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Metabolism Unit, Shriners Burns Institute, and the Departments of Surgery and Anesthesiology, University of Texas Medical Branch, Galveston, Texas 77550
We have recently shown that increased
carbohydrate flux decreases fat oxidation during exercise by inhibition
of fatty acid entry into the mitochondria. Because endurance training
reduces the rate of carbohydrate flux during exercise, we hypothesized that training increases fat oxidation by relieving this inhibition. To
test this hypothesis, five sedentary and five endurance-trained men
exercised on a cycle ergometer at an oxygen consumption
(
O2) of ~2.0 l/min,
representing 80 and 40% peak
O2, respectively. [1-13C]oleate and
[1-14C]octanoate,
long- and medium-chain fatty acids, respectively, were infused for the
duration of the studies. Carbohydrate oxidation was significantly
higher in the sedentary group (196 ± 9 vs. 102 ± 17 µmol · kg
1 · min
1,
P < 0.05). Oleate oxidation was
higher in the trained group (3.8 ± 0.6 vs. 1.9 ± 0.3 µmol · kg
1 · min
1,
P < 0.05), whereas octanoate
oxidation was not different between the two groups. The percentage of
oleate that was taken up by tissues and oxidized was higher in the
trained group (76 ± 7 vs. 58 ± 3%,
P < 0.05). However, the percentage
of octanoate taken up and oxidized was not different (82 ± 3 vs. 85 ± 4%, not significant). Because octanoate, unlike oleate, can
freely diffuse across the mitochondrial membrane, the present results
suggest that the difference in fatty acid oxidation between trained and
untrained individuals may be due to enhanced fatty acid entry into the
mitochondria.
mitochondria; malonyl-coenzyme A; carnitine palmitoyltransferase; medium-chain fatty acids; endurance training; muscle
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