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Airway injury as a mechanism for exercise-induced bronchoconstriction in elite athletes
Abstract
Exercise-induced bronchoconstriction (EIB) is a consequence of evaporative water loss in conditioning the inspired air. The water loss causes cooling and dehydration of the airway surface. One acute effect of dehydration is the release of mediators, such as prostaglandins, leukotrienes, and histamine, that can stimulate smooth muscle, causing contraction and a change in vascular permeability. Inspiring cold air increases dehydration of the surface area and causes changes in bronchial blood flow. This article proposes that the pathogenesis of EIB in elite athletes relates to the epithelial injury arising from breathing poorly conditioned air at high flows for long periods of time or high volumes of irritant particles or gases. The evidence to support this proposal comes from many markers of injury. The restorative process after injury involves plasma exudation and movement of cells into the airways, a process repeated many times during a season of training. This process has the potential to expose smooth muscle to a wide variety of plasma- and cell-derived substances. The exposure to these substances over time can lead to an alteration in the contractile properties of the smooth muscle, making it more sensitive to mediators of bronchoconstriction. It is proposed that cold-weather athletes have airway hyperresponsiveness (AHR) to pharmacologic agents as a result of epithelial injury. In those who are allergic, AHR can also be expressed as EIB. The role of beta(2)-receptor agonists in inhibiting and enhancing the development of AHR and EIB is discussed.
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“Furthermore, in the general community the acute respiratory symptoms usually have a viral cause, but it is not obvious that similar symptoms occurring after heavy exercise are caused by a viral infection because they can also result from exercise‐induced bronchoconstriction (EIB) symptoms caused by an injury to the airways because of exceptional ventilatory exertion (Anderson 2008).”
From Vitamin C for preventing and treating the common cold (2013) · cites this paper as Anderson 2008
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Metadata
- Authors
- Anderson, S. D., & Kippelen, P.
- Affiliations
- Royal Prince Alfred Hospital (AU)
- University of Aberdeen (GB)
- Corresponding author
- Anderson, Sandra D.
- Venue
- Journal of Allergy and Clinical Immunology
- Publisher
- Elsevier BV
- Published
- 2008-08
- Volume
- 122
- Issue
- 2
- Pages
- 225-235
- ISSN
- 0091-6749 (ISSN-L)
- OpenAlex
- W1966370024
- Semantic Scholar
- 4b75678f6bce41311a4bde4f6ec899f7a7355e94
- Cited by
- 237
- References
- 165
- Citations by year
- 2026: 8 · 2025: 6 · 2024: 7 · 2023: 5 · 2022: 13 · 2021: 5 · 2020: 17 · 2019: 12 · 2018: 17 · 2017: 11 · 2016: 16 · 2015: 8 · 2014: 10 · 2013: 19 · 2012: 18
- FWCI
- 1.99
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Allergy and Clinical Immunology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Asthma and respiratory diseases
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Respiratory and Cough-Related Research
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Occupational exposure and asthma
- Keywords
- exercise-induced bronchoconstriction, airway injury, airway epithelial injury, airway cooling, airway hyperresponsiveness, elite athletes, plasma exudation, beta2-adrenergic agonists, allergic airway disease, bronchial blood flow, airway irritants
- MeSH terms
- Adrenergic beta-Agonists, Asthma, Exercise-Induced, Bronchi, Capillary Permeability, Epithelial Cells, Humans, Inflammation, Mast Cells, Muscle, Smooth, Sports, Exercise, Eicosanoids, Bronchoconstriction, Bronchoconstrictor Agents, Methacholine Chloride, Bronchial Hyperreactivity
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