Pflügers Archiv - European Journal of Physiology

, Volume 456, Issue 3, pp 587–600

Cellular and molecular events controlling skeletal muscle mass in response to altered use

  • François B. Favier
  • Henri Benoit
  • Damien Freyssenet
Skeletal Muscle

DOI: 10.1007/s00424-007-0423-z

Cite this article as:
Favier, F.B., Benoit, H. & Freyssenet, D. Pflugers Arch - Eur J Physiol (2008) 456: 587. doi:10.1007/s00424-007-0423-z

Abstract

Gain or loss of skeletal muscle mass occurs in situations of altered use such as strength training, aging, denervation, or immobilization. This review examines our current understanding of the cellular and molecular events involved in the control of muscle mass under conditions of muscle use and disuse, with particular attention to the effects of resistance exercise/training. The DNA content, which is a critical determinant of protein synthesis by providing the amount of DNA necessary to sustain gene transcription, can be either increased (activation of satellite cells) or decreased (apoptosis) depending on muscle activity and ongoing physiological processes. In addition, several transcription factors are sensitive to functional demand and may control muscle-specific protein expression to promote or repress myofiber enlargement. The control of skeletal muscle mass is also markedly mediated by the regulation of transduction pathways that promote the synthesis and/or the degradation of proteins. Insulin-like growth factor-I plays a key role in this balance by activating the Akt/tuberous sclerosis complex 2/mammalian target of rapamycin pathway. Stimulation of this pathway leads to the concomitant activation of initiation and elongation factors resulting in the elevation of protein translation and the downregulation of ubiquitin proteasome components through Forkhead-box O transcription factors.

Keywords

AgeingGene expressionHypertrophyIGFProtein metabolism

Copyright information

© Springer-Verlag 2007

Authors and Affiliations

  • François B. Favier
    • 1
  • Henri Benoit
    • 1
  • Damien Freyssenet
    • 1
  1. 1.Unité Physiologie et Physiopathologie de l’Exercice et Handicap, IFR143Université Jean MonnetSaint Etienne, cedex 2France