抄録
Feedback regulation by activation of group III and IV thin fiber afferents in exercising muscle causes the cardiovascular and sympathetic nerve responses (termed exercise pressor reflex). Mechanical stimuli activate mainly group III afferents, some of which are sensitive to a change in temperature. The mechanical response of group III afferents might be modulated by thermal stimuli. However, the effect of intramuscular temperature on the exercise pressor reflex remained little known. To test the hypothesis that the mechanoreflex might be altered by decreasing temperature of the exercising muscle, we studied the effect of local muscle cooling on the increases in cardiac sympathetic nerve activity (CSNA), heart rate (HR), and mean arterial blood pressure (MAP) during evoked static contraction and passive stretch of the triceps surae muscle in anesthetized cats. Gadolinium, a blocker of mechanosensitive ion channels, blunted the increases in CSNA, HR, and MAP during static contraction as well as passive stretch, suggesting the significant contribution of muscle mechanoreceptors to the exercise pressor reflex. Intramuscular temperature of the triceps surae muscle decreased from 35±1 °C to 19±1 °C by muscle cooling. The baseline HR and MAP were reduced by muscle cooling, while the baseline CSNA was increased. Local muscle cooling blunted the increases in CSNA, HR, and MAP during static contraction, despite the same tension development. We suggest that the exercise pressor reflex is influenced by muscle cooling, probably due to decreasing discharge of muscle mechanosensitive afferents. [J Physiol Sci. 2007;57 Suppl:S201]
