Interaction of neural and local mechanisms in the control of skeletal muscle blood flow.

摘要

The current project sought to characterize the interaction of neural and local mechanisms of skeletal muscle blood flow control through exogenous and endogenous alpha-adrenoreceptor activation. We hypothesized that alpha1- and alpha2-adrenoreceptors in the human leg would exhibit differential distribution and responsiveness, and that unilateral knee-extensor exercise would attenuate alpha-adrenoreceptor-mediated vasoconstriction in an intensity-dependant manner. We also hypothesized that carotid baroreflex (CBR)-mediated sympathoexcitation would provoke less vasoconstriction during exercise than at rest. Intra-arterial infusion of phenylephrine (PE, alpha 1-agonist) or BHT-933 (alpha2-agonist) reduced femoral blood flow (FBF) by approximately 60% at rest, but during exercise (27W) the degree of vasoconstriction evoked by PE and BHT was significantly reduced. During ramped (7W--37W) exercise, BHT did not reduce FBF at any intensity, while some degree of PE-induced vasoconstriction was evident at all but the highest exercise intensity. Using sinusoidal neck pressure, CBR-mediated changes in heart rate (HR), arterial blood pressure (ABP) muscle sympathetic nerve activity (MSNA), FBF, and tissue oxygenation (TOm) were seen at rest. During 7W exercise, CBR-mediated control of ABP, FBF, and TOm was attenuated. We conclude that exercise attenuates alpha-adrenergic responsiveness to exogenous and endogenous activation to ensure sufficient muscle blood flow while maintaining systemic ABP homeostasis.