Stimulus and mechanisms of exercise-induced bronchoconstriction

Abstract

<h3>Educational aims</h3> To describe the stimulus for exercise-induced bronchoconstriction. To describe the different mechanisms whereby this stimulus may act to cause the airways to narrow in asthmatics and athletes. To describe the relevance of the stimulus and mechanism to protocols to diagnose exercise-induced bronchoconstriction. To describe the inflammatory mediators involved in exercise-induced bronchoconstriction. To describe how and why airway injury could contribute to the pathogenesis of airway hyperresponsiveness and exercise-induced bronchoconstriction in athletes. <h3>Summary</h3> The stimulus for exercise-induced bronchoconstriction (EIB) is the loss of water by humidifying large volumes of air during exercise. The mechanism for EIB relates to the thermal and osmotic effects of water loss. The thermal theory proposes that EIB is a vascular event comprising vasoconstriction during exercise followed by rapid rewarming and a reactive hyperaemia at the end of exercise. The osmotic theory proposes that water loss induces an increase in osmolarity in the airways, which causes the release of mediators that cause bronchial smooth muscle to contract. Increased vascular permeability and leakage are common to both theories.