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- Title
Skeletal Muscle Adaptation to Exercise Training: AMP-Activated Protein Kinase Mediates Muscle Fiber Type Shift.
- Authors
Roeckl, Katja S.; Hirshman, Michael F.; Brandauer, Josef; Fujii, Nobuharu; Witters, Lee A.; Goodyear, Laurie J.
- Abstract
Endurance exercise training has profound benefits on overall health, including the prevention of obesity, cardiovascular disease, and diabetes. The goal of this study was to determine whether AMPK mediates commonly observed adaptive responses to exercise training in skeletal muscle. Six weeks of voluntary wheel cage running induced a fiber type fib to IIa shift in triceps muscle of wild type mice (p < 0.01). This training-induced shift was significantly reduced in transgenic mice expressing a muscle-specific AMPK alpha-2 inactive subunit (p < 0.05). Sedentary mice carrying an AMPK-activating mutation (gamma-1TG) showed a significantly elevated level of type IIa fibers compared to wild type littermates (p < 0.01), which did not increase further with training. To determine if AMPK is also involved in concomitant metabolic adaptations to exercise training, we measured markers of mitochondria (citrate synthase, succinate dehydrogenase) and glucose uptake capacity (GLUT4, hexokinase II). Training resulted in similar increases in mitochondrial markers in wild type and AMPK alpha-2 inactive mice. Increased AMPK activity in sedentary gamma-1TG mice was associated with an increase in mitochondrial markers (P < 0.01), but there was no further increase with training. In the sedentary state, GLUT4 protein expression was not different in either line of transgenic mice compared to corresponding wild type animals, and was not increased by exercise training. In contrast, training increased hexokinase II protein in wild type mice (p < 0.01), but not in the AMPK alpha-2 inactive mice. Hexokinase II was increased in sedentary gamma-1TG mice (p < 0.05), without an additional increase by training. In summary, AMPK alpha-2 activity is important for training-induced fiber type shifts from IIb to IIa, and the upregulation of hexokinase II protein. However, AMPK activity is not necessary for training-induced increases in mitochondrial markers. These results suggest that AMPK activation mediates some, but not all, skeletal muscle adaptations to endurance exercise training. ADA-Funded Research
- Subjects
PHYSIOLOGICAL adaptation; MUSCLES; EXERCISE; PROTEIN kinases; ADENOSINE monophosphate
- Publication
Diabetes, 2007, Vol 56, pA37
- ISSN
0012-1797
- Publication type
Article