title: Mechanical load plays little role in contraction-mediated glucose transport in mouse skeletal muscle.
abstract: 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.
authors.affiliation: Department of Physiology and Pharmacology, Karolinska Institutet, 171 77, Stockholm, Sweden. marie.sandstrom@ki.se
authors.forename: Marie E
authors.initials: ME
authors.lastname: Sandström
authors.forename: Shi-Jin
authors.initials: SJ
authors.lastname: Zhang
authors.forename: Håkan
authors.initials: H
authors.lastname: Westerblad
authors.forename: Abram
authors.initials: A
authors.lastname: Katz
mesh_terms: D000091162:AMP-Activated Protein Kinase Kinases; D000251:Adenosine Triphosphatases / Q000037:antagonists & inhibitors; D000818:Animals; D001692:Biological Transport / Q000187:drug effects / Q000502:physiology; D001696:Biomechanical Phenomena; D002118:Calcium / Q000378:metabolism; D005947:Glucose / Q000378:metabolism*; D005978:Glutathione / Q000378:metabolism; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D009119:Muscle Contraction / Q000502:physiology*; D018656:Muscle Fibers, Fast-Twitch / Q000502:physiology; D018482:Muscle, Skeletal / Q000378:metabolism*; D010766:Phosphorylation; D011494:Protein Kinases / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D013449:Sulfonamides / Q000494:pharmacology; D014050:Toluene / Q000031:analogs & derivatives / Q000494:pharmacology
chemical_list: C444880:N-benzyl-p-toluene sulfonamide; D013449:Sulfonamides; D014050:Toluene; D011494:Protein Kinases; D000091162:AMP-Activated Protein Kinase Kinases; D000251:Adenosine Triphosphatases; D005978:Glutathione; D005947:Glucose; D002118:Calcium