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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
-1 and
-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
-1 and
-2 subunits increased in response to exercise with the
magnitude of this rise being similar post training. ACC-
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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