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Am J Physiol Endocrinol Metab 276: E352-E357, 1999;
0193-1849/99 $5.00
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Vol. 276, Issue 2, E352-E357, February 1999

Muscular long-chain fatty acid content during graded exercise in humans

Bente Kiens1, Theo H. M. Roemen2, and Ger J. van der Vusse2

1 Copenhagen Muscle Research Centre, August Krogh Institute, University of Copenhagen, DK-2100 Copenhagen, Denmark; and 2 Department of Physiology, Cardiovascular Research Institute Maastricht, Maastricht University, 6200 MD Maastricht, The Netherlands

We measured the content of long-chain fatty acids (LCFA) in biopsies obtained from the vastus lateralis muscle in humans at rest and after different exercise intensities. Nine volunteers exercised at 65% of maximal oxygen uptake (VO2 max) for 40 min and at 90% of VO2 max for another 15 min on a Krogh bicycle ergometer. LCFA measured in muscle tissue averaged 76 ± 5 nmol/g wet wt at rest, decreased significantly after exercise at 65% VO2 max to 48 ± 4 nmol/g wet wt, and increased to 68 ± 5 nmol/g wet wt (P < 0.05) after high-intensity exercise. The calculated myocyte LCFA content at rest amounted to 69 ± 5 nmol/g wet wt, decreased by 43% (P < 0.05) after exercise at 65% of VO2 max, and subsequently increased by 54% after exercise at 90% of VO2 max (P < 0.05) compared with the values obtained at the lower workload. The blood plasma LCFA concentration during the low-intensity exercise (366 ± 23 nmol/ml) was similar to the values obtained at rest (372 ± 31 nmol/ml) but decreased significantly during the high-intensity workload (249 ± 49 nmol/ml). From these data it is proposed that 1) in human skeletal muscle, metabolism rather than cellular availability of LCFA governs the rate of LCFA utilization at rest and during exercise, and 2) consequently reduction in muscle LCFA oxidation during high-intensity exercise (e.g., 90% VO2 max) is due primarily to a decrease in mitochondrial LCFA oxidation rate rather than an insufficient cellular availability of LCFA.

skeletal muscle; exercise


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