Neural and humoral signals for pulmonary ventilation arising in exercising muscle.

Abstract

This review analyzes attempts to isolate and quantify the neurally and humorally mediated portions of the ventilatory response to moderate exercise. 1. Dejours' "neuro-humoral theory" postulates that, following a change from rest to moderate, constant-load exercise in man, the abrupt initial increase in VE is neurally mediated, and the subsequent gradual rise in VE is humorally mediated. However, no compelling evidence exists to support either of these hypotheses. Moreover, there is a plausible alternative method of partitioning VE into fast and slow components: the steady-state value of VE may be entirely due to the slow component. 2. The similarity between the kinetics of VE and VCO2 during exercise suggests that the ventilatory response may be primarily triggered by a signal that has its origin in the CO2 flux to the lung. Intravenous CO2 loading in resting animals produces such a flux, unaccompanied by possible neural signals arising from contracting muscles. However, experiments of this type have produced drastically conflicting results. 3. With cross-circulation techniques, the ventilatory response to neural signals from exercising limbs can be isolated, by sending the blood leaving these limbs directly into the venous system of another animal. Experiments of this type with anesthetized dogs led Kao and co-workers to conclude that the increase in VE during steady-state exercise is entirely due to neural signals originating in the exercising limbs. 4. In skeletal muscle, the kinetics of VO2 closely follow those of the concentrations of creatine phosphate and free creatine: a sensor of either of these concentrations could thus theoretically serve as a useful "metaboreceptor". The extracellular concentration of K+ in contracting muscles also changes rapidly enough to lead cardio-ventilatory adjustments, and thus might possibly trigger a neural signal involved in their control.