Allergy and Sports: Exercise-Induced Asthma

Abstract

In some asthmatic subjects exercise is followed by a bronchospastic response that generally lasts 30-60 minutes and regresses spontaneously. The initiating stimulus is thought to be the cooling and/or dehydration of airways caused by hyperpnea. The mechanisms leading from thermodynamic changes to airway narrowing are object of controversy. Two hypotheses have been proposed, one suggesting that an increase in the osmolarity of airway lining fluid following water loss causes mediator release, and the other suggesting that an excessive vasodilation during airway rewarming causes vascular engorgement, thus reducing airway caliber. Other controversial issues in exercise-induced asthma are the role of airway inflammation and the question whether a late-phase response may occur. That inflammatory cells and mediators play a role is suggested by increased numbers of eosinophil and epithelial cells in bronchoalveolar lavage and by the efficacy of cromolyn and leukotriene antagonists in preventing EIA. The existence of late-phase response to exercise is questionable because exercise does not cause an increase in airway responsiveness, which usually accompanies late-phase responses to allergens. Furthermore, data of bronchoalveolar lavage and bronchial biopsy suggest that the delayed bronchoconstriction that may be observed after exercise reflects airway instability in subjects with more prominent eosinophilic inflammation of airways and is not specific to exercise.

Key words

Bronchoconstriction - heat exchange - water exchange - airway inflammation