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1 Department of Human Physiology, The Copenhagen Muscle Research Centre, Institute of Exercise and Sport Sciences, University of Copenhagen, DK-2100 Copenhagen, Denmark
2 Structural Cell Biology Unit, Department of Medical Anatomy, University of Copenhagen, DK-2200 Copenhagen, Denmark
* To whom correspondence should be addressed. E-mail: croepstorff{at}ifi.ku.dk.
In the present study we investigated possible sites of regulation of long-chain fatty acid (LCFA) oxidation in contracting human skeletal muscle. Leg plasma LCFA kinetics were determined in eight healthy men during bicycling (60 min, 65% VO2 peak) with either high (H-FOX) or low (L-FOX) leg fat oxidation (H-FOX: 1098±140; L-FOX: 494±84 µmol FA.min-1, p<0.001) which was achieved by manipulating pre-exercise muscle glycogen (H-FOX: 197±21; L-FOX: 504±25 mmol/kg dry weight, p<0.001). Several blood metabolites and hormones were kept nearly similar between trials by allocating a pre-exercise meal and infusing glucose intravenously during exercise. During exercise, leg plasma LCFA fractional extraction was identical between trials (H-FOX: 17.8±1.6; L-FOX: 18.2±1.8%, NS), suggesting similar LCFA transport capacity in muscle. On the contrary, leg plasma LCFA oxidation was 99% higher in H-FOX than in L-FOX (421±47 vs. 212±37 µmol/min, p<0.001). Probably due to the slightly higher (p<0.01) plasma LCFA concentration in H-FOX than in L-FOX, leg plasma LCFA uptake was non-significantly (p=0.17) higher (25%) in H-FOX than in L-FOX, yet the fraction of plasma LCFA uptake oxidized was 61% higher (p<0.05) in H-FOX than in L-FOX. Accordingly, the muscle content of several lipid-binding proteins did not differ significantly between trials, although FAT/CD36 and caveolin-1 were elevated (p<0.05) by the high-intensity exercise and dietary manipulation allocated on the day before the experimental trial. The present data suggest that in contracting human skeletal muscle with different fat oxidation rates, achieved by manipulating pre-exercise glycogen content, transsarcolemmal transport is not limiting plasma LCFA oxidation. Rather the latter seems to be limited by intracellular regulatory mechanisms.
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