Gadolinium does not blunt the cardiovascular responses at the onset of voluntary static exercise in cats: a predominant role of central command

Abstract

The cardiovascular adaptation to voluntary static exercise is controlled by the autonomic nervous system. Two neural mechanisms are responsible for the cardiovascular adaptation at the onset of exercise. One is central command descending from higher brain centers, and the other is muscle mechanosensitive reflex from activation of mechanoreceptors in the contracting muscles. To examine which mechanism played a major role in the initial cardiovascular adaptation during static exercise, we studied the effect of intravenous injection of gadolinium (55μM), a blocker of stretch-activated ion channels, on the increases in heart rate (HR) and mean arterial blood pressure (MAP) at the onset of static exercise (pressing a bar with a forelimb) in conscious cats. Gadolinium did not blunt the initial increases in HR and MAP at the onset of exercise, although the peak force applied to the bar was gradually decreased following gadolinium. Next, we examined the effect of gadolinium on the reflex changes in HR and MAP in response to passive mechanical stretch of a forelimb or hindlimb in anesthetized cats. Gadolinium significantly blunted their increases during passive stretch, indicating that the cardiovascular responses to passive limb stretch is evoked by a reflex from stimulation of muscle mechanosensitive receptors. It appeared that gadolinium blocked the stretch-activated ion channels and thereby attenuated the reflex responses. Therefore it is concluded that the initial cardiovascular adaptation at the onset of voluntary exercise in conscious cats is induced by feedforward control from direct descending signal from higher brain centers, but not by the muscle mechanoreflex.