Exercise attenuates alpha-adrenergic-receptor responsiveness in skeletal muscle vasculature

Attenuation of sympathetic vasoconstriction (sympatholysis) in working musc les during dynamic exercise is controversial. A potential mechanism is a re duction in alpha -adrenergic-receptor responsiveness. The purpose of this s tudy was to examine alpha (1)- and alpha (2)-adrenergic-receptor-mediated v asoconstriction in resting and exercising skeletal muscle using intra-arter ial infusions of selective agonists. Thirteen mongrel dogs were instrumente d chronically with flow probes on the external iliac arteries of both hindl imbs and a catheter in one femoral artery. The selective alpha (1)-adrenerg ic agonist (phenylephrine) or the selective alpha (2)-adrenergic agonist (c lonidine) was infused as a bolus into the femoral artery catheter at rest a nd during mild and heavy exercise. Intra-arterial infusions of phenylephrin e elicited reductions in vascular conductance of 76 +/- 4, 71 +/- 5, and 31 +/- 2% at rest, 3 miles/h, and 6 miles/h and 10% grade, respectively. Intr a-arterial clonidine reduced vascular conductance by 81 +/- 5, 49 +/- 4, an d 14 +/- 2%, respectively. The response to intra-arterial infusion of cloni dine was unaffected by surgical sympathetic denervation. Agonist infusion d id not affect either systemic blood pressure, heart rate, or blood flow in the contralateral iliac artery, alpha (1)-Adrenergic-receptor responsivenes s was attenuated during heavy exercise. In contrast, alpha (2)-adrenergic-r eceptor responsiveness was attenuated even at a mild exercise intensity. Th ese results suggest that the mechanism of exercise sympatholysis may involv e reductions in postsynaptic alpha -adrenergic-receptor responsiveness.