The arterioles in skeletal muscles, like those of the coronary circulation, have a high vascular resistance at rest as a result of alpha-adrenergic sympathetic stimulation. This produces a relatively low blood flow. Because muscles have such a large mass, however, they still receive from 20% to 25% of the total blood flow in the body at rest. Also, as in the heart, blood flow in a skeletal muscle decreases when the muscle contracts and squeezes its arterioles, and in fact blood flow stops entirely when the muscle contracts beyond about 70% of its maximum. Pain and fatigue thus occur much more quickly when an isometric contraction is sustained than when rhythmic isotonic contractions are performed.
In addition to adrenergic fibers, which promote vasoconstriction by stimulation of alpha-adrenergic receptors, there are also sympathetic cholinergic fibers in skeletal muscles. These cholinergic fibers, together with the stimulation of beta-adrenergic receptors by the hormone epinephrine, stimulate vasodilation as part of the fight-or-flight response to any stressful state, including that existing just prior to exercise (table 14.5). These extrinsic controls have been previously discussed and function to regulate blood flow through muscles at rest and upon anticipation of exercise.
As exercise progresses, the vasodilation and increased skeletal muscle blood flow that occur are almost entirely due to intrinsic metabolic control. The high metabolic rate of skeletal muscles during exercise causes local changes, such as increased carbon dioxide concentrations, decreased pH (due to carbonic acid and lactic acid), decreased oxygen, increased extracellular K+, and the secretion of adenosine. As in the intrinsic control of the coronary circulation, these changes cause vasodilation of ar-terioles in skeletal muscles. This decreases the vascular resistance and increases the rate of blood flow. As a result of these changes, skeletal muscles can receive as much as 85% of the total blood flow in the body during maximal exercise.
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