IntroductionNeural mechanisms closely regulate cardiovascular changes during exercise, including the increases in cardiac output, blood pressure and the redistribution of blood flow to match the metabolic demands of skeletal muscle. Blood flow to skeletal muscle is controlled by the amount of sympathetic vasoconstrictor drive, and it has been shown that the peak reduction in muscle blood flow occurs five or six cardiac cycles after a burst of muscle sympathetic nerve activity (MSNA) to that muscle (Fairfax et al. ). During volitional exercise, MSNA is governed by the activation of a centrally mediated efferent pathway (central command), a reflex generated by peripheral stimulation of chemically (metaboreflex) or mechanically (mechanoreflex) sensitive group IV and III afferent nerve fibre endings within the contracting muscle, and resetting of the arterial baroreflex. Sympathetic vasoconstrictor drive could also be linked to muscle activity (Seals, ; Boulton et al. , ) because the perfusion demands of skeletal muscle and other organs can vary greatly and in proportion to the level of activity (Andersen & Saltin, ; Saunders et al. ; Reeder & Green, ). Active skeletal muscle has a tremendous capacity to vasodilate and thereby increase its blood flow, especially at the onset of contraction (Reeder & Green, ).
The Journal of Physiology – Wiley
Published: Jan 15, 2018
Keywords: ; ; ;
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