Serum IGF-I-deficiency does not prevent compensatory skeletal muscle hypertrophy in resistance exercise.
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.
Matheny
Ronald W
RW
Department of Biochemistry, The Sam and Ann Barshop Institute for Longevity and Aging Studies, MSC 7760, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229-3900, USA.
Matheny
Wayne
W
Merritt
Edward
E
Zannikos
Symeon V
SV
Farrar
Roger P
RP
Adamo
Martin L
ML
D000818:Animals; D001835:Body Weight; D005786:Gene Expression Regulation; D006984:Hypertrophy; D007334:Insulin-Like Growth Factor I / Q000172:deficiency* / Q000235:genetics; D008297:Male; D051379:Mice; D018482:Muscle, Skeletal / Q000378:metabolism* / Q000473:pathology*; D009929:Organ Size; D010805:Physical Conditioning, Animal / Q000502:physiology*; D052097:Quadriceps Muscle / Q000378:metabolism / Q000473:pathology; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism
D012333:RNA, Messenger; D007334:Insulin-Like Growth Factor I