Ventilatory response to muscular exercise: observations regarding a humoral pathway.

To assess the role of humoral mechanisms in eliciting the hyperpnea of muscular exercise, anesthetized dogs underwent complete spinal transection at the second lumbar level (L2). Muscular exercise of the denervated hindlimbs was then induced by electrical stimulation. Coincident with hindlimb muscle contraction, oxygen consumption (VO2) increased 173% and ventilation (VE) increased 163%; no statistically significant changes occurred in arterial carbon dioxide tension (PCO2), arterial pH, or arterial oxygen saturation. Similar results were obtained after peripheral chemodenervation and vagotomy plus spinal transection. In order to evaluate the possibility that extracranial receptors mediate the increases in VE elicited by exercise-induced humoral factors, heads of vagotomized L2 spinal-transected dogs were perfused entirely by a support dog with blood of unchanging gas composition via both carotid and both vertebral arteries. The carotid bodies lay within the region of the perfused head; the aortic bodies were denervated. These L2 spinal-transected head-perfused animals still responded to hindlimb exercise with a 156% increase in VO2 and a 122% increase in VE. We conclude that muscular exercise can stimulate VE via humoral factors other than usual chemical stimuli in arterial blood (i.e., PCO2, pH, or O2 saturation). Extracranial receptors (other than conventional peripheral arterial chemoreceptors) appear to mediate a major portion of the increase in VE elicited by exercise-induced humoral factors.