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. In this study we examined which mechanism played a major role in the initial cardiovascular adaptation during static exercise. To solve this, we studied the effect of intravenous injection of gadolinium (Gd, 55μM), a blocker of stretch-activated ion channel, 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. Gd 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 Gd. Next, we examined the effect of Gd on the reflex changes in HR and MAP in response to passive mechanical stretch of a forelimb or hindlimb in anesthetized cats. Gd significantly blunted their increases during passive stretch, indicating that Gd may block the stretch-activated ion channel and thereby attenuate the reflex responses. In conclusion, the present finding that Gd did not affect the initial cardiovascular responses at the onset of voluntary static exercise suggests that central command predominantly contributes to the initial cardiovascular adaptation. [Jpn J Physiol 55 Suppl:S92 (2005)]
