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Am J Physiol Endocrinol Metab (December 23, 2003). doi:10.1152/ajpendo.00462.2003
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Submitted on October 14, 2003
Accepted on December 14, 2003

Intensified exercise training does not alter AMPK signalling in human skeletal muscle

S. A. Clark1, Z- P. Chen2, K. T. Murphy3, R. J. Aughey3, M. J. McKenna3, B. E. Kemp2, and J. A. Hawley1*

1 Exercise Metabolism Group, School of Medical Sciences, RMIT University, Melbourne, Victoria, Australia
2 St. Vincent's Institute of Medical Research and Department of Medicine, University of Melbourne, Melbourne, Victoria, Australia
3 Muscle, Ions and Exercise Group, School of Human Movement, Recreation and Performance, Centre for Rehabilitation, Exercise and Sports Science, Victoria University of Technology, Melbourne, Victoria, Australia

* To whom correspondence should be addressed. E-mail: john.hawley{at}rmit.edu.au.

The AMPK cascade has been linked to many of the acute effects of exercise on skeletal muscle substrate metabolism, as well as some of the chronic training-induced adaptations. We determined the effect of 3 wk of intensified training (7 sessions of 8 x 5 min @ 85% of VO2peak) in skeletal muscle from well-trained athletes on AMPK responsiveness to exercise. Rates of whole-body substrate oxidation were determined during a 90 min steady-state ride pre- and post-training. Muscle metabolites and AMPK signalling were determined from biopsies taken at rest and immediately after exercise during the 1st and 7th intensified training session, performed at the same (absolute) pre-training workrate. Training decreased rates of whole-body CHO oxidation (P<0.05) and increased rates of fat oxidation (P<0.05) during SS. Resting muscle glycogen and its utilization during intense exercise was unaffected by training. However training induced a two-fold decrease in muscle [lactate] (P<0.05) and resulted in tighter metabolic regulation (i.e. attenuation of the decrease in the PCr/(PCr + Cr) ratio and of the increase in [AMP free]/ATP). The resting activities of AMPK{alpha}-1 and {alpha}-2 were similar after training, with the magnitude of the rise in response to exercise similar before and after training. AMPK phosphorylation at Thr172 on both the {alpha}-1 and {alpha}-2 subunits increased in response to exercise with the magnitude of this rise being similar post training. ACC-{beta} phosphorylation was similar at rest and, despite training-induced increases in whole-body rates of fat oxidation, did not increase after intensified training. Our results indicate that in well-trained individuals, short-term intensified training improves metabolic control but does not blunt AMPK signalling in response to intense exercise.




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