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Am J Physiol Endocrinol Metab 288: E133-E142, 2005. First published September 21, 2004; doi:10.1152/ajpendo.00379.2004
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Malonyl-CoA and carnitine in regulation of fat oxidation in human skeletal muscle during exercise

Carsten Roepstorff,1 Nils Halberg,1 Thore Hillig,1 Asish K. Saha,2 Neil B. Ruderman,2 Jørgen F. P. Wojtaszewski,1 Erik A. Richter,1 and Bente Kiens1

1The Copenhagen Muscle Research Centre, Department of Human Physiology, Institute of Exercise and Sport Sciences, University of Copenhagen, Copenhagen, Denmark; and 2Diabetes Research Unit, Departments of Medicine, Physiology, and Biophysics, Section of Endocrinology, Boston University School of Medicine, Boston, Massachusetts

Submitted 16 August 2004 ; accepted in final form 17 September 2004

Intracellular mechanisms regulating fat oxidation were investigated in human skeletal muscle during exercise. Eight young, healthy, moderately trained men performed bicycle exercise (60 min, 65% peak O2 consumption) on two occasions, where they ingested either 1) a high-carbohydrate diet (H-CHO) or 2) a low-carbohydrate diet (L-CHO) before exercise 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 than in H-CHO (P < 0.001). In keeping with this, the activity of {alpha}2-AMP-activated protein kinase ({alpha}2-AMPK) was increased twice as much in L-CHO as in H-CHO (P < 0.01) at 60 min of exercise. However, acetyl-CoA carboxylase (ACC){beta} Ser221 phosphorylation was increased to the same extent (6-fold) under the two conditions. The concentration of malonyl-CoA was reduced 13% by exercise in both conditions (P < 0.05). Pyruvate dehydrogenase activity was higher during exercise in H-CHO than in 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 {alpha}2-AMPK 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.

acetylcarnitine; acetyl coenzyme A; pyruvate dehydrogenase activity; adenosine 5'-monosphosphate-activated protein kinase; acetyl coenzyme A carboxylase


Address for reprint requests and other correspondence: C. Roepstorff, The Copenhagen Muscle Research Centre, Institute of Exercise and Sport Sciences, Dept. of Human Physiology, Universitetsparken 13, DK-2100 Copenhagen Ø, Denmark (E-mail: croepstorff{at}ifi.ku.dk)




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