Journal
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
Volume 279, Issue 2, Pages E348-E355Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpendo.2000.279.2.E348
Keywords
exercise; lipolysis; fatty acid; intramuscular triglyceride; stable isotopes
Categories
Funding
- NIDDK NIH HHS [DK-45416, DK-37948, DK-09749-01A1] Funding Source: Medline
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Endurance training increases fatty acid oxidation (FAO) and skeletal muscle oxidative capacity. However, the source of the additional fat and the mechanisms for increasing FAO capacity in muscle are not clear. We measured whole body and regional lipolytic activity and whole body and plasma FAO in six lean women during 90 min of bicycling exercise (50% pretraining peak O-2 consumption) before and after 12 wk of endurance training. We also assessed skeletal muscle content of peroxisome proliferator-activated receptor-alpha (PPAR alpha) and its target proteins that regulate FAO [medium-chain and very long chain acyl-CoA dehydrogenase (MCAD and VLCAD)]. Despite a 25% increase in whole body FAO during exercise after training (P < 0.05), training did not alter regional adipose tissue lipolysis (abdominal: 0.56 +/- 0.26 and 0.57 +/- 0.10 mmol . 100 g(-1) . min(-1); femoral: 0.13 +/- 0.07 and 0.09 +/- 0.02 mmol . 100 g(-1) . min(-1)), whole body palmitate rate of appearance in plasma (168 +/- 18 and 150 +/- 25 mu mol/ min), and plasma FAO (554 +/- 61 and 601 +/- 45 mu mol/ min). However, training doubled the levels of muscle PPAR alpha, MCAD, and VLCAD. We conclude that training increases the use of nonplasma fatty acids and may enhance skeletal muscle oxidative capacity by PPAR alpha regulation of gene expression.
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