Contributions of nerves and metabolites to exercise vasodilation: a unifying hypothesis.
Neuronal cell bodies exist in arterioles of skeletal muscle and appear to initiate vasodilation during phasic contraction. The following findings indicate that intrinsic nerves rather than metabolites maintain vasodilation during sustained phasic contraction with free flow. 1) Under certain conditions maximal vasodilation can occur without detectable release of metabolites. 2) When metabolites are released during exercise, their concentrations in blood or tissue do not always determine the extent of vasodilation. 3) Vasodilation during sustained contraction can be partly blocked by local anesthetics. The extent of block is inversely proportional to the concentration of metabolites. Dose, time course of block, and other tests of specificity indicate that local anesthetics act on the intrinsic nerves rather than smooth or striated muscle. When contraction stops, neurogenic vasodilation decays rapidly (half time less than 1 min). Sustained vasodilation during recovery is therefore fully accounted for by metabolites. A hypothesis is suggested that integrates the roles of extrinsic nerves, intrinsic nerves, and metabolites in support of muscle contraction.
D000200:Action Potentials; D000818:Animals; D001158:Arteries / Q000294:innervation; D004176:Dipyridamole / Q000494:pharmacology; D004285:Dogs; D008012:Lidocaine / Q000494:pharmacology; D009132:Muscles / Q000098:blood supply / Q000502:physiology*; D009474:Neurons / Q000502:physiology*; D010101:Oxygen Consumption; D005082:Physical Exertion; D014664:Vasodilation
D004176:Dipyridamole; D008012:Lidocaine