The Regulation of Muscle Blood Flow Depends on Many Mechanisms to Provide Oxygen for Muscular Contractions

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As discussed in Chapter 16, many potential local regulatory mechanisms adjust blood flow to the metabolic needs of the tissues. In fast-twitch muscles, which primarily depend on anaerobic metabolism, the accumulation of hydrogen ions from lactic acid is potentially a major contributor to the va-sodilation that occurs. In slow-twitch skeletal muscles, which can easily increase oxidative metabolic requirements by more than 10 to 20 times during heavy exercise, it is not hard to imagine that whatever causes metabolically linked vasodi-lation is in ample supply at high metabolic rates.

During rhythmic muscle contractions, the blood flow during the relaxation phase can be high, and it is unlikely that the muscle becomes significantly hypoxic during submaximal aerobic exercise. Studies in humans and animals indicate that lactic acid formation, an indication of hypoxia and anaerobic metabolism, is present only during the first several minutes of submaximal exercise. Once the vasodila-tion and increased blood flow associated with exercise are established, after 1 to 2 minutes, the microvasculature is probably capable of maintaining ample oxygen for most workloads, perhaps up to 75 to 80% of maximum perform ance because remarkably little additional lactic acid accumulates in the blood. While the tissue oxygen content likely decreases as exercise intensity increases, the reduction does not compromise the high aerobic metabolic rate except with the most demanding forms of exercise. The changes in oxygen tensions before, during, and after a period of muscle contractions in an animal model were illustrated in Figure 16.7.

To ensure the best possible supply of nutrients, particularly oxygen, even mild exercise causes sufficient vasodilation to perfuse virtually all of the capillaries, rather than just 25 to 50% of them, as occurs at rest. However, near-maximum or maximum exercise exhausts the ability of the mi-crovasculature to meet tissue oxygen needs and hypoxic conditions rapidly develop, limiting the performance of the muscles. The burning sensation and muscle fatigue during maximum exercise or at any time muscle blood flow is inadequate to provide adequate oxygen is partially a consequence of hypoxia. This type of burning sensation is particularly evident when a muscle must hold a weight in a steady position. In this situation, the contraction of the muscle compresses the microvessels, stopping the blood flow and, with it, the availability of oxygen.

The vasodilation associated with exercise is dependent upon NO. However, exactly which chemicals released or consumed by skeletal muscle induce the increased release of NO from endothelial cells is unknown. In addition, skeletal muscle cells can make NO and, although not yet tested, may produce a substantial fraction of the NO that causes the dilation of the arterioles. If endothelial production of NO is curtailed by the inhibition of endothelial nitric oxide synthase, the increased muscle blood flow during contractions is strongly suppressed. However, there is concern that the resting vasoconstriction caused by suppressed NO formation diminishes the ability of the vasculature to dilate in response a variety of mechanisms. Flow-mediated vasodilation, for example, appears to be used to dilate smaller arteries and larger arterioles to maximize the increase in blood flow initiated by the dilation of smaller arterioles in contact with active skeletal muscle cells. Studies in animals indicate these vessels make a major contribution to vascular regulation in skeletal muscle and must be participants in any significant increase in blood flow.

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  • Calleigh
    What are the mechanisms which produce increase muscle blood flow?
    7 years ago

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