Vascular smooth muscle is under the influence of local (metabolic, autoregulatory and endothelial), reflex (autonomic nervous system), and hormonal (norepinephrine, epinephrine, angiotensin, and vasopressin) regulatory mechanisms.
At the onset of exercise, skeletal muscle fiber activation sets in motion a series of biochemical events that increase metabolic demand and produce cellular metabolites (adenosine} .
These metabolites have their greatest influence on vascular smooth muscle of the smallest terminal arterioles and cause relaxation. The relaxation/dilation of the terminal arteriole reduces the perfusion pressure on the upstream arterioles and the vessels relax (autoregulation) in response.
Autoregulation increases blood flow which stimulates the release of endothelial derived relaxing factors. These events mediate a cascade, or 'migrating upstream vasodilation'. This vasodilation increases blood now to working muscles and improves oxygen supply. As exercise continues, an increased sympathetic nervous system activity and vasoactive hormones modulate vasodilation of vascular smooth muscle.
Thus, during exercise, vascular smooth muscle is regulated by several mechanisms that are designed to redistribute cardiac output and assure adequate tissue blood flow while maintaining arterial blood pressure.
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