PDF(Pubmed)
Abstract：
We sought to examine how resistance exercise (RE), cycling exercise, and disuse atrophy affect myosin heavy chain (MyHC) protein fragmentation in humans. In the first study (1boutRE), younger adult men (n=8; 5±2 years of RE experience) performed a lower body RE bout with vastus lateralis (VL) biopsies obtained immediately before, 3-, and 6-hours post-exercise. In the second study (10weekRT), VL biopsies were obtained in untrained younger adults (n=36, 18 men and 18 women) before and 24 hours (24h) after their first/naïve RE bout. These participants also engaged in 10 weeks (24 sessions) of resistance training and donated VL biopsies before and 24h after their last RE bout. VL biopsies were also examined from a third acute cycling study (n=7) and a fourth study involving two weeks of leg immobilization (n=20, 15 men and 5 women) to determine how MyHC fragmentation was affected. In the 1boutRE study, the fragmentation of all MyHC isoforms (MyHCTotal) increased 3 hours post-RE (~ +200%, p=0.018) and returned to pre-exercise levels by 6 hours post-RE. Immunoprecipitation of MyHCTotal revealed ubiquitination levels remained unaffected at the 3- and 6-hour post-RE time points. Interestingly, a greater increase in magnitude for MyHC type IIa versus I isoform fragmentation occurred 3-hours post-RE (8.6±6.3-fold versus 2.1±0.7-fold, p=0.018). In all 10weekRT participants, the first/naïve and last RE bouts increased MyHCTotal fragmentation 24h post-RE (+65% and +36%, respectively; p<0.001); however, the last RE bout response was attenuated compared to the first bout (p=0.045). The first/naïve bout response was significantly elevated in females only (p<0.001), albeit females also demonstrated a last bout attenuation response (p=0.002). Although an acute cycling bout did not alter MyHCTotal fragmentation, ~8% VL atrophy with two weeks of leg immobilization led to robust MyHCTotal fragmentation (+108%, p<0.001), and no sex-based differences were observed. In summary, RE and disuse atrophy increase MyHC protein fragmentation. A dampened response with 10 weeks of resistance training, and more refined responses in well-trained men, suggest this is an adaptive process. Given the null polyubiquitination IP findings, more research is needed to determine how MyHC fragments are processed. Moreover, further research is needed to determine how aging and disease-associated muscle atrophy affect these outcomes, and whether MyHC fragmentation is a viable surrogate for muscle protein turnover rates.
摘要：
我们试图研究阻力运动(RE)，骑自行车运动,废用性萎缩会影响人类肌球蛋白重链（MyHC）蛋白片段。在第一项研究(1boutRE)中，年轻的成年男性（n=8;5±2年的RE经验）进行了下半身RE发作，并在之前立即进行了股外侧肌（VL）活检，3-,运动后6小时。在第二项研究(10周RT)中，VL活检是在未经训练的年轻成年人（n=36，18名男性和18名女性）之前和之后24小时（24小时）进行的第一次/首次RE发作。这些参与者还进行了10周（24次）的阻力训练，并在最后一次RE发作之前和之后24小时捐赠了VL活检。还从第三次急性循环研究（n=7）和涉及两周腿部固定的第四项研究（n=20，15名男性和5名女性）中检查了VL活检，以确定MyHC碎片如何受到影响。在1boutRE研究中，所有MyHC同工型的碎片化(MyHC总计)在RE后3小时增加(~+200%，p=0.018），并在RE后6小时恢复到运动前水平。MyHCTotal的免疫沉淀显示泛素化水平在RE后3小时和6小时时间点未受影响。有趣的是,MyHCIIa型与I同工型片段的幅度增加更大，发生在RE后3小时（8.6±6.3倍对2.1±0.7倍，p=0.018)。在所有10周RT参与者中，第一次/幼稚和最后一次RE发作增加了RE后24hMyHC总碎片(+65%和+36%，分别；p<0.001)；然而，与第一次发作相比，最后一次RE发作的反应减弱（p=0.045）。第一次/幼稚发作反应仅在女性中显著升高(p<0.001)，尽管女性也表现出最后一次回合衰减反应（p=0.002）。尽管急性自行车比赛并没有改变MyHC总碎片，~8%的VL萎缩和两周的腿部固定导致强烈的MyHC总碎片化(+108%，p<0.001)，并且没有观察到基于性别的差异。总之,RE和废用萎缩增加MyHC蛋