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High-fat, low-carbohydrate (CHO) diets increase whole-body rates of fat oxidation and down-regulate CHO metabolism. We measured substrate utilization and skeletal muscle mitochondrial respiration to determine whether these adaptations are driven by high fat or lowCHOavailability. In a randomized crossover design, 8male cyclists consumed5dof ahigh-CHOdiet [ > 70%energy intake (EI)], followedby 5dof either anisoenergetic high-fat (HFAT; > 65% EI) or high-protein diet (HPRO; > 65% EI) with CHO intake clamped at < 20% EI. During the intervention, participants undertook daily exercise training. On d 6, participants consumed a high-CHO diet before performing 100 min of submaximal steady-state cycling plus an ∼30-min time trial. After 5 d of HFAT, skeletal muscle mitochondrial respiration supported by octanoylcarnitine and pyruvate, as well as uncoupled respiration, was decreased at rest, and rates of whole-body fat oxidationwere higher during exercise compared with HPRO. After 1 d of high-CHOdiet intake,mitochondrial respiration returned to baseline values inHFAT,whereas rates of substrate oxidation returned toward baseline in both conditions. These findings demonstrate that high dietary fat intake, rather than low-CHOintake, contributes to reductions inmitochondrial respiration and increases in wholebody rates of fat oxidation after a consuming a high-fat, low-CHO diet


Mary MacKillop Institute for Health Research

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Journal Article

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