Muscle protein metabolism and the sarcopenia of aging

Int J Sport Nutr Exerc Metab. 2001 Dec:11 Suppl:S119-27. doi: 10.1123/ijsnem.11.s1.s119.

Abstract

Loss of muscle mass, strength, and oxidative capacity accompanies normal aging in humans. The mechanisms responsible for these changes remain to be clearly defined. Muscle protein mass and function depend on protein turnover. Synthesis rate of the major muscle contractile protein, myosin heavy chain (MHC), and transcript levels of fast MHC isoforms decrease in association with strength reductions, while mitochondrial protein synthesis rate declines in parallel with activities of mitochondrial enzymes and maximal oxidative capacity (VO2max). Resistance exercise training increases the synthesis rate of MHC and transcript levels of the slow MHC isoform in older humans, along with increasing muscle strength. The relationship between the synthesis of muscle proteins, and muscle size and function, with aging and exercise training are discussed in this review.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Aged
  • Aged, 80 and over
  • Aging / metabolism*
  • Aging / physiology
  • Exercise / physiology*
  • Female
  • Humans
  • Male
  • Muscle Proteins / metabolism*
  • Muscle, Skeletal / metabolism*
  • Muscular Atrophy / metabolism*
  • Muscular Atrophy / physiopathology
  • Myosin Heavy Chains / biosynthesis
  • Oxygen Consumption / physiology
  • Protein Isoforms

Substances

  • Muscle Proteins
  • Protein Isoforms
  • Myosin Heavy Chains