Exercise-induced bronchoconstriction: pathogenesis.

S. D. Anderson, Pascale Kippelen

    Research output: Contribution to journalEditorial

    102 Citations (Scopus)

    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.

    Original languageEnglish
    Pages (from-to)116-122
    Number of pages6
    JournalCurrent Allergy and Asthma Reports
    Volume5
    Issue number2
    Publication statusPublished - 2005

    Keywords

    • CANINE PERIPHERAL AIRWAYS
    • THERMALLY-INDUCED ASTHMA
    • CROSS-COUNTRY SKIERS
    • MAST-CELL
    • BRONCHIAL HYPERRESPONSIVENESS
    • INDUCED BRONCHOSPASM
    • BETA(2)-ADRENOCEPTOR-MEDIATED RESPONSES
    • NONASTHMATIC SUBJECTS
    • ISOCAPNIC HYPERPNEA
    • ALLERGIC RHINITIS

    Cite this

    Anderson, S. D., & Kippelen, P. (2005). Exercise-induced bronchoconstriction: pathogenesis. Current Allergy and Asthma Reports, 5(2), 116-122.