, prostaglandins and, especially leukotrienes are important. Airway narrowing occurs post-exercise as a result of the mediator release, which is possibly produced along with warming of the airway, resulting bronchoconstriction, vascular engorgement and leakage, and increased mucus production.

• #140 Exercise-Induced Asthma: Managing Respiratory Issues in Athletes

  https://www.mdpi.com/2411-5142/9/1/15

  The pathogenesis of EIB in athletes is multi-faceted and influenced by various factors, including the type of sport, training environment, genetics, and individual sensitivities. It involves a complex interplay of physiological and environmental factors. […] Bronchoconstriction during Exercise: The hallmark feature of EIA is the narrowing of the airways during or after physical exertion. In athletes, this EIB typically occurs due to increased ventilation during intense exercise. As athletes breathe more deeply and rapidly, they inhale larger volumes of cold dry air, leading to airway cooling and dehydration of the airway surface. […] Airway Inflammation: Underlying airway inflammation is a common factor in both EIBA and EIBwA. Exercise, particularly in challenging environmental conditions, such as cold or dry air, can irritate and inflame the airway epithelium. This inflammation triggers the release of various inflammatory mediators, leading to bronchoconstriction.

• #141 Exercise-induced bronchoconstriction: new evidence in pathogenesis, diagnosis and treatment | Asthma Research and Practice | Full Text

  https://asthmarp.biomedcentral.com/articles/10.1186/s40733-015-0004-4

  A direct effect of viral infections, occupational agents and exercise may in fact represent a causal mechanism of bronchoconstriction, alternative to the classic eosinophilic mast cell-dependent pathway occurring in allergic asthma. […] The role of epithelial damage and of substances released by the epithelium and found in sputum, such as interleukin-8 and leukotrienes, and in serum or urines, such as Nerve Growth Factor (NGF) and the Clara cell protein CC16, may also explain the heterogeneous inflammatory response reported in EIBwA. […] The importance of aquaporin, expressed by the subepithelial glandular cells, in regulating the water transport through the epithelium, as well as the increased mucus production, as shown by the increased expression of MUC5AC in induced sputum, may be also relevant in EIBwA. […] At last, autonomic dysregulation may also have a role in causing bronchial obstruction in EIBwA, both through the basal increased parasympathetic tone shown in athletes and through reflex mechanisms induced by exercise.

• #142

  https://www.termedia.pl/Asthma-and-exercise-induced-respiratory-disorders-r-nin-athletes-The-position-paper-of-the-Polish-Society-r-nof-Allergology-and-Polish-Society-of-Sports-Medicine,123,36304,1,0.html

  Asthma is a heterogeneous disease typically associated with a chronic respiratory inflammation which is defined as a syndrome of such respiratory symptoms as wheezing, dyspnoea, chest tightening and coughing which differ in time and intensity and are connected with variable airways obstruction. Currently discussed pathogenic mechanisms potentially responsible for exercise-induced bronchoconstriction in people who practice high-intensity exercise on a regular basis include: osmotic and thermal changes in airways mucosa caused by exercise-induced hyperventilation (osmotic and thermal hypothesis); damage to respiratory epithelium; increasing severity of the airway inflammation; neural activation. Osmotic and thermal changes to bronchial mucosa are the rationale behind the osmotic and thermal hypotheses which are considered as classical ones in the attempts to explain the pathogenesis of EIB in athletes. Increased water evaporation from the mucosa during exercise leads to the increase in the osmolarity of the fluid covering the respiratory epithelium. The changes to osmotic relations result in the lysis of the cells and the release of the mediators including cysteinyl leukotrienes which have strong bronchoconstrictive properties. Furthermore, the airway cooling activates cholinergic receptors, which causes increased tension of bronchial smooth muscles and enhanced fluid secretion in airways. Directly after exercise completion the respiratory tract warming commences and leads to secondary hyperaemia and increased capillary permeability in the bronchial wall. A rise in the number of inflammatory cells (eosinophils, neutrophils, epithelial cells) has been observed in the respiratory tract of athletes. A large body of evidence has already proven that damage to respiratory epithelium during exercise (particularly in adverse environmental conditions) significantly increases susceptibility to EIB. The conclusions mentioned above were drawn from the analyses of the markers of respiratory epithelium damage (e.g. protein CC16). Unfavourable and harmful environmental conditions for exercise can also contribute to respiratory tract damage and increased susceptibility to EIB. The most spectacular associations were found in the relations between exposure to chlorine compounds (trichloramine) while swimming and the increase in bronchial hyperreactivity (BHR). Exposure to dry and cold air while practicing endurance winter sports can be another factor which increases the risk of EIB. Some other studies, however, do not provide results which are compelling enough to significantly associate exercise in adverse conditions with predisposition to EIB. It is suggested that damage to respiratory epithelium occurs only in the presence of BHR symptoms or exercise-induced bronchoconstriction. Consequently, mutual causation and the sequence of the described phenomena are still open to discussion. The innervation of the respiratory tract is mainly composed of parasympathetic fibres. Stimulation of parasympathetic cholinergic fibres results in bronchoconstriction. In the light of the recent research, high-intensity exercise is thought to magnify para-sympathomimetic activity, thereby increasing the tension of bronchial smooth muscles and, consequently, increasing the probability of EIB. The relationship between BHR and some autonomic nervous system-dependent responses, e.g. perspiration, tearing, saliva production, have been reported. However, although chronically enhanced parasympathomimetic nervous system activity is observed there are data which do not confirm the correlation between BHR and dysfunctional autonomic regulation. Some authors suggest that autonomic modulation may be involved in BHR development but only when accompanied by the risk of inspiring harmful components of the air. Neurogenic inflammation is also considered in the investigation of EIB pathogenesis. High-intensity exercise elevates the concentration of substance P which is one of the key mediators of neurogenic inflammation. Acetylcholine and nerve growth factor (NGF) have also been put forward as potentially involved in the development of the EIB-provoking inflammation. Since none of the aforementioned mechanisms fully explains the pathogenesis of EIB, potential interaction of several mechanisms should be taken into account while assessing individual predisposition to exercise-induced respiratory symptoms. The identification of the athletes susceptible to EIB appears to be the key issue here as it may contribute to the improvement of preventive measures. The observations made within the last 20-30 years indicate that the asthma rate is higher in athletes, especially those practicing endurance sports. The risk of asthma in the athletes with atopy symptoms is several times higher than in healthy population.

