Mechanical load plays little role in contraction-mediated glucose transport in mouse skeletal muscle.

The factors responsible for control of glucose transport during exercise are not fully understood. We investigated the role of mechanical load in contraction-mediated glucose transport in an isolated muscle preparation. Mouse extensor digitorum longus muscles were stimulated with repeated contractions for 10 min with or without N-benzyl-p-toluene sulphonamide (BTS, an inhibitor of myosin II ATPase) to block crossbridge activity. BTS inhibited force production during repeated contraction to approximately 5% of control. In contrast, BTS had little effect on glucose transport in the basal state (control = 0.55 +/- 0.04; BTS = 0.47 +/- 0.09 micromol (20 min)(-1) ml(-1)) or after contraction (control = 2.27 +/- 0.15; BTS = 2.10 +/- 0.16 micromol (20 min)(-1) ml(-1)). BTS did not significantly alter the contraction-mediated changes in high-energy phosphates, glutathione status (a measure of oxidant status) or AMP-activated protein kinase activity. In conclusion, these data show that mechanical load plays little role in contraction-mediated glucose transport. Instead, it is likely that the increased glucose transport during contraction is a consequence of the increase in myoplasmic Ca(2+) and the subsequent alterations in metabolism, e.g. increased energy turnover and production of reactive oxygen species.