Control of skeletal muscle perfusion at the onset of dynamic exercise

At the onset of exercise there is a rapid increase in skeletal muscle vascu lar conductance and blood flow. Several mechanisms involved in the regulati on of muscle perfusion have been proposed to initiate this hyperemic respon se, including neural, metabolic, endothelial, myogenic, and muscle pump mec hanisms. Investigators utilizing pharmacological blockade of cholinergic mu scarinic receptors and sympathectomy have concluded that neither sympatheti c cholinergic nor adrenergic neural mechanisms are involved in the initial hyperemia. Studies have also shown that the time course for vasoactive meta bolite release, diffusion, accumulation, and action is too long to account for the rapid increase in vascular conductance at the initiation of exercis e. Furthermore, there is little or no evidence to support an endothelium or myogenic mechanism as the initiating factor in the muscle hyperemia. Thus, the rise in muscle blood flow does not appear to be explained by known neu ral, metabolic, endothelial, or myogenic influences. However, the initial h yperemia is consistent with the mechanical effects of the muscle pump to in crease the arteriovenous pressure gradient across muscle. Because skeletal muscle blood flow is regulated by multiple and redundant mechanisms, it is likely that neural, metabolic, and possibly endothelial factors become impo rtant modulators of mechanically induced exercise hyperemia following the f irst 5-10 s of exercise.