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1Faculty of Applied Health Sciences, Brock University, St. Catharines, Ontario; and 2Department of Medicine, McMaster University, Hamilton, Ontario, Canada
Submitted 13 June 2007 ; accepted in final form 10 October 2007
Pyruvate dehydrogenase (PDH) is an important regulator of carbohydrate oxidation during exercise, and its activity can be downregulated by an increase in dietary fat. The purpose of this study was to determine the acute metabolic effects of differential dietary fatty acids on the activation of the PDH complex (PDHa activity) at rest and at the onset of moderate-intensity exercise. University-aged male subjects (n = 7) underwent two fat-loading trials spaced at least 2 wk apart. Subjects consumed
300 g saturated (SFA) or n-6 polyunsaturated fatty acid (PUFA) fat over the course of 5 h. Following this, participants cycled at 65% of their maximum oxygen uptake for 15 min. Muscle biopsies were taken before and following fat loading and at 1 min exercise. Plasma free fatty acids increased from 0.15 ± 0.07 to 0.54 ± 0.19 mM over 5 h with SFA and from 0.11 ± 0.04 to 0.35 ± 0.13 mM with n-6 PUFA and were significantly lower throughout the n-6 PUFA trial. PDHa activity was unchanged following fat loading but increased at the onset of exercise in the SFA trial, from 1.18 ± 0.27 to 2.16 ± 0.37 mmol·min–1·kg wet wt–1. This effect was negated in the n-6 PUFA trial (1.04 ± 0.20 to 1.28 ± 0.36 mmol·min–1·kg wet wt–1). PDH kinase was unchanged in both trials, suggesting that the attenuation of PDHa activity with n-6 PUFA was a result of changes in the concentrations of intramitochondrial effectors, potentially intramitochondrial NADH or Ca2+. Our findings suggest that attenuated PDHa activity contributes to the preferential oxidation of n-6 PUFA during moderate-intensity exercise.
active fraction of pyruvate dehydrogenase; carbohydrate oxidation; moderate-intensity exercise; saturated fatty acids; polyunsaturated fatty acids; n-6 fatty acids
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