| 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. |
