Effects of nitric oxide on the contraction of skeletal muscle

G Maréchal1, P Gailly

  • 1Department of Physiology and Pharmacology, Faculty of Medicine, Catholic University of Louvain, Brussels, Belgium. marechal@fymu.ucl.ac.be

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.

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