Because the oxygen and waste removal requirements of the muscle cells change in response to exercise, local body tissues (blood vessels that serve muscle cells) possess an intrinsic capability to regulate local blood flow.

Through a process known as autoregulation, local blood vessels dilate or constrict in response to the prevailing blood pressure at that site in the vascular bed and the metabolic needs of the local cells to assure that appropriate blood flow is maintained.

In this regard local factors in one part of the circulatory system can maintain blood flow under conditions of heightened blood pressure, while appropriate blood flow can be maintained in other parts of the circulatory system under conditions of reduced blood pressure.

What this suggests is that although blood flow is affected by signals from the nervous and neuroendocrine systems, blood flow also can be regulated locally in the absence of these influences.

Under conditions of exercise or physical exertion, blood flow increases to the striate muscles due to the increased metabolic demand of those tissues. In recent years, increased attention has been paid to the identification of the mechanisms involved in the local regulation of blood flow.

Nitric oxide, for example, has been isolated as a ‘relaxing’ factor that operates as a vasodilator released by local blood vessels in the circulatory system based upon the prevailing blood pressure at those sites.

As pressure increases are detected in local blood vessels, nitric oxide is released, causing the vessel to dilate and lower blood pressure. This action presumably explains how diastolic blood pressure remains relatively unaffected during cardiovascular activation that accompanies bouts of exercise.

Unfortunately, circulating proteins, like C-reactive protein, that increase one’s risk for atherosclerosis, appear to reduce quantities of nitric oxide, preventing adaptive blood pressure regulation at the local level.