Serum IGF-I-deficiency does not prevent compensatory skeletal muscle hypertrophy in resistance exercise

Wayne Matheny, Edward Merritt, Symeon V. Zannikos, Roger P. Farrar, Martin L. Adamo

Research output: Contribution to journalArticlepeer-review

53 Scopus citations


The involvement of circulating insulin-like growth factor-I (IGF-I) in the skeletal muscle response to resistance exercise is currently unclear. To address this, we utilized the liver IGF-I- deficient (LID) mouse model, in which the igf1 gene has been disrupted in the hepatocytes, resulting in ∼80% reduction in serum IGF-I. Twelve- to 13-month-old male LID and control (L/L) mice were subjected to 16 weeks of resistance training. Resistance exercise resulted in equal strength gains in both L/ L and LID mice. Basal IGF-I mRNA levels were greater in LID muscles than in L/L, and exercise increased IGF-I mRNA in quadriceps, gastrocnemius, and plantaris muscles. LID mice had elevated tyrosine phosphorylation of IGF-IR and Stat5b, the latter possibly reflective of increased serum GH. Tyrosine phosphorylation of IGF-IR was increased, while phospho-Stat5b was reduced after resistance training of both wild-type and LID mice. These data suggest that: 1) performance and recovery in response to resistance training is normal even when there is severe deficiency of circulating IGF-I; and 2) upregulation of local IGF-I may be involved in the compensatory growth of muscle that occurs in response to resistance training. Decreased levels of p-Stat5b in exercised mice suggests that the upregulation of local IGF-I gene expression in response to exercise may be GH-independent.

Original languageEnglish (US)
Pages (from-to)164-170
Number of pages7
JournalExperimental Biology and Medicine
Issue number2
StatePublished - Feb 1 2009


  • Hypertrophy
  • Insulin-like growth factor-i
  • Mouse
  • Resistance training

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)


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