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

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.