title: Effects of nitric oxide on the contraction of skeletal muscle.
abstract: A review of the literature suggests that the effects of nitric oxide (NO) on skeletal muscles fibers can be classified in two groups. In the first, the effects of NO are direct, due to nitrosation or metal nitrosylation of target proteins: depression of isometric force, shortening velocity of loaded or unloaded contractions, glycolysis and mitochondrial respiration. The effect on calcium release channels varies, being inhibitory at low and stimulatory at high NO concentrations. The general consequence of the direct effects of NO is to 'brake' the contraction and its associated metabolism. In the second group, the effects of NO are mediated by cGMP: increase of the shortening velocity of loaded or unloaded contractions, maximal mechanical power, initial rate of force development, frequency of tetanic fusion, glucose uptake, glycolysis and mitochondrial respiration; decreases of half relaxation time of tetanus and twitch, twitch time-to-peak, force maintained during unfused tetanus and of stimulus-associated calcium release. There is negligible effect on maximal force of isometric twitch and tetanus. The general consequence of cGMP-mediated effects of NO is to improve mechanical and metabolic muscle power, similar to a transformation of slow-twitch to fast-twitch muscle, an effect that we may summarize as a 'slow-to-fast' shift.
authors.affiliation: Department of Physiology and Pharmacology, Faculty of Medicine, Catholic University of Louvain, Brussels, Belgium. marechal@fymu.ucl.ac.be
authors.forename: G
authors.initials: G
authors.lastname: Maréchal
authors.forename: P
authors.initials: P
authors.lastname: Gailly
mesh_terms: D000818:Animals; D001120:Arginine / Q000378:metabolism; D006152:Cyclic GMP / Q000378:metabolism; D003864:Depression, Chemical; D004285:Dogs; D004558:Electric Stimulation; D004734:Energy Metabolism / Q000187:drug effects; D051275:Glucose Transporter Type 4; D006801:Humans; D007537:Isometric Contraction / Q000187:drug effects; D051379:Mice; D009004:Monosaccharide Transport Proteins / Q000378:metabolism; D009119:Muscle Contraction / Q000187:drug effects* / Q000502:physiology; D009124:Muscle Proteins / Q000378:metabolism; D018482:Muscle, Skeletal / Q000098:blood supply / Q000187:drug effects* / Q000378:metabolism; D009200:Myocardial Contraction / Q000187:drug effects; D009569:Nitric Oxide / Q000494:pharmacology* / Q000502:physiology; D020030:Nitric Oxide Donors / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D010101:Oxygen Consumption / Q000187:drug effects; D011499:Protein Processing, Post-Translational; D011817:Rabbits; D051381:Rats; D017382:Reactive Oxygen Species; D013314:Stress, Mechanical; D013552:Swine; D013746:Tetany / Q000378:metabolism; D014664:Vasodilation
chemical_list: D051275:Glucose Transporter Type 4; D009004:Monosaccharide Transport Proteins; D009124:Muscle Proteins; D020030:Nitric Oxide Donors; D017382:Reactive Oxygen Species; C495692:SLC2A4 protein, human; C495693:Slc2a4 protein, mouse; C495694:Slc2a4 protein, rat; D009569:Nitric Oxide; D001120:Arginine; D019001:Nitric Oxide Synthase; D006152:Cyclic GMP