Journal of Applied Physiology, Vol 47, Issue 1 126-137, Copyright © 1979 by American Physiological Society
Ventilatory response to muscular exercise: observations regarding a humoral pathway
S. Levine
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.
