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1 Department of Kinesiology and Health Education, The University of Texas at Austin, Austin, TX, USA
2 Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, LA, USA
* To whom correspondence should be addressed. E-mail: coyle{at}mail.utexas.edu.
This study determined the role of intramuscular triglyceride (IMTG) and adipose lipolysis in the elevated fat oxidation during exercise caused by a high-fat diet. In four separate trials, six endurance-trained cyclists exercised at 50% VO2peak for 1 h after a two-day control diet (22% fat, CON) or an isocaloric high-fat diet (60% fat, HF) with or without the ingestion of Acipimox, an adipose lipolysis inhibitor, before exercise. During exercise, HF elevated fat oxidation by 72% and whole body lipolysis (i.e., Ra glycerol) by 79% compared to CON (P<0.05) and this was associated with a 36% increase (P<0.05) in pre-exercise IMTG concentration. Although Acipimox lowered plasma FFA availability, HF still increased fat oxidation and Ra glycerol to the same magnitude above control as the increase caused by HF without Acipimox (i.e.; both increased fat oxidation 13-14 µmol/kg/min). In conclusion, the marked increase in fat oxidation following a HF diet is associated with elevated IMTG concentration and whole body lipolysis, and does not require increased adipose tissue lipolysis and plasma FFA concentration during exercise. This suggests that altered substrate storage in skeletal muscle is responsible for increased fat oxidation during exercise after two days of a high-fat diet.
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