Yeo Wee Kian, Lessard Sarah J, Chen Zhi-Ping, Garnham Andrew P, Burke Louise M, Rivas Donato A, Kemp Bruce E, Hawley John A
Exercise Metabolism Group, School of Medical Sciences, RMIT University, Victoria, Australia.
J Appl Physiol (1985). 2008 Nov;105(5):1519-26. doi: 10.1152/japplphysiol.90540.2008. Epub 2008 Sep 18.
We have previously reported that 5 days of a high-fat diet followed by 1 day of high-carbohydrate intake (Fat-adapt) increased rates of fat oxidation and decreased rates of muscle glycogenolysis during submaximal cycling compared with consumption of an isoenergetic high-carbohydrate diet (HCHO) for 6 days (Burke et al. J Appl Physiol 89: 2413-2421, 2000; Stellingwerff et al. Am J Physiol Endocrinol Metab 290: E380-E388, 2006). To determine potential mechanisms underlying shifts in substrate selection, eight trained subjects performed Fat-adapt and HCHO. On day 7, subjects performed 1-h cycling at 70% peak O2 uptake. Muscle biopsies were taken immediately before and after exercise. Resting muscle glycogen content was similar between treatments, but muscle triglyceride levels were higher after Fat-adapt (P < 0.05). Resting AMPK-alpha1 and -alpha2 activity was higher after Fat-adapt (P = 0.02 and P = 0.05, respectively), while the phosphorylation of AMPK's downstream target, acetyl-CoA carboxylase (pACC at Ser221), tended to be elevated after Fat-adapt (P = 0.09). Both the respiratory exchange ratio (P < 0.01) and muscle glycogen utilization (P < 0.05) were lower during exercise after Fat-adapt. Exercise increased AMPK-alpha1 activity after HCHO (P = 0.03) but not Fat-adapt. Exercise was associated with an increase in pACC at Ser221 for both dietary treatments (P < 0.05), with postexercise pACC Ser221 higher after Fat-adapt (P = 0.02). In conclusion, compared with HCHO, Fat-adapt increased resting muscle triglyceride stores and resting AMPK-alpha1 and -alpha2 activity. Fat-adapt also resulted in higher rates of whole body fat oxidation, reduced muscle glycogenolysis, and attenuated the exercise-induced rise in AMPK-alpha1 and AMPK-alpha2 activity compared with HCHO. Our results demonstrate that AMPK-alpha1 and AMPK-alpha2 activity and fuel selection in skeletal muscle in response to exercise can be manipulated by diet and/or the interactive effects of diet and exercise training.
我们之前曾报道，与连续6天摄入等能量的高碳水化合物饮食（HCHO）相比，先进行5天高脂肪饮食，随后1天高碳水化合物摄入（脂肪适应），在次最大强度骑行过程中可提高脂肪氧化率，并降低肌肉糖原分解率（Burke等人，《应用生理学杂志》89: 2413 - 2421, 2000；Stellingwerff等人，《美国生理学杂志 - 内分泌与代谢》290: E380 - E388, 2006）。为了确定底物选择变化背后的潜在机制，八名受过训练的受试者进行了脂肪适应和HCHO饮食方案。在第7天，受试者以70%峰值摄氧量进行1小时的骑行。在运动前后立即采集肌肉活检样本。两种饮食方案下静息肌肉糖原含量相似，但脂肪适应后肌肉甘油三酯水平更高（P < 0.05）。脂肪适应后静息AMPK - alpha1和 - alpha2活性更高（分别为P = 0.02和P = 0.05），而AMPK下游靶点乙酰辅酶A羧化酶（Ser221位点的pACC）的磷酸化在脂肪适应后有升高趋势（P = 0.09）。脂肪适应后运动期间呼吸交换率（P < 0.01）和肌肉糖原利用率（P < 0.05）均较低。HCHO饮食后运动增加了AMPK - alpha1活性（P = 0.03），但脂肪适应饮食后未增加。两种饮食方案下运动均与Ser221位点的pACC增加有关（P < 0.05），脂肪适应后运动后pACC Ser221更高（P = 0.02）。总之，与HCHO相比，脂肪适应增加了静息肌肉甘油三酯储备以及静息AMPK - alpha1和 - alpha2活性。与HCHO相比，脂肪适应还导致全身脂肪氧化率更高、肌肉糖原分解减少，并且减弱了运动诱导的AMPK - alpha1和AMPK - alpha2活性升高。我们的结果表明，饮食和/或饮食与运动训练的交互作用可调控骨骼肌中AMPK - alpha1和AMPK - alpha2活性以及运动时的燃料选择。
