PMID: 15683611Feb 3, 2005

Exercise-induced bronchoconstriction: pathogenesis

Current Allergy and Asthma Reports
Sandra D Anderson, Pascale Kippelen

Abstract

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.

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Related Concepts

Pathogenic Aspects
Bronchial System
Pathogenesis
Mast Cell
Exercise, Isometric
Pathologic Vasoconstriction
Response to Water Deprivation
Smooth Muscle
Adrenergic beta-Agonists
Adrenergic beta-2 Receptor Agonists

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