Nordby Pernille, Rosenkilde Mads, Ploug Thorkil, Westh Karina, Feigh Michael, Nielsen Ninna B, Helge Jørn W, Stallknecht Bente
Department of Biomedical Sciences, University of Copenhagen, Denmark; and.
Department of Biomedical Sciences, University of Copenhagen, Denmark; and
J Appl Physiol (1985). 2015 Apr 1;118(7):803-10. doi: 10.1152/japplphysiol.00715.2014. Epub 2015 Jan 22.
Endurance training increases peak fat oxidation (PFO) during exercise, but whether this is independent of changes in body weight is not known. The aim of the present study was to investigate the effects of endurance training with or without weight loss or a diet-induced weight loss on PFO and on key skeletal muscle mitochondrial proteins involved in fat oxidation. Sixty moderately overweight, sedentary but otherwise healthy men were randomized to 12 wk of training (T), diet (D), training and increased caloric intake (T-iD), or continuous sedentary control (C). Isoenergetic deficits corresponding to 600 kcal/day were comprised of endurance exercise for T and caloric restriction for D. T-iD completed similar training but was not in 600 kcal deficit because of dietary replacement. PFO and the exercise intensity at which this occurred (FatMax) were measured by a submaximal exercise test and calculated by polynomial regression. As intended by study design, a similar weight loss was observed in T (-5.9 ± 0.7 kg) and D (-5.2 ± 0.8 kg), whereas T-iD (-1.0 ± 0.5 kg) and C (0.1 ± 0.6 kg) remained weight stable. PFO increased to a similar extent with 42% in T [0.16 g/min; 95% confidence intervals (CI): 0.02; 0.30, P = 0.02] and 41% in T-iD (0.16 g/min; 95% CI: 0.01; 0.30, P = 0.04) compared with C, but did not increase in D (P = 0.96). In addition, the analysis of covariance showed that changes in both PFO (0.10 g/min; 95% CI: 0.03; 0.17, P = 0.03) and FatMax (6.3% V̇o2max; 95% CI: 1.4; 11.3, P < 0.01) were independently explained by endurance training. In conclusion, endurance training per se increases PFO in moderately overweight men.
耐力训练可提高运动期间的峰值脂肪氧化（PFO），但这是否独立于体重变化尚不清楚。本研究的目的是调查有无体重减轻的耐力训练或饮食诱导的体重减轻对PFO以及参与脂肪氧化的关键骨骼肌线粒体蛋白的影响。60名中度超重、久坐但其他方面健康的男性被随机分为12周的训练组（T）、饮食组（D）、训练并增加热量摄入组（T-iD）或持续久坐对照组（C）。相当于每天600千卡的等能量亏空在T组通过耐力运动实现，在D组通过热量限制实现。T-iD组完成了类似的训练，但由于饮食替代没有处于600千卡的亏空状态。通过次极量运动测试测量PFO以及发生PFO时的运动强度（脂肪最大摄氧量），并通过多项式回归计算。按照研究设计，T组（-5.9±0.7千克）和D组（-5.2±0.8千克）观察到类似的体重减轻，而T-iD组（-1.0±0.5千克）和C组（0.1±0.6千克）体重保持稳定。与C组相比，T组的PFO增加了42%[0.16克/分钟；95%置信区间（CI）：0.02；0.30，P=0.02]，T-iD组增加了41%（0.16克/分钟；95%CI：0.01；0.30，P=0.04），而D组没有增加（P=0.96）。此外，协方差分析表明，耐力训练可独立解释PFO（0.10克/分钟；95%CI：0.03；0.17，P=0.03）和脂肪最大摄氧量（6.3%最大摄氧量；95%CI：1.4；11.3，P<0.01）的变化。总之，耐力训练本身可提高中度超重男性的PFO。
