Hyperpnea and heat flux: initial reaction sequence in exercise-induced asthma

Abstract

The magnitude of postexertional asthma is apparently proportional to the heat exchange that occurs within the airways. Because the ventilation level is an important determinant of the quantity of heat transferred from the mucosa, if the hyperpnea of exercise was simulated by hyperventilation, heat exchange similar to that seen with exercise and equivalent bronchial obstruction would be produced. To test this hypothesis, 8 asthmatics performed eucapnic hyperventilation to mean levels of 63 and 44 1/min while they breathed dry air at subfreezing (-12.degree. C) and room temperature (23.degree. C), and fully saturated air at room and body temperature, through a heat exchanger in a random order. Multiple aspects of pulmonary mechanics were measured before and after each challenge. 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, increasing the thermal burden on the airways at maximal ventilation (.ovrhdot.VE), the bronchospastic response progressively increased. Decreasing the thermal burden by decreasing .ovrhdot.VE proportionally reduced the response. The major stimulus for exercise-induced asthma is apparently heat loss from the mucosa with subsequent cooling precipitated by the hyperpnea of exercise but not exercise per se.