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This Article Full Text Full Text (PDF) All Versions of this Article: 579/2/527    most recent jphysiol.2006.123372v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Sandström, M. E. Articles by Katz, A. Search for Related Content PubMed PubMed Citation Articles by Sandström, M. E. Articles by Katz, A. Related Collections Skeletal Muscle and Exercise

¹ Department of Physiology and Pharmacology, Karolinska Institutet, 171 77 Stockholm, Sweden

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 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 µmol (20 min)^–1 ml^–1) or after contraction (control = 2.27 ± 0.15; BTS = 2.10 ± 0.16 µmol (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 Ca²⁺ and the subsequent alterations in metabolism, e.g. increased energy turnover and production of reactive oxygen species.

(Received 23 October 2006; accepted after revision 18 December 2006; first published online 21 December 2006)
Corresponding author M. Sandström: Department of Physiology and Pharmacology, Karolinska Institutet, 171 77, Stockholm, Sweden. Email: marie.sandstrom{at}ki.se

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