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It was previously demonstrated that the magnitude of post exertional asthma is proportional to the heat exchange that occurs within the airways. Since the level of ventilation is an important determinant of the quantity of heat transferred from the mucosa, it was reasoned that if we simulated the hyperpnea of exercise by hyperventilation, heat exchange would be produced similar to that seen with exercise, and thus equivalent bronchial obstruction. To test this hypothesis, 8 asthmatics performed eucapnic hyperventilation to mean levels of 63 and 44 L/min while they breathed dry air at subfreezing (-12 C) and room temperature (23 C) and fully saturated air at room and body temperature through a heat exchanger in a random order. Hyperventilation at body conditions (0 heat flux) did not result in any change in pulmonary mechanics. However, as the water content and temperature of the inspirate were decreased, thus increasing the thermal burden on the airways at maximal ventilation (V sub E), the bronchospastic response progressively increased. Decreasing the thermal burden by decreasing V sub E proportionally reduced the response. From this we conclude that the major stimulus for exercise-induced asthma is heat loss from the mucosa with subsequent cooling, which is precipitated by the hyperpnea of exercise but not exercise per se.
Deal et al. (Thu,) studied this question.