Jacob Kathryn J, Sonjak Vita, Spendiff Sally, Hepple Russell T, Chevalier Stéphanie, Perez Anna, Morais José A
Research Institute of the McGill University Health Center, Montreal, QC, Canada.
Children's Hospital of Eastern Ontario Research Institute, University of Ottawa, Ottawa, ON, Canada.
Front Nutr. 2021 Jan 22;7:619216. doi: 10.3389/fnut.2020.619216. eCollection 2020.
Frailty is a clinical condition associated with loss of muscle mass and strength (sarcopenia). Mitochondria are centrally implicated in frailty and sarcopenia. Leucine (Leu) can alter mitochondrial content in myocytes, while resistance training (RT) is the strongest stimulus to counteract sarcopenia and may enhance mitochondrial biogenesis. We determined the effects of Leu supplementation and RT on mitochondrial content and function in pre/frail elderly women in a randomized double-blinded placebo-controlled study. Nineteen pre/frail elderly women (77.5 ± 1.3 y, BMI: 25.1 ± 0.9 kg/m), based on the Frailty Phenotype, underwent 3-months of RT 3×/week with protein-optimized diet and were randomized to 7.5 g/d of Leu supplementation or placebo alanine (Ala). Pre/post-intervention mitochondrial respiration, reactive oxygen species (ROS) production, calcium retention capacity (CRC), time to permeability transition pore (mPTP) opening, mitochondrial voltage-dependent anion channel (VDAC) protein content, leg press 1-repetition maximum (1RM), and 6-min walk test (6MWT) were measured. No time, supplementation, or interaction effects were observed for respiration, ROS, time to mPTP opening, and CRC. VDAC levels significantly increased in the Leu group post-intervention ( = 0.012). Both groups significantly increased leg press 1RM and 6MWT, with no effect of supplementation. Leu supplementation with 3 months of RT increased mitochondrial content. Future studies should investigate if there is an increase in mitochondrial turnover or a shift in quality control (mitophagy) in leucine supplemented pre/frail elderly women who undergo 12 weeks of RT. ClinicalTrials.gov, identifier: NCT01922167.
衰弱是一种与肌肉质量和力量丧失（肌肉减少症）相关的临床状况。线粒体在衰弱和肌肉减少症中起着核心作用。亮氨酸（Leu）可改变肌细胞中的线粒体含量，而抗阻训练（RT）是对抗肌肉减少症的最强刺激因素，可能会增强线粒体生物发生。在一项随机双盲安慰剂对照研究中，我们确定了补充亮氨酸和抗阻训练对虚弱/衰弱老年女性线粒体含量和功能的影响。根据衰弱表型，19名虚弱/衰弱老年女性（77.5±1.3岁，体重指数：25.1±0.9kg/m²）接受了为期3个月、每周3次的抗阻训练，并采用蛋白质优化饮食，随机分为补充7.5g/d亮氨酸组或安慰剂丙氨酸（Ala）组。测量干预前后的线粒体呼吸、活性氧（ROS）产生、钙保留能力（CRC）、通透性转换孔（mPTP）开放时间、线粒体电压依赖性阴离子通道（VDAC）蛋白含量、腿举1次重复最大值（1RM）和6分钟步行试验（6MWT）。在呼吸、ROS、mPTP开放时间和CRC方面，未观察到时间、补充剂或交互作用的影响。干预后亮氨酸组的VDAC水平显著升高（P = 0.012）。两组的腿举1RM和6MWT均显著增加，补充剂无影响。补充亮氨酸并进行3个月抗阻训练可增加线粒体含量。未来的研究应调查，在接受12周抗阻训练的补充亮氨酸的虚弱/衰弱老年女性中，线粒体周转率是否增加或质量控制（线粒体自噬）是否发生变化。ClinicalTrials.gov标识符：NCT01922167。
