Stellingwerff Trent, Spriet Lawrence L, Watt Matthew J, Kimber Nicholas E, Hargreaves Mark, Hawley John A, Burke Louise M
Department of Human Biology and Nutritional Sciences, University of Guelph, Ontario, Canada.
Am J Physiol Endocrinol Metab. 2006 Feb;290(2):E380-8. doi: 10.1152/ajpendo.00268.2005. Epub 2005 Sep 27.
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% VO2peak 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% VO2peak 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 x kg(-1) x day(-1) CHO, or approximately 70% of total energy intake) or an isoenergetic high-fat (FAT-adapt) diet (4.6 g x kg(-1) x 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 micromol glucosyl units/g dry wt). However, the respiratory exchange ratio was lower during cycling at 70% VO2peak in the FAT-adapt trial, which resulted in an approximately 45% increase and an approximately 30% decrease in fat and CHO oxidation, respectively. PDH activity was lower at rest and throughout exercise at 70% VO2peak (1.69 +/- 0.25 vs. 2.39 +/- 0.19 mmol x kg wet wt(-1) x 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% VO2peak 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 x kg dry wt(-1) x min(-1)). HSL activity was approximately 20% higher (P = 0.12) during exercise at 70% VO2peak 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% VO2peak 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.
训练期间进行五天高脂饮食，随后一天进行碳水化合物（CHO）恢复，可提高全身脂肪氧化率，并降低有氧骑行过程中的CHO氧化率。导致燃料氧化发生这些变化的机制尚不清楚，但分别涉及骨骼肌脂肪和CHO代谢途径中关键调节酶的上调和下调。本研究测量了在70%最大摄氧量（VO2peak）下骑行20分钟以及在150%峰值功率输出（PPO）下冲刺1分钟前后的肌肉丙酮酸脱氢酶（PDH）和激素敏感性脂肪酶（HSL）活性。在70%VO2peak运动的最初一分钟以及1分钟冲刺期间对肌肉糖原分解进行了估算。七名男性自行车运动员分两次进行了此运动方案。连续5天，受试者随机摄入高CHO（HCHO）饮食（10.3 g·kg⁻¹·天⁻¹ CHO，约占总能量摄入的70%）或等能量高脂（FAT-adapt）饮食（4.6 g·kg⁻¹·天⁻¹ FAT，占总能量的67%），同时进行有监督的有氧耐力训练。在两种饮食方案的第6天，受试者摄入HCHO饮食并休息，然后在第7天进行实验测试。这种CHO恢复导致静息糖原含量相似（FAT-adapt组为873±121 vs. HCHO组为868±120微摩尔葡萄糖基单位/克干重）。然而，在FAT-adapt试验中，70%VO2peak骑行期间的呼吸交换率较低，这导致脂肪和CHO氧化分别增加约45%和减少约30%。在FAT-adapt试验与HCHO试验中，静息时以及70%VO2peak全程运动（1.69±0.25 vs. 2.39±0.19 mmol·kg湿重⁻¹·分钟⁻¹）和1分钟冲刺时，PDH活性较低。在70%VO2peak运动的第1分钟以及1分钟冲刺期间，FAT-adapt后的糖原分解估算值也较低（9.1±1.1 vs. 13.4±2.1以及37.3±5.1 vs. 50.5±2.7葡萄糖基单位·kg干重⁻¹·分钟⁻¹）。FAT-adapt后，70%VO2peak运动期间HSL活性大约高20%（P = 0.12）。结果表明，先前报道的FAT-adapt方案后全身CHO氧化减少和脂肪氧化增加是骨骼肌内代谢变化的结果。在70%VO2peak骑行期间负责肌肉底物利用转变的代谢信号尚不清楚，但FAT-adapt试验后游离ADP和AMP积累较低可能是冲刺期间糖原分解减少和PDH激活降低的原因。
