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Skeletal Muscle Adaptation to Exercise Training: AMP-Activated Protein Kinase Mediates Muscle Fiber Type Shift

Katja S.C. Röckl, MD^*, Michael F. Hirshman, BS^*, Josef Brandauer, PhD^*, Nobuharu Fujii, PhD^*, Lee A. Witters, MD, and Laurie J. Goodyear, PhD^*

*Research Division, Joslin Diabetes Center and Department of Medicine, Brigham and Women's Hospital, and Harvard Medical School, Boston MA;
Dartmouth Medical School, Hanover NH

Correspondence: Laurie.Goodyear{at}joslin.harvard.edu

Regular endurance exercise has profound benefits on overall health, including the prevention of obesity, cardiovascular disease, and diabetes.

Objective.: To determine whether AMPK mediates commonly observed adaptive responses to exercise training in skeletal muscle.

Research Design/Methods and Results.: Six weeks of voluntary wheel running induced a significant (p < 0.05) fiber type IIb to IIa/x shift in triceps muscle of wild type mice. Despite similar wheel running capacities, this training-induced shift was reduced by 40% in transgenic mice expressing a muscle-specific AMPK2 inactive subunit. Sedentary mice carrying an AMPK-activating mutation (1TG) showed a 2.6-fold increase in type IIa/x fibers but no further increase with training. To determine if AMPK is involved in concomitant metabolic adaptations to training, we measured markers of mitochondria (citrate synthase, succinate dehydrogenase) and glucose uptake capacity (GLUT4, hexokinase II). Mitochondrial markers increased similarly in wild type and AMPK2 inactive mice. Sedentary 1TG mice showed a 25% increase in citrate synthase activity, but no further increase with training. GLUT4 protein expression was not different in either line of transgenic mice compared to wild type, and tended to increase with training, although this was not statistically significant. Training induced a 65% increase in hexokinase II protein in wild type, but not in AMPK2 inactive mice. Hexokinase II was significantly elevated in sedentary 1TG mice, without an additional increase with training.

Conclusions.: AMPK is not necessary for exercise training-induced increases in mitochondrial markers, but is essential for fiber type IIb to IIa/x transformation and increases in hexokinase II protein.

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