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Am J Physiol Endocrinol Metab 277: E208-E214, 1999;
0193-1849/99 $5.00
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Vol. 277, Issue 2, E208-E214, August 1999

Effect of tension on contraction-induced glucose transport in rat skeletal muscle

Jacob Ihlemann, Thorkil Ploug, Ylva Hellsten, and Henrik Galbo

Copenhagen Muscle Research Center, Rigshospitalet, and Department of Medical Physiology, The Panum Institute, University of Copenhagen, 2200 Copenhagen N, Denmark

We questioned the general view that contraction-induced muscle glucose transport only depends on stimulation frequency and not on workload. Incubated soleus muscles were electrically stimulated at a given pattern for 5 min. Resting length was adjusted to achieve either no force (0% P), maximum force (100% P), or 50% of maximum force (50% P). Glucose transport (2-deoxy-D-glucose uptake) increased directly with force development (P < 0.05) [27 ± 2 (basal), 45 ± 2 (0% P), 68 ± 3 (50% P), and 94 ± 3 (100% P) nmol · g-1 · 5 min-1]. Glycogen decreased at 0% P but did not change further with force development (P > 0.05). Lactate, AMP, and IMP concentrations were higher (P < 0.05) and ATP concentrations lower (P < 0.05) when force was produced than when it was not. 5'-AMP-activated protein kinase (AMPK) activity increased directly with force [20 ± 2 (basal), 60 ± 11 (0% P), 91 ± 12 (50% P), and 109 ± 12 (100% P) pmol · mg-1 · min-1]. Passive stretch (~86% P) doubled glucose transport without altering metabolism. In conclusion, contraction-induced muscle glucose transport varies directly with force development and is not solely determined by stimulation frequency. AMPK activity is probably an essential determinant of contraction-induced glucose transport. In contrast, glycogen concentrations per se do not play a major role. Finally, passive stretch per se increases glucose transport in muscle.

2-deoxy-D-glucose; metabolism; exercise; GLUT-4; signal transduction


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