AENDO August 40/2

Ihlemann, Jacob, Thorkil Ploug, Ylva Hellsten, and Henrik Galbo. Effect of tension on contraction-induced glucose transport in rat skeletal muscle. Am. J. Physiol. 277 (Endocrinol. Metab. 40): E208–E214, 1999.—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 6 2 (basal), 45 6 2 (0% P), 68 6 3 (50% P), and 94 6 3 (100% P) nmol ·g21 ·5 min21]. 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. 58-AMP-activated protein kinase (AMPK) activity increased directly with force [20 6 2 (basal), 60 6 11 (0% P), 91 6 12 (50% P), and 109 6 12 (100% P) pmol ·mg21 ·min21]. 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 contractioninduced glucose transport. In contrast, glycogen concentrations per se do not play a major role. Finally, passive stretch per se increases glucose transport in muscle.