earticle

영어

Maximal whole body exercise leads skeletal muscle blood flow to markedly increase to match metabolic demands, a phenomenon termed exercise hyperaemia that is accomplished by increasing vaso-dilation. However, local vasodilatory mechanisms in response to skele-tal muscle contraction remain uncertain. This review highlights meta-bolic vasodilators released from contracting skeletal muscle, endotheli-um, or blood cells. As a considerable skeletal muscle vasodilation po-tentially results in hypotension, sympathetic nerve activity needs to be augmented to elevate cardiac output and blood pressure during dy-namic exercise. However, since the enhanced sympathetic vasocon-striction restrains skeletal muscle blood flow, intramuscular arteries have an indispensable ability to blunt sympathetic activity for exercise hyperaemia. In addition, we discuss that mechanical compression of the intramuscular vasculature contributes to causing the initial phase of increasing vasodilation following a single muscle contraction. We have also chosen to focus on conducted (or ascending) electrical signals that evoke vasodilation of proximal feed arteries to elevate blood flow in the microcirculation of skeletal muscle. Endothelial hyperpolarization originating within distal arterioles ascends into the proximal feed arter-ies, thereby increasing total blood flow in contracting skeletal muscle. This brief review summarizes molecular mechanisms underlying the regulation of skeletal muscle blood flow to a single or sustained muscle contraction.