Resistance Exercise and Insulin Regulate AS160 and Interaction With 14-3-3 in Human Skeletal Muscle

  1. Kirsten F. Howlett1,
  2. Kei Sakamoto2,
  3. Andrew Garnham1,
  4. David Cameron-Smith1 and
  5. Mark Hargreaves3
  1. 1School of Exercise and Nutrition Sciences, Deakin University, Burwood, Victoria, Australia
  2. 2Medical Research Council (MRC) Protein Phosphorylation Unit, College of Life Sciences, University of Dundee, Dundee, Scotland, United Kingdom
  3. 3Department of Physiology, The University of Melbourne, Parkville, Australia
  1. Address correspondence and reprint requests to Kirsten Howlett, School of Exercise and Nutrition Sciences, Deakin University, Burwood, Victoria, 3125, Australia. E-mail: kirsten.howlett{at}deakin.edu.au

Abstract

A single bout of aerobic exercise can enhance insulin action, but whether a similar effect occurs after resistance exercise is unknown. Hyperinsulinemic-euglycemic clamps were performed on eight male subjects at rest and after a single bout and three repeated bouts of resistance exercise over 7 days. Skeletal muscle biopsies were taken before and after the clamp and immediately after a single exercise bout. Whole-body insulin action measured by glucose infusion rate decreased (P < 0.05) after a single exercise bout, whereas in response to repeated bouts of resistance exercise, the glucose infusion rate was similar to the rest trial. In skeletal muscle, Akt substrate of 160 kDa (AS160) phosphorylation, an Akt substrate implicated in the regulation of GLUT4 translocation, and its interaction with 14-3-3 was decreased (P < 0.05) only after a single exercise bout. Insulin increased (P < 0.05) phosphorylation of AS160 and its interaction with 14-3-3, but the insulin response was not influenced by resistance exercise. Phosphorylation of insulin receptor substrate-1 and Akt were similar to changes in AS160 phosphorylation after exercise and/or insulin. In conclusion, a single bout of resistance exercise impairs whole-body insulin action. Regulation of AS160 and interaction with 14-3-3 in skeletal muscle are influenced by resistance exercise and insulin but do not fully explain the effect of resistance exercise on whole-body insulin action.

Footnotes

  • Published ahead of print at http://diabetes.diabetesjournals.org on 16 March 2007. DOI: 10.2337/db06-1398.

    The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

    • Accepted March 2, 2007.
    • Received October 4, 2006.
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  1. Published online before print March 16, 2007, doi: 10.2337/db06-1398 Diabetes June 2007 vol. 56 no. 6 1608-1614
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