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Am J Physiol Endocrinol Metab 282: E348-E354, 2002; doi:10.1152/ajpendo.00085.2001
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Vol. 282, Issue 2, E348-E354, February 2002

Increased muscle fatigability in GLUT-4-deficient mice

M. Gorselink1, M. R. Drost2, K. F. J. de Brouwer1, G. Schaart2, G. P. J. van Kranenburg2, T. H. M. Roemen1, M. van Bilsen1, M. J. Charron3, and G. J. van der Vusse1

Departments of 1 Physiology and 2 Movement Sciences, University of Maastricht, 6200 MD Maastricht, The Netherlands; and 3 Department of Biochemistry, Albert Einstein College of Medicine, Bronx, New York 10461

GLUT-4 plays a predominant role in glucose uptake during muscle contraction. In the present study, we have investigated in mice whether disruption of the GLUT-4 gene affects isometric and shortening contractile performance of the dorsal flexor muscle complex in situ. Moreover, we have explored the hypothesis that lack of GLUT-4 enhances muscle fatigability. Isometric performance normalized to muscle mass during a single tetanic contraction did not differ between wild-type (WT) and GLUT-4-deficient [GLUT-4(-/-)] mice. Shortening contractions, however, revealed a significant 1.4-fold decrease in peak power per unit mass, most likely caused by the fiber-type transition from fast-glycolytic fibers (IIB) to fast-oxidative fibers (IIA) in GLUT-4(-/-) dorsal flexors. In addition, the resting glycogen content was significantly lower (34%) in the dorsal flexor complex of GLUT-4(-/-) mice than in WT mice. Moreover, the muscle complex of GLUT-4(-/-) mice showed enhanced susceptibility to fatigue, which may be related to the decline in the muscle carbohydrate store. The significant decrease in relative work output during the steady-state phase of the fatigue protocol suggests that energy supply via alternative routes is not capable to compensate fully for the lack of GLUT-4.

skeletal muscle; electrical stimulation


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