Related Experiment Videos
Effects of nitric oxide on the contraction of skeletal muscle
1Department of Physiology and Pharmacology, Faculty of Medicine, Catholic University of Louvain, Brussels, Belgium. marechal@fymu.ucl.ac.be
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.
Insights
Nitric oxide (NO) directly brakes skeletal muscle contraction and metabolism. However, NO indirectly enhances muscle power and metabolism via cGMP, promoting a slow-to-fast muscle fiber shift.
Area of Science:
- Muscle physiology
- Biochemistry
- Cell signaling
Background:
- Nitric oxide (NO) plays a crucial role in regulating various physiological processes, including skeletal muscle function.
- The dual role of NO in skeletal muscle, acting both directly and indirectly, requires detailed elucidation.
- Understanding NO's impact is vital for comprehending muscle adaptation and performance.
Purpose of the Study:
- To review and classify the effects of nitric oxide (NO) on skeletal muscle fibers.
- To differentiate between direct NO effects and those mediated by cyclic guanosine monophosphate (cGMP).
- To elucidate the functional consequences of NO signaling on muscle contraction and metabolism.
Main Methods:
- Literature review of studies investigating nitric oxide's effects on skeletal muscle.
- Analysis of direct effects of NO on proteins (nitrosation, nitrosylation).
- Analysis of indirect effects mediated by cGMP signaling pathways.
Main Results:
- Direct NO effects: Depression of force, shortening velocity, glycolysis, and mitochondrial respiration; variable effects on calcium release channels, generally 'braking' contraction and metabolism.
- cGMP-mediated NO effects: Increased shortening velocity, mechanical power, force development rate, glucose uptake, and mitochondrial respiration; decreased relaxation time; 'slow-to-fast' muscle shift.
- Negligible impact on maximal isometric force for both direct and indirect pathways.
Conclusions:
- Nitric oxide exerts distinct effects on skeletal muscle fibers through direct and cGMP-mediated pathways.
- Direct NO actions tend to inhibit muscle contraction and metabolism.
- cGMP-mediated NO signaling enhances muscle power and metabolic efficiency, inducing a 'slow-to-fast' fiber type transformation.