• #143 Exercise-Induced Asthma: Managing Respiratory Issues in Athletes

  https://www.mdpi.com/2411-5142/9/1/15

  Asthma is a complex respiratory condition characterized by chronic airway inflammation and variable expiratory airflow limitation, affecting millions globally. Among athletes, particularly those competing at elite levels, the prevalence of respiratory conditions is notably heightened, varying between 20% and 70% across specific sports. […] Exercise-induced bronchoconstriction (EIB) is a common issue among athletes, impacting their performance and well-being. The pathogenesis of EIB involves complex interactions between physiological and environmental factors. Airway dehydration and cooling are key mechanisms, leading to osmotic and thermal theories. Airway inflammation and hyper-responsiveness are common factors. Elite athletes often exhibit distinct inflammatory responses and heightened airway sensitivity, influenced by sport type, training, and environment.

• #144 Exercise-Induced Asthma: Managing Respiratory Issues in Athletes

  https://www.mdpi.com/2411-5142/9/1/15

  The pathogenesis of EIB in athletes is multi-faceted and influenced by various factors, including the type of sport, training environment, genetics, and individual sensitivities. It involves a complex interplay of physiological and environmental factors. […] Bronchoconstriction during Exercise: The hallmark feature of EIA is the narrowing of the airways during or after physical exertion. In athletes, this EIB typically occurs due to increased ventilation during intense exercise. As athletes breathe more deeply and rapidly, they inhale larger volumes of cold dry air, leading to airway cooling and dehydration of the airway surface. […] Airway Inflammation: Underlying airway inflammation is a common factor in both EIBA and EIBwA. Exercise, particularly in challenging environmental conditions, such as cold or dry air, can irritate and inflame the airway epithelium. This inflammation triggers the release of various inflammatory mediators, leading to bronchoconstriction.

• #145 Exercise-Induced Asthma: Managing Respiratory Issues in Athletes

  https://www.mdpi.com/2411-5142/9/1/15

  The principles for diagnosing EIBA in athletes closely align with those used in the general population, primarily centering on demonstrating airflow limitation. […] The overall management of EIB, whether with or without underlying asthma, should align with similar principles for both athletes and non-athletes. Therefore, the general guidelines for symptom control, prevention of exacerbations, avoidance of airflow limitation, and reducing the risk of asthma-related complications should be followed diligently. […] Inhaled corticosteroids (ICS) are the cornerstone of asthma therapy in athletes. Short-acting beta agonists (SABA) are discouraged as sole treatments. […] The pharmacological therapy for EIB in individuals with asthma follows the same principles as the general therapy for asthma, with the approach being based on the severity and frequency of symptoms. The primary long-term goal is to reduce airway inflammation and prevent bronchoconstriction.

• #146 Exercise-Induced Asthma: Managing Respiratory Issues in Athletes

  https://www.mdpi.com/2411-5142/9/1/15

  The paradox of asthma in sports lies in the fact that while exercise can trigger asthma symptoms, it is still recommended, and asthma should not deter individuals from participating in sports because sport reduces the minute ventilation required for a given level of exercise and decreases the stimulus for bronchoconstriction.

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