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This Article Full Text Full Text (PDF) All Versions of this Article: 586/1/283    most recent jphysiol.2007.141507v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Spangenburg, E. E. Articles by Bodine, S. C. Search for Related Content PubMed PubMed Citation Articles by Spangenburg, E. E. Articles by Bodine, S. C. Related Collections Skeletal Muscle and Exercise Related Article

¹ University of Maryland, School of Public Health, Department of Kinesiology, College Park, MD 21045, USA
² Division of Endocrinology, Diabetes, and Bone Diseases, Department of, Medicine, The Mount Sinai School of Medicine, New York, NY 10029, USA
³ University of Maryland Baltimore, School of Nursing, 655 West Lombard Street, Baltimore, MD 21201, USA
⁴ Section of Neurobiology, Physiology and Behavior, University of California Davis, Davis, CA 95616, USA

Increasing the mechanical load on skeletal muscle results in increased expression of insulin-like growth factor I (IGF-I), which is thought to be a critical step in the induction of muscle hypertrophy. To determine the role of the IGF-I receptor in load-induced skeletal muscle hypertrophy, we utilized a transgenic mouse model (MKR) that expresses a dominant negative IGF-I receptor specifically in skeletal muscle. Skeletal muscle hypertrophy was induced in the plantaris muscle using the functional overload (FO) model, a model which has previously been shown to induce significant elevations of IGF-I expression in skeletal muscle. Adult male wild-type (WT) and MKR mice were subjected to 0, 7 or 35 days of FO. In control or unchallenged animals, the plantaris mass was 11% greater in WT compared to the MKR mice (P < 0.05). After 7 days of FO, plantaris mass increased significantly by 26% and 62% in WT and MKR mice, respectively (P < 0.05). After 35 days of FO, WT and MKR mice demonstrated significant increases of 100% and 122%, respectively, in plantaris mass (P < 0.05). Further, at no time point was the degree of hypertrophy significantly different between the WT and MKR mice. Previous research suggests that IGF-I induces muscle growth through activation of the Akt–mTOR signalling pathway; therefore, we measured the phosphorylation status of Akt and p70^s6k in the WT and MKR mice after 7 days of FO. Significant increases of 100% and 200% in Akt (Ser-473) and p70^s6k (Thr-389) phosphorylation were measured in overloaded plantaris from both WT and MKR mice, respectively. Moreover, no differences were detected between the WT and MKR mice. These data suggest that increased mechanical load can induce muscle hypertrophy and activate the Akt and p70^s6k independent of a functioning IGF-I receptor.

(Received 26 July 2007; accepted after revision 29 October 2007; first published online 1 November 2007)
Corresponding author E. E. Spangenburg: University of Maryland, Department of Kinesiology, College Park, MD 21045, USA. Email: espen{at}umd.edu

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