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Decreased PDH activation and glycogenolysis during exercise following fat adaptation with carbohydrate restoration

¹Department of Human Biology and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada; ²School of Medical Sciences, RMIT University, Bundoora; ³School of Exercise and Nutrition Sciences, Deakin University, Burwood; ⁴Department of Physiology, The University of Melbourne, Victoria; and ⁵Department of Sports Nutrition, Australia Institute of Sport, Belconnen, Australia

Submitted 15 June 2005 ; accepted in final form 22 September 2005

Five days of a high-fat diet while training, followed by 1 day of carbohydrate (CHO) restoration, increases rates of whole body fat oxidation and decreases CHO oxidation during aerobic cycling. The mechanisms responsible for these shifts in fuel oxidation are unknown but involve up- and downregulation of key regulatory enzymes in the pathways of skeletal muscle fat and CHO metabolism, respectively. This study measured muscle PDH and HSL activities before and after 20 min of cycling at 70% O_{2 peak} and 1 min of sprinting at 150% peak power output (PPO). Estimations of muscle glycogenolysis were made during the initial minute of exercise at 70% O_{2 peak} and during the 1-min sprint. Seven male cyclists undertook this exercise protocol on two occasions. For 5 days, subjects consumed in random order either a high-CHO (HCHO) diet (10.3 g·kg^–1·day^–1 CHO, or 70% of total energy intake) or an isoenergetic high-fat (FAT-adapt) diet (4.6 g·kg^–1·day^–1 FAT, or 67% of total energy) while undertaking supervised aerobic endurance training. On day 6 for both treatments, subjects ingested an HCHO diet and rested before their experimental trials on day 7. This CHO restoration resulted in similar resting glycogen contents (FAT-adapt 873 ± 121 vs. HCHO 868 ± 120 µmol glucosyl units/g dry wt). However, the respiratory exchange ratio was lower during cycling at 70% O_{2 peak} in the FAT-adapt trial, which resulted in an 45% increase and an 30% decrease in fat and CHO oxidation, respectively. PDH activity was lower at rest and throughout exercise at 70% O_{2 peak} (1.69 ± 0.25 vs. 2.39 ± 0.19 mmol·kg wet wt^–1·min^–1) and the 1-min sprint in the FAT-adapt vs. the HCHO trial. Estimates of glycogenolysis during the 1st min of exercise at 70% O_{2 peak} and the 1-min sprint were also lower after FAT-adapt (9.1 ± 1.1 vs. 13.4 ± 2.1 and 37.3 ± 5.1 vs. 50.5 ± 2.7 glucosyl units·kg dry wt^–1·min^–1). HSL activity was 20% higher (P = 0.12) during exercise at 70% O_{2 peak} after FAT-adapt. Results indicate that previously reported decreases in whole body CHO oxidation and increases in fat oxidation after the FAT-adapt protocol are a function of metabolic changes within skeletal muscle. The metabolic signals responsible for the shift in muscle substrate use during cycling at 70% O_{2 peak} remain unclear, but lower accumulation of free ADP and AMP after the FAT-adapt trial may be responsible for the decreased glycogenolysis and PDH activation during sprinting.

skeletal muscle metabolism; pyruvate dehydrogenase; substrate phosphorylation; fat oxidation; carbohydrate oxidation

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