Airways inflammatory and atopy-related responses in athletes

Authors

  • AJ McKune
  • LL Smith

DOI:

https://doi.org/10.17159/2078-516X/2006/v18i2a243

Abstract



The prevalence of asthma and airway hyperresponsiveness (AHR) in highly trained endurance athletes is rising. The type of training (i.e. endurance, or speed and power) seems to influence the airway symptoms. High-intensity exercise and training might contribute to the development of asthma or AHR in athletes previously unaffected by these airway disorders. Repeated hyperventilation of unconditioned air, as well as air containing irritants and/or allergens has been suggested to cause thermal, mechanical, or osmotic airway trauma resulting in damage to the airway epithelium. Subsequent airway inflammatory responses may be responsible for the development of atopy-related symptoms in endurance athletes such as those observed in asthma and AHR. Eosinophils and neutrophils are the inflammatory cells that have been frequently observed to be elevated in the airways of endurance athletes. The trafficking of these cells to the airways may possibly be regulated by TH2 cytokines that are expressed in the airways in response to epithelial cell damage. In addition, these airway inflammatory responses may lead to airway remodelling similar to that which occurs in asthma. The effect of the exercise challenge itself may initiate airway atopy-related and inflammatory responses in endurance athletes. While the literature seems to support the role of local airway conditions and/or events in inducing atopy-related symptoms in athletes, it is proposed that alterations in the hormonal and/or cytokine milieu with intense competition and/or training may also play a role.

South African Journal of Sports Medicine Vol. 18 (2) 2006: pp. 46-51

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Published

2006-02-03

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Articles

How to Cite

McKune, A., & Smith, L. (2006). Airways inflammatory and atopy-related responses in athletes. South African Journal of Sports Medicine, 18(2), 46-51. https://doi.org/10.17159/2078-516X/2006/v18i2a243
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