Effect of tension on contraction-induced glucose transport in rat skeletalmuscle

We questioned the general view that contraction-induced muscle glucose tran sport only depends on stimulation frequency and not on workload. Incubated soleus muscles were electrically stimulated at a given pattern for 5 min. R esting 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-gl ucose 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 hig her (P < 0.05) and ATP concentrations lower (P < 0.05) when force was produ ced than when it was not. 5'-AMP-activated protein kinase (AMPK) activity i ncreased 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 (si milar to 86% P) doubled glucose transport without altering metabolism. In c onclusion, contraction-induced muscle glucose transport varies directly wit h force development and is not solely determined by stimulation frequency. AMPK activity is probably an essential determinant of contraction-induced g lucose transport. In contrast, glycogen concentrations per se do not play a major role. Finally, passive stretch per se increases glucose transport in muscle.