Exercise-induced bronchoconstriction: pathogenesis

There is still active debate on the acute mechanism of exercise-induced bronchoconstriction (EIB). Although it is unlikely that vasoconstriction and hyperemia of the bronchial vasculature are essential events for EIB, it is likely that this vasculature enhances the airway response to dehydration and...

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Bibliographic Details
Published in:Current allergy and asthma reports 2005-03, Vol.5 (2), p.116-122
Main Authors: Anderson, Sandra D, Kippelen, Pascale
Format: Article
Language:English
Subjects:
Adrenergic beta-2 Receptor Agonists
Adrenergic beta-Agonists - pharmacology
Bronchial Hyperreactivity - etiology
Bronchoconstriction
Exercise
Humans
Mast Cells - physiology
Muscle, Smooth - physiology
Muscular system
Pathogenesis
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Summary:There is still active debate on the acute mechanism of exercise-induced bronchoconstriction (EIB). Although it is unlikely that vasoconstriction and hyperemia of the bronchial vasculature are essential events for 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 beta(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.
ISSN:1529-7322
1534-6315
DOI:10.1007/s11882-005-0084-y