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J. Biol. Chem., Vol. 280, Issue 17, 17260-17265, April 29, 2005

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Exercise Capacity of Mice Genetically Lacking Muscle Glycogen Synthase

IN MICE, MUSCLE GLYCOGEN IS NOT ESSENTIAL FOR EXERCISE^*

Bartholomew A. Pederson, Carlie R. Cope, Jill M. Schroeder, Micah W. Smith, José M. Irimia¶, Beth L. Thurberg||, Anna A. DePaoli-Roach, and Peter J. Roach**

From the Department of Biochemistry and Molecular Biology and Indiana University Center for Diabetes Research, Indiana University School of Medicine, Indianapolis, Indiana 46202-5122 and ^||Department of Pathology, Genzyme Corporation, Framingham, Massachusetts 01701-9322

The glucose storage polymer glycogen is generally considered to be an important source of energy for skeletal muscle contraction and a factor in exercise endurance. A genetically modified mouse model lacking muscle glycogen was used to examine whether the absence of the polysaccharide affects the ability of mice to run on a treadmill. The MGSKO mouse has the GYS1 gene, encoding the muscle isoform of glycogen synthase, disrupted so that skeletal muscle totally lacks glycogen. The morphology of the soleus and quadriceps muscles from MGSKO mice appeared normal. MGSKO-null mice, along with wild type littermates, were exercised to exhaustion. There were no significant differences in the work performed by MGSKO mice as compared with their wild type littermates. The amount of liver glycogen consumed during exercise was similar for MGSKO and wild type animals. Fasting reduced exercise endurance, and after overnight fasting, there was a trend to reduced exercise endurance for the MGSKO mice. These studies provide genetic evidence that in mice muscle glycogen is not essential for strenuous exercise and has relatively little effect on endurance.

Received for publication, September 10, 2004 , and in revised form, February 11, 2005.

^* This work was supported by in part by National Institutes of Health Grant DK27221. 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.

Supported by a mentor-based postdoctoral research award from the American Diabetes Association (to P. J. R.).

^¶ Supported by a grant from the Fondo de Investigación Sanitaria of the Instituto de Salud Carlos III, Red de centros en Metabolismo y Nutrición (C03/08), Madrid, Spain. Present address: Unitat de Bioquímica, Departament de Ciències Fisiològiques I, Institut d'Investigaciones Biomèdiques August Pi i Sunyer, Universitat de Barcelona, Barcelona, Spain.

^** To whom correspondence should be addressed: Dept. of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, IN 46202-5122. Tel.: 317-274-1582; Fax: 317-274-4686; E-mail: proach{at}iupui.edu.

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