Does sympathetic vasoconstriction contribute to metabolism: Perfusion matching in exercising skeletal muscle?

Abstract

The process of matching skeletal muscle blood flow to metabolism is complex and multi-factorial. In response to exercise, increases in cardiac output, perfusion pressure and local vasodilation facilitate an intensity-dependent increase in muscle blood flow. Concomitantly, sympathetic nerve activity directed to both exercising and non-active muscles increases as a function of exercise intensity. Several studies have reported the presence of tonic sympathetic vasoconstriction in the vasculature of exercising muscle at the onset of exercise that persists through prolonged exercise bouts, though it is blunted in an exercise-intensity dependent manner (functional sympatholysis). The collective evidence has resulted in the current dogma that vasoactive molecules released from skeletal muscle, the vascular endothelium, and possibly red blood cells produce local vasodilation, while sympathetic vasoconstriction restrains vasodilation to direct blood flow to the most metabolically active muscles/fibers. Vascular smooth muscle is assumed to integrate a host of vasoactive signals resulting in a precise matching of muscle blood flow to metabolism. Unfortunately, a critical review of the available literature reveals that published studies have largely focused on bulk blood flow and existing experimental approaches with limited ability to reveal the matching of perfusion with metabolism, particularly between and within muscles. This paper will review our current understanding of the regulation of sympathetic vasoconstriction in contracting skeletal muscle and highlight areas where further investigation is necessary.

Features of immediate adaptation of the circulatory system to static load in persons with different body mass index

“…Further growth of the pumping function of the heart in individuals of both groups has a compensatory nature and is characterized by the desire to restore blood circulation in vessels that were compressed during static stress [7,25]. The increase in both types of blood pressure under the influence of SL can be explained by the increase in pressure inside the aorta during the maintenance of static tension, which, according to the logic of the Anrep phenomenon (loading the heart with outflow), leads to an increase in the force of heart contraction, and as a result -to an increase in the value of sAT and dAT [8,9].…”

Features of functional changes in blood vessels during the period of early recovery after static physical exercise

“…Already 1 min after SL, all examined young men observed a decrease in the SPR, TPR, and tone of large-caliber arteries, which is evidence of the fact that the initial narrowing of the main arteries, arterioles, and venules is replaced by their significant expansion. This phenomenon can be explained by the leveling of the effect of catecholamines under the action of the powerful release of metabolitesvasodilators from skeletal muscles, a greater proportion of beta-than alpha-adrenoceptors in the cell membranes of myocytes of blood vessels of skeletal muscles and a local increase in temperature in actively working skeletal muscles [5,9]. This is most pronounced in bodybuilders, who have the most developed and hypertrophied muscles, compared to untrained young men and those who engage in fitness.…”

The Importance of Physical Activity for the Normalization of High Blood Pressure

“…Введение. В настоящее время значительно увеличилась продолжительность жизни человека, а особенно стал намного больше период результативного труда в зрелом возрасте [2,4]. Но с увеличением продолжительности жизни стали чаще проявляться различные заболевания, особенно гипертоническая болезнь [2].…”

“…Показано, что функциональный симпатолизис [4] усиливает кровоток к активным мышцам. Авторы работы [6] считают, что усиленный кровоток в работающие мышцы обеспечивается рабочей мышечной гиперемией (симпатолизисом).…”