Fat adaptation followed by carbohydrate loading compromises high-intensity sprint performance

Sep 6, 2005Journal of applied physiology (Bethesda, Md. : 1985)

High-intensity sprint performance may decline after switching to fat-based fuel then loading carbohydrates

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Abstract

Ingestion of a high-fat diet followed by carbohydrate loading increased fat utilization but reduced 1-km sprint power output during a 100-km cycling time trial.

A high-fat diet decreased the respiratory exchange ratio at rest and during exercise, indicating enhanced fat utilization.
Plasma free fatty acid levels increased significantly after the high-fat diet.
There was a tendency for increased sympathetic activation in response to the high-fat diet, as indicated by low-frequency power in heart rate variability.
Overall performance in the 100-km time trial was similar between dietary conditions.
1-km sprint power output was significantly lower after the high-fat diet compared to the high-carbohydrate diet, despite similar ratings of perceived exertion, heart rate, and muscle recruitment.

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The aim of this study was to investigate the effect of a high-fat diet (HFD) followed by 1 day of carbohydrate (CHO) loading on substrate utilization, heart rate variability (HRV), effort perception [rating or perceived exertion (RPE)], muscle recruitment [electromyograph (EMG)], and performance during a 100-km cycling time trial. In this randomized single-blind crossover study, eight well-trained cyclists completed two trials, ingesting either a high-CHO diet (HCD) (68% CHO energy) or an isoenergetic HFD (68% fat energy) for 6 days, followed by 1 day of CHO loading (8-10 g CHO/kg). Subjects completed a 100-km time trial on day 1 and a 1-h cycle at 70% of peak oxygen consumption on days 3, 5, and 7, during which resting HRV and resting and exercising respiratory exchange ratio (RER) were measured. On day 8, subjects completed a 100-km performance time trial, during which blood samples were drawn and EMG was recorded. Ingestion of the HFD reduced RER at rest (P < 0.005) and during exercise (P < 0.01) and increased plasma free fatty acid levels (P < 0.01), indicating increased fat utilization. There was a tendency for the low-frequency power component of HRV to be greater for HFD-CHO (P = 0.056), suggestive of increased sympathetic activation. Overall 100-km time-trial performance was not different between diets; however, 1-km sprint power output after HFD-CHO was lower (P < 0.05) compared with HCD-CHO. Despite a reduced power output with HFD-CHO, RPE, heart rate, and EMG were not different between trials. In conclusion, the HFD-CHO dietary strategy increased fat oxidation, but compromised high intensity sprint performance, possibly by increased sympathetic activation or altered contractile function.

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