Abstract
1. The present review examines the control of muscle vascular conductance by the sympathetic nervous system during exercise. 2. Evidence for tonic sympathetic neural control of active muscle rests on three findings: (i) directly measured muscle sympathetic nerve traffic is increased; (ii) spillover of noradrenaline from active muscles is also increased; and (iii) withdrawal of sympathetic outflow to active muscle either by acute blockade of its sympathetic nerve supply or by reflex inhibition of sympathetic nervous activity raises muscle vascular conductance via inhibition of tonic vasoconstriction. 3. Loss of tonic sympathetic control of muscle vascular conductance during mild to severe exercise caused marked hypotension despite maintenance of a normal cardiac output. 4. The extent to which active muscle can vasodilate in intact animals appears to have been hidden by tonic vasoconstriction. This vasoconstriction appears to be minimally affected by metabolites in oxidative (red) muscle, but may be inhibited in predominantly glycolytic (white) muscle owing to different spatial distributions of alpha 1- and alpha 2-adrenoceptors in the two muscle types and to the different susceptibilities of the two receptor types to interference by metabolites. 5. The reflexes causing vasoconstriction in active and inactive muscles are unknown. One hypothesis is that a flow-sensitive muscle chemoreflex raises sympathetic outflow to reduce accumulations of muscle metabolites caused by mismatches between muscle blood flow and metabolism, called 'flow errors'. Another hypothesis is that the arterial baroreflex corrects mismatches between cardiac output and vascular conductance called 'pressure errors'. This review argues for a dominance of control by the baroreflex based on the following observations: (i) the arterial baroreflex is essential to the normal rise in sympathetic nervous activity and arterial pressure at the onset of exercise; (ii) during submaximal exercise, a functioning arterial baroreflex is required to maintain tonic sympathetic activity and prevent arterial hypotension; and (iii) whereas a muscle chemoreflex may be needed to guard against hypoperfusion of active muscle, the arterial baroreflex must oppose hypotension by initiating sympathetic vasoconstriction to oppose muscle vasodilation.