Evidence in man for a fast neural mechanism during the early phase of exercise hyperpnea.

Recently, the rapid increase in ventilation at the onset of exercise has been attributed to reflexes stimulated by the concomitant increase in cardiac output. To evaluate these 'fast-humoral' hypotheses in supine man, the heart rate, ventilation, and end-tidal PCO2 and PO2 were observed during four procedures: the onset of mild dynamic exercise by the lower legs (1) with and (2) without inflation of occluding cuffs around the upper thighs, (3) rapid induction of circulatory occlusion at the level of the upper thighs, and (4) abrupt release of circulatory occlusion after 2.5 min of ischemia. Exercise resulted in abrupt hyperpnea, alveolar hyperventilation, and tachycardia whether or not there was circulatory occlusion. Circulatory occlusion engendered abrupt bradycardia and transient, hyperventilatory hyperpnea. Release of circulatory occlusion resulted in relatively large tachycardia and, after a delay, small hyperpnea and alveolar hypoventilation. The results demonstrate that the early response to exercise is not inherently isocapnic hyperpnea and that, contrary to the prediction of the fast-humoral hypotheses, the presumed increase in cardiac output following cuff release does not produce a ventilatory response similar to that of exercise. These findings support the existence of a neurally mediated factor during the early stages of exercise hyperpnea.