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
