Abstract

Skeletal muscle blood flow increases nearly 20-fold during exercise. Despite experimental work in this area for more than a century, the physiological mechanisms responsible for the regulation of skeletal muscle blood flow during contractions remain relatively unknown. Historically, experiments have focused on identifying chemical factors associated with increased tissue metabolism that also act as vasodilators. However, functional vasodilation cannot be attributed to changes in the local concentration of any single metabolic factor. The rapid increase in muscle blood flow during the initial moments of exercise led others to consider a role for neural mechanisms in the development of functional hyperemia. However, a specific neural pathway has not been identified. Mechanical factors, such as vascular compression and increases in perfusion pressure, also affect vascular resistance and skeletal muscle blood flow. Yet the specific manner in which these mechanical factors interact during muscle contractions is not well understood. The recent determination that arterial feed vessels, upstream from the active tissue and microcirculation, also dilate during muscle contractions has led to the consideration that the vessels are primarily responsible for the regulation of bulk flow to the tissue. Since these vessels are anatomically separated from the active tissue, more complex, indirect regulatory mechanisms must be explored. It is also likely that the specific factors responsible for functional vasodilation and increased muscle blood during exercise differ between muscle fiber types and relative contraction intensities. Consideration of these factors may lead to a better understanding of the regulation of muscle blood flow.

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