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in the metabolic response to
training
Department of Internal Medicine and Center for Cardiovascular Research, Washington University School of Medicine, St. Louis, Missouri 63110
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 O2 consumption) before and after 12 wk of endurance training. We also assessed skeletal muscle content of
peroxisome proliferator-activated receptor-
(PPAR) 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 µmol · 100 g
1
· min1; femoral: 0.13 ± 0.07 and 0.09 ± 0.02 µmol · 100 g1 · min1),
whole body palmitate rate of appearance in plasma (168 ± 18 and
150 ± 25 µmol/min), and plasma FAO (554 ± 61 and 601 ± 45 µmol/min). However, training doubled the levels of muscle
PPAR, MCAD, and VLCAD. We conclude that training increases the use
of nonplasma fatty acids and may enhance skeletal muscle oxidative capacity by PPAR regulation of gene expression.
exercise; lipolysis; fatty acid; intramuscular triglyceride; stable isotopes
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