Section for Sport Science, Department of Public Health, Aarhus University, Aarhus, Denmark.
Research Laboratory for Biochemical Pathology, Department of Clinical Medicine, Aarhus University, Aarhus, Denmark.
Scand J Med Sci Sports. 2019 Dec;29(12):1866-1880. doi: 10.1111/sms.13541. Epub 2019 Sep 30.
Repeated periodization of carbohydrate (CHO) intake using a diet-exercise strategy called the sleep-low model can potentially induce mitochondrial biogenesis and improve endurance performance in endurance-trained individuals. However, more studies are needed to confirm the performance-related effects and to investigate the sustained effects on maximal fat oxidation (MFO) rate and proteins involved in intramuscular lipid metabolism. Thirteen endurance-trained males (age 23-44 years; O -max, 63.9 ± 4.6 mL·kg ·min ) were randomized into two groups: sleep-low (LOW-CHO) or high CHO availability (HIGH-CHO) in three weekly training blocks over 4 weeks. The acute metabolic response was investigated during 60 minutes of exercise within the last 3 weeks of the intervention. Pre- and post-intervention, 30-minute time-trial performance was investigated after a 90-minute pre-load, which as a novel approach included nine intense intervals (and estimation of MFO). Additionally, muscle biopsies (v. lateralis) were obtained to investigate expression of proteins involved in intramuscular lipid metabolism using Western blotting. During acute exercise, average fat oxidation rate was ~36% higher in LOW-CHO compared to HIGH-CHO (P = .03). This did not translate into sustained effects on MFO. Time-trial performance increased equally in both groups (overall time effect: P = .005). We observed no effect on intramuscular proteins involved in lipolysis (ATGL, G0S2, CGI-58, HSL) or fatty acid transport and β-oxidation (CD-36 and HAD, respectively). In conclusion, the sleep-low model did not induce sustained effects on MFO, endurance performance, or proteins involved in intramuscular lipid metabolism when compared to HIGH-CHO. Our study therefore questions the transferability of acute effects of the sleep-low model to superior sustained adaptations.
采用一种称为睡眠低氧模型的饮食-运动策略，反复周期性地摄入碳水化合物（CHO），可能会诱导线粒体生物发生，并提高耐力训练个体的耐力表现。然而，还需要更多的研究来证实与性能相关的影响，并研究对最大脂肪氧化（MFO）率和涉及肌肉内脂质代谢的蛋白质的持续影响。13 名耐力训练男性（年龄 23-44 岁；O max ，63.9 ± 4.6 mL·kg·min）被随机分为两组：睡眠低氧（LOW-CHO）或高 CHO 可利用性（HIGH-CHO），在 4 周内的三个每周训练块中。在干预的最后 3 周内，进行了 60 分钟运动期间的急性代谢反应研究。在干预前后，在 90 分钟预负荷后进行了 30 分钟计时赛性能测试，这是一种新方法，包括 9 个剧烈间隔（并估计 MFO）。此外，还采集了肌肉活检（v.外侧），使用 Western 印迹法研究参与肌肉内脂质代谢的蛋白质的表达。在急性运动期间，LOW-CHO 组的平均脂肪氧化率比 HIGH-CHO 组高约 36%（P =.03）。这并没有转化为对 MFO 的持续影响。两组的计时赛性能均同等增加（总体时间效应：P =.005）。我们没有观察到脂肪分解（ATGL、G0S2、CGI-58、HSL）或脂肪酸转运和β氧化（CD-36 和 HAD）相关的肌肉内蛋白质的影响。总之，与 HIGH-CHO 相比，睡眠低氧模型并未引起 MFO、耐力表现或参与肌肉内脂质代谢的蛋白质的持续影响。因此，我们的研究对睡眠低氧模型的急性效应转化为优越的持续适应提出了质疑。
