Increased muscle fatigability in GLUT-4-deficient mice

M. Gorselink, W.A. Bemelman, K.F.J. de Brouwer, G. Schaart, G.P.J. van Kranenburg, T.H.M. Roemen, M. van Bilsen, M.J. Charron, G.J. van der Vusse*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review


Department of Physiology, University of Maastricht, 6200 MD Maastricht, The Netherlands.

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.
Original languageEnglish
Pages (from-to)E348-E354
Number of pages7
JournalAmerican Journal of Physiology : Endocrinology and Metabolism
Issue number2
Publication statusPublished - 1 Jan 2002


Dive into the research topics of 'Increased muscle fatigability in GLUT-4-deficient mice'. Together they form a unique fingerprint.

Cite this