Institute for Health and Sport, Victoria University, Melbourne, Australia; Sports Cardiology, Baker Heart and Diabetes Institute, Melbourne, Australia.
Institute for Health and Sport, Victoria University, Melbourne, Australia.
Mol Metab. 2021 Jan;43:101110. doi: 10.1016/j.molmet.2020.101110. Epub 2020 Oct 31.
Sleep loss has emerged as a risk factor for the development of impaired glucose tolerance. The mechanisms underpinning this observation are unknown; however, both mitochondrial dysfunction and circadian misalignment have been proposed. Because exercise improves glucose tolerance and mitochondrial function, and alters circadian rhythms, we investigated whether exercise may counteract the effects induced by inadequate sleep.
To minimize between-group differences of baseline characteristics, 24 healthy young males were allocated into one of the three experimental groups: a Normal Sleep (NS) group (8 h time in bed (TIB) per night, for five nights), a Sleep Restriction (SR) group (4 h TIB per night, for five nights), and a Sleep Restriction and Exercise group (SR+EX) (4 h TIB per night, for five nights and three high-intensity interval exercise (HIIE) sessions). Glucose tolerance, mitochondrial respiratory function, sarcoplasmic protein synthesis (SarcPS), and diurnal measures of peripheral skin temperature were assessed pre- and post-intervention.
We report that the SR group had reduced glucose tolerance post-intervention (mean change ± SD, P value, SR glucose AUC: 149 ± 115 A.U., P = 0.002), which was also associated with reductions in mitochondrial respiratory function (SR: -15.9 ± 12.4 pmol O.s.mg, P = 0.001), a lower rate of SarcPS (FSR%/day SR: 1.11 ± 0.25%, P < 0.001), and reduced amplitude of diurnal rhythms. These effects were not observed when incorporating three sessions of HIIE during this period (SR+EX: glucose AUC 67 ± 57, P = 0.239, mitochondrial respiratory function: 0.6 ± 11.8 pmol O.s.mg, P = 0.997, and SarcPS (FSR%/day): 1.77 ± 0.22%, P = 0.971).
A five-night period of sleep restriction leads to reductions in mitochondrial respiratory function, SarcPS, and amplitude of skin temperature diurnal rhythms, with a concurrent reduction in glucose tolerance. We provide novel data demonstrating that these same detrimental effects are not observed when HIIE is performed during the period of sleep restriction. These data therefore provide evidence in support of the use of HIIE as an intervention to mitigate the detrimental physiological effects of sleep loss.
睡眠不足已成为糖耐量受损的一个风险因素。其背后的机制尚不清楚；然而，线粒体功能障碍和昼夜节律紊乱都被提出来了。因为运动可以改善葡萄糖耐量和线粒体功能，并改变昼夜节律，所以我们研究了运动是否可以抵消睡眠不足引起的影响。
为了尽量减少基线特征的组间差异，将 24 名健康年轻男性分配到以下三个实验组之一：正常睡眠（NS）组（每晚 8 小时床上时间（TIB），连续五晚）、睡眠限制（SR）组（每晚 4 小时 TIB，连续五晚）和睡眠限制和运动（SR+EX）组（每晚 4 小时 TIB，连续五晚和三次高强度间歇运动（HIIE））。在干预前后评估葡萄糖耐量、线粒体呼吸功能、肌浆蛋白合成（SarcPS）和外周皮肤温度的昼夜测量值。
我们报告说，SR 组在干预后葡萄糖耐量降低（平均变化 ± 标准差，P 值，SR 葡萄糖 AUC：149 ± 115 A.U.，P = 0.002），这也与线粒体呼吸功能降低有关（SR：-15.9 ± 12.4 pmol O.s.mg，P = 0.001），肌浆蛋白合成率较低（FSR%/天 SR：1.11 ± 0.25%，P < 0.001），以及昼夜节律振幅降低。当在此期间进行三次 HIIE 时，这些影响并未观察到（SR+EX：葡萄糖 AUC 67 ± 57，P = 0.239，线粒体呼吸功能：0.6 ± 11.8 pmol O.s.mg，P = 0.997，和肌浆蛋白合成（FSR%/天）：1.77 ± 0.22%，P = 0.971）。
五晚的睡眠限制导致线粒体呼吸功能、SarcPS 和皮肤温度昼夜节律振幅降低，同时葡萄糖耐量降低。我们提供了新的数据，证明当在睡眠限制期间进行高强度间歇运动时，这些相同的有害影响不会被观察到。因此，这些数据为高强度间歇运动作为减轻睡眠不足对生理的有害影响的干预措施提供了证据。
