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1 The Copenhagen Muscle Research Centre, Department of Human Physiology, Institute of Exercise and Sport Sciences, University of Copenhagen, Copenhagen, Denmark
2 Diabetes Research Unit, Departmens of Medicine, Physiology, and Biophysics, Section of Endocrinology, Boston University School of Medicine, Boston, MA, USA
* To whom correspondence should be addressed. E-mail: croepstorff{at}ifi.ku.dk.
Intracellular mechanisms to regulate fat oxidation were investigated in human skeletal muscle
during exercise. Eight young, healthy moderately trained men performed bicycle exercise (60 min,
65% VO2 peak) on two occasions, one on which they ingested a high carbohydrate diet (H-CHO)
prior to the exercise and the other a low carbohydrate diet (L-CHO) to alter muscle glycogen
content as well as to induce, respectively, low and high rates of fat oxidation. Leg fat oxidation was
122% higher during exercise in L-CHO vs. H-CHO (p<0.001). In keeping with this, the activity of
2AMPK was increased twice as much in L-CHO vs. H-CHO (p<0.01) at 60 min of exercise.
However, ACC
Ser221 phosphorylation was increased to the same extent (6-fold) under the two
conditions. The concentration of malonyl-CoA was reduced by 13% by exercise in both conditions
(p<0.05). PDH activity was higher during exercise in H-CHO vs. L-CHO (p<0.01). In H-CHO only,
the concentrations of acetyl-CoA and acetylcarnitine were increased (p<0.001) and the
concentration of free carnitine was decreased (p<0.01) by exercise. The data suggest that a decrease
in the concentration of malonyl-CoA, secondary to 2AMPK activation and ACC inhibition (by
phosphorylation), contributes to the increase in fat oxidation observed at the onset of exercise
regardless of muscle glycogen levels. They also suggest that with high muscle glycogen, the
availability of free carnitine may limit fat oxidation during exercise, due to its increased use for
acetylcarnitine formation.
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