HYPERPNEA AND HEAT-FLUX - INITIAL REACTION SEQUENCE IN EXERCISE-INDUCED ASTHMA

The authors have previously demonstrated that the magnitude of postexertional asthma is proportional to the heat exchange that occurs within the airways. Because the level of ventilation is an important determinant of the quantity of heat transferred from the mucosa, they reasoned that if they simulated the hyperpnea of exercise by hyperventilation, they could produce heat exchange similar to that seen with exercise, and equivalent bronchial obstruction. To test this hypothesis, they had 8 asthmatics perform 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. 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 terminal burden on the airways at maximal ventilation (VE), the bronchospastic response progressively increased. Decreasing the thermal burden by decreasing VE proportionally reduced the response. From this the authors conclude that the major stimulus for exercise-induced asthma is heat loss from the mucosa with subsequent cooling precipitated by the hyperpnea of exercise but not exercise per se.