Resistance training, and IGF involvement in the maintenance of muscle mass during the aging process

Martin L. Adamo, Roger P. Farrar

Research output: Contribution to journalShort surveypeer-review

80 Scopus citations

Abstract

Sarcopenia is the decline of muscle mass and strength with age. Sarcopenia leads to significant impairment in the ability to carry out normal daily function and thus there is a great need for interventions that will lead to muscle regeneration and repair in the aging population. Age-related sarcopenia in humans, characterized by loss of type I and type II muscle fibers and a decrease in fiber cross-sectional area primarily in type II fibers, can be attenuated by mechanical load on the muscle, which increases cross-sectional area of the remaining fibers, but does not restore fiber numbers characteristic of young muscle. Considerable evidence also implicates age-related declines in muscle insulin-like growth factor action in sarcopenia. IGF-I promotes myoblast proliferation, differentiation, and protein accretion in muscle through multiple signaling mechanisms, including the PI3-kinase, MAP kinase and calcineurin pathways. Exercise and injury induce increases in IGF-I, IGF-I receptors and IGF-I-activated signaling pathways. Although there is evidence that aging muscle retains the ability to synthesize IGF-I, there is also evidence that aging may be associated with attenuation of the ability of exercise to induce an isoform of IGF-I that promotes satellite cell proliferation. Moreover, aging muscle may be resistant to IGF-I, an effect that is reversed by exercise. However, it is clear that over-expression of IGF-I in muscle can protect against age-related sarcopenia.

Original languageEnglish (US)
Pages (from-to)310-331
Number of pages22
JournalAgeing Research Reviews
Volume5
Issue number3
DOIs
StatePublished - Aug 1 2006

Keywords

  • Exercise
  • IGF
  • Muscle mass
  • Sarcopenia

ASJC Scopus subject areas

  • Biotechnology
  • Biochemistry
  • Aging
  • Molecular Biology
  • Neurology

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