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AJP - Endocrinology and Metabolism, Vol 264, Issue 2 E215-E220, Copyright © 1993 by American Physiological Society
ARTICLES |
A. R. Coggan, R. J. Spina, W. M. Kohrt and J. O. Holloszy
Section of Applied Physiology, Washington University School of Medicine, St. Louis, Missouri 63110.
It has been hypothesized that endurance training reduces carbohydrate utilization during exercise via citrate-mediated inhibition of phosphofructokinase (PFK). To test this hypothesis, vastus lateralis muscle biopsy samples were obtained from eight men before and immediately (approximately 10 s) after 2 h of cycle ergometer exercise at 60% of pretraining peak O2 uptake, both before and after 12 wk of endurance exercise training (3 days/wk running, 3 days/wk interval cycling). Training increased muscle citrate synthase (CS) activity from 3.69 +/- 0.48 (SE) to 5.30 +/- 0.42 mol.h-1.kg protein-1 and decreased the mean respiratory exchange ratio during exercise from 0.92 +/- 0.01 to 0.88 +/- 0.01 (both P < 0.001). Muscle citrate concentration at the end of exercise correlated significantly with CS activity (r = 0.70; P < 0.005) and was slightly but not significantly higher after training (0.80 +/- 0.19 vs. 0.54 +/- 0.19 mmol/kg dry wt; P = 0.16). Muscle glucose 6-phosphate (G-6-P) concentration at the end of exercise, however, was 31% lower in the trained state (1.17 +/- 0.10 vs. 1.66 +/- 0.27 mmol/kg dry wt; P < 0.05), in keeping with a 36% decrease in the amount of muscle glycogen utilized (133 +/- 22 vs. 209 +/- 19 mmol.kg dry wt-1.2 h-1; P < 0.01). The lower G-6-P concentration after training suggests that the training-induced reduction in carbohydrate utilization results from attenuation of flux before the PFK step in glycolysis and is not due to citrate-mediated inhibition of PFK.
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