Regulation of 5′AMP-activated protein kinase activity and substrate utilization in exercising human skeletal muscle

American Journal of Physiology - Endocrinology and Metabolism - Tập 284 Số 4 - Trang E813-E822 - 2003
Jørgen F. P. Wojtaszewski1, Christopher MacDonald1, Jakob N. Nielsen1, Ylva Hellsten1, D. Grahame Hardie2, Bruce E. Kemp3, Bente Kiens1, Erik A. Richter1
1Copenhagen Muscle Research Centre, Department of Human Physiology, Institute of Exercise and Sport Sciences, University of Copenhagen, 2100 Copenhagen, Denmark;
2Division of Molecular Physiology, School of Life Science, Dundee University, Dundee DD1 5EH, Scotland, United Kingdom; and
3St. Vincent's Institute of Medical Research, Fitzroy, Victoria 3065, Australia

Tóm tắt

The metabolic role of 5′AMP-activated protein kinase (AMPK) in regulation of skeletal muscle metabolism in humans is unresolved. We measured isoform-specific AMPK activity and β-acetyl-CoA carboxylase (ACCβ) Ser221phosphorylation and substrate balance in skeletal muscle of eight athletes at rest, during cycling exercise for 1 h at 70% peak oxygen consumption, and 1 h into recovery. The experiment was performed twice, once in a glycogen-loaded (glycogen concentration ∼900 mmol/kg dry wt) and once in a glycogen-depleted (glycogen concentration ∼160 mmol/kg dry wt) state. At rest, plasma long-chain fatty acids (FA) were twofold higher in the glycogen-depleted than in the loaded state, and muscle α1 AMPK (160%) and α2 AMPK (145%) activities and ACCβ Ser221phosphorylation (137%) were also significantly higher in the glycogen-depleted state. During exercise, α2 AMPK activity, ACCβ Ser221phosphorylation, plasma catecholamines, and leg glucose and net FA uptake were significantly higher in the glycogen-depleted than in the glycogen-loaded state without apparent differences in muscle high-energy phosphates. Thus exercise in the glycogen-depleted state elicits an enhanced uptake of circulating fuels that might be associated with elevated muscle AMPK activation. It is concluded that muscle AMPK activity and ACCβ Ser221phosphorylation at rest and during exercise are sensitive to the fuel status of the muscle. During exercise, this dependence may in part be mediated by humoral factors.

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Tài liệu tham khảo

10.1042/bj3340233

10.1113/jphysiol.1985.sp015794

10.2337/diabetes.49.7.1078

10.1249/00005768-198205000-00012

10.1152/ajpendo.2000.279.5.E1202

10.1042/bj3460659

10.1152/ajpendo.2000.279.2.E259

10.1111/j.1432-1033.1990.tb15293.x

10.2337/diabetes.49.8.1295

10.2337/diabetes.49.8.1281

10.1152/ajpendo.1999.277.6.E1103

10.1152/jappl.1983.55.2.628

10.1074/jbc.M202489200

10.1006/bbrc.2000.3073

10.1111/j.1475-097X.1981.tb00872.x

Goodyear LJ., 2000, Exerc Sports Sci Rev, 28, 113

Ha J, 1994, J Biol Chem, 269, 22162, 10.1016/S0021-9258(17)31770-2

10.1006/abbi.2001.2589

10.1146/annurev.biochem.67.1.821

10.2337/diabetes.51.8.2420

10.2337/diabetes.49.4.527

Hayashi T, 1998, Diabetes, 47, 1369

10.1113/jphysiol.1990.sp018175

10.1152/ajpendo.2001.281.2.E335

10.1152/ajpendo.2000.279.6.E1311

10.1074/jbc.274.35.24896

10.1152/ajpendo.1997.273.6.E1107

10.1038/415339a

10.1016/S0014-5793(98)01392-1

10.1016/S1097-2765(01)00251-9

10.2337/diabetes.50.5.921

10.1152/ajpendo.2001.280.5.E677

10.1152/japplphysiol.00642.2002

10.1113/jphysiol.2002.018044

10.1152/ajpendo.1996.270.3.E541

10.1152/ajpendo.1998.274.6.E1080

10.1152/ajpendo.00118.2002

10.1074/jbc.M201692200

10.1006/bbrc.2001.5275

10.1152/jappl.1986.61.3.827

10.1152/jappl.1989.66.2.876

10.1152/ajpendo.1995.269.2.E283

10.1152/ajpendo.00455.2001

10.1042/bj3350533

10.1172/JCI119034

10.1016/0003-2697(79)90151-9

10.1074/jbc.271.2.611

10.1152/ajpendo.00101.2001

10.1074/jbc.273.20.12443

Tullson PC, 1990, J Physiol, 520, 909

10.1074/jbc.272.20.13255

10.1152/ajpendo.1999.277.1.E1

10.1152/jappl.1997.82.1.219

10.1006/abbi.1994.1058

10.2337/diabetes.51.2.284

10.1016/S0006-291X(02)02465-8

10.1111/j.1469-7793.2000.t01-1-00221.x

Woods A, 1994, J Biol Chem, 269, 19509, 10.1016/S0021-9258(17)32198-1

10.1042/bst0290537

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American Journal of Physiology - Endocrinology and Metabolism

Tập 284 Số 4

E813-E822

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