| First Author | Gorselink M | Year | 2002 |
| Journal | Am J Physiol Endocrinol Metab | Volume | 282 |
| Issue | 2 | Pages | E348-54 |
| PubMed ID | 11788366 | Mgi Jnum | J:75600 |
| Mgi Id | MGI:2177110 | Doi | 10.1152/ajpendo.00085.2001 |
| Citation | Gorselink M, et al. (2002) Increased muscle fatigability in GLUT-4-deficient mice. Am J Physiol Endocrinol Metab 282(2):E348-54 |
| abstractText | 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. |
