No effect of five days of bed rest or short-term resistance exercise prehabilitation on markers of skeletal muscle mitochondrial content and dynamics in older adults.
No effect of five days of bed rest or short-term resistance exercise prehabilitation on markers of skeletal muscle mitochondrial content and dynamics in older adults.
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卧床休息五天或短期阻力运动康复训练对老年人骨骼肌线粒体含量和动力学标志物没有影响。
DOI：
10.14814/phy2.15345
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发表时间：
2022-07
影响因子：
2.5
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中科院分区：
文献类型：
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卧床休息（BR）导致骨骼肌代谢的显著损害。据报道，线粒体代谢对废用高度敏感，先前报道了失调的裂变融合事件和受损的氧化功能。临床相关短期BR（≤5天）对线粒体蛋白表达的影响目前尚不清楚，运动预刺激作为一种潜在的对抗性干预措施的影响也不清楚。本研究考察了5天BR和短期抗阻运动预适应（ST-REP）对线粒体蛋白质含量的影响。10名老年男性（71 ± 4岁）接受了5天的BR，提前7天完成了4次高容量单侧抗阻运动训练。从非运动对照和运动腿的股外侧肌中获取肌肉活检，包括运动前和运动后以及BR前和BR后，以确定柠檬酸合酶活性的变化以及线粒体电子传递链中关键蛋白的表达和裂变融合动力学、生物合成和线粒体自噬的分子调节因子。我们未观察到BR或ST-REP对柠檬酸合酶蛋白含量、酶活性或ETC复合物I-V蛋白含量的显著影响。此外，我们没有观察到线粒体分裂和融合标志物（p-DRP 1 S616、p-DRP 1 S637、p-DRP 1 S616/S637比值、p-MFFS 146、Mitofillin、OPA 1或MFN 2）的显著变化（全部p > 0.05）。最后，我们观察到生物合成标志物（p-AMPKT 172，p-ACCS 79，PGC 1a，TFAM）或线粒体自噬相关信号（ULK-1，BNIP 3/NIX，LC 3B I/II）无差异（所有p > 0.05）。与以前长期的肌肉骨骼废用期（即，7-14天），在健康老年人中，临床相关的5天BR期未导致肌肉线粒体蛋白信号传导的显著扰动，ST-REP在BR前一周无影响。因此，废用诱导的肌肉萎缩可能先于线粒体含量的改变。与之前长期的肌肉骨骼废用期相比，临床相关的5天卧床休息不会干扰健康老年人的肌肉线粒体蛋白信号传导。卧床前一周的短期抗阻运动预适应也不会影响肌肉线粒体信号传导。因此，废用诱导的肌肉萎缩可能先于线粒体含量的改变。
Bed rest (BR) results in significant impairments in skeletal muscle metabolism. Mitochondrial metabolism is reportedly highly sensitive to disuse, with dysregulated fission‐fusion events and impaired oxidative function previously reported. The effects of clinically relevant short‐term BR (≤5 days) on mitochondrial protein expression are presently unclear, as are the effects of exercise prehabilitation as a potential counteractive intervention. The present study examined the effects of a 5‐day period of BR and short‐term resistance exercise prehabilitation (ST‐REP) on mitochondrial‐protein content. Ten older men (71 ± 4 years) underwent 5 days of BR, completing four sessions of high‐volume unilateral resistance exercise prehabilitation over 7 days beforehand. Muscle biopsies were obtained from the vastus lateralis in the non‐exercised control and exercised legs, both pre‐ and post‐prehabilitation and pre‐ and post‐BR, to determine changes in citrate synthase enzyme activity and the expression of key proteins in the mitochondrial electron transport chain and molecular regulators of fission‐fusion dynamics, biosynthesis, and mitophagy. We observed no significant effect of either BR or ST‐REP on citrate synthase protein content, enzyme activity, or ETC complex I‐V protein content. Moreover, we observed no significant changes in markers of mitochondrial fission and fusion (p‐DRP1S616, p‐DRP1S637, p‐DRP1S616/S637 ratio, p‐MFFS146, Mitofillin, OPA1, or MFN2 (p > 0.05 for all). Finally, we observed no differences in markers of biosynthesis (p‐AMPKT172, p‐ACCS79, PGC1a, TFAM) or mitophagy‐related signaling (ULK‐1, BNIP3/NIX, LC3B I/II) (p > 0.05 for all). In contrast to previous longer‐term periods of musculoskeletal disuse (i.e., 7–14 days), a clinically relevant, 5‐day period of BR resulted in no significant perturbation in muscle mitochondrial protein signaling in healthy older adults, with no effect of ST‐REP in the week prior to BR. Accordingly, disuse‐induced muscle atrophy may precede alterations in mitochondrial content. In contrast to previous longer‐term periods of musculoskeletal disuse, a clinically relevant 5‐day period of bed‐rest did not perturbate muscle mitochondrial protein signaling in healthy older adults. short‐term resistance exercise prehabilitation the week prior to bed‐rest also did not influence muscle mitochondrial signaling. Accordingly, disuse‐induced muscle atrophy may precede alterations in mitochondrial content.