Sympathetic Vasoconstriction in Skeletal Muscle: Adaptations to Exercise Training

Abstract

Sympathetic vasoconstriction in the skeletal muscle vascular bed is essential for the regulation of vascular resistance and therefore control of blood pressure and muscle blood flow at rest and during exercise. In this article, we address the hypothesis that aerobic exercise training alters sympathetic vasoconstrictor responsiveness and enhances contraction-mediated inhibition of sympathetic vasoconstriction (functional sympatholysis) through a nitric oxide–dependent mechanism.

Vascular characteristics in young women—Effect of extensive endurance training or a sedentary lifestyle

“…There is some evidence that endurance training may lower muscle sympathetic nerve traffic, but other data argue against this notion . Irrespective of this, it has been shown that aerobic exercise training may modulate sympathetic vasoconstriction in resting skeletal muscle and enhance functional sympatholysis through a nitric oxide‐dependent mechanism . That lower muscle sympathetic vasoconstriction could to some extent explain the lower AI in the physically trained groups is, however, contradicted by the finding that the calculated value of TPR was not significantly different between any of the groups of the present study (Table ).…”

“…41,42 Irrespective of this, it has been shown that aerobic exercise training may modulate sympathetic vasoconstriction in resting skeletal muscle and enhance functional sympatholysis through a nitric oxide-dependent mechanism. 43,44 That lower muscle sympathetic vasoconstriction could to some extent explain the lower AI in the physically trained groups is, however, contradicted by the finding that the calculated value of TPR was not significantly different between any of the groups of the present study (Table 2). Therefore, an alternative and more likely explanation of the detected differences in AI with exercise training or sedentary lifestyle, in spite of the fact that indicators of central arterial distensibility were not different, may be changes in endothelial function as a result of the level of exercise-induced increase in shear stress.…”

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

“…Exercise training has also been used to investigate sympatholysis ( Jendzjowsky and DeLorey, 2013b ; Jendzjowsky and DeLorey, 2013c ; Jendzjowsky et al, 2014a ; Mizuno et al, 2014 ; Mortensen et al, 2014 ; Just and DeLorey, 2016 ; Just et al, 2016 ; Cooper et al, 2021 ). In rats, exercise training enhanced sympatholysis through an NO dependent mechanism ( Jendzjowsky and DeLorey, 2013c ; Mizuno et al, 2014 ).…”

“…This contraction-mediated inhibition of sympathetic vasoconstriction was termed functional sympatholysis by Remensnyder et al (1962) . While the precise mechanism(s) responsible for sympatholysis have not been fully elucidated, the available evidence suggests that vasoactive molecules released from skeletal muscle, the vascular endothelium, and possibly red blood cells decrease the responsiveness of post-synaptic sympathetic receptors ( Figure 1 ) ( Thomas and Segal, 2004 ; Just et al, 2016 ; Mueller et al, 2017 ; DeLorey, 2021 ). The current dogma, oft repeated over the past several decades, is that functional sympatholysis is responsible for directing blood flow to the most metabolically active muscles/fibers.…”

The perceptions of natural compounds against dipeptidyl peptidase 4 in diabetes: from in silico to in vivo

“…18 Secreted sDPP-4 can reduce vasoconstriction that is caused by neuropeptide Y (NPY) and subsequently increase the arteriolar diameter of skeletal muscle that provides a physiological explanation for raising training efficiency caused by sDPP-4. 19,20 In addition to arteriolar diameter of skeletal muscle, secreted sDPP-4 acts as myokine, which stimulates inflammation in smooth muscles from blood vessel through activating protease-activated receptor 2 (PAR2)/ERK/NF-κB signaling pathway, increasing proinflammatory cytokine release and finally stimulating smooth muscle cell proliferation. 21 However, sDPP-4-induced smooth muscle inflammation is not always good to the body.…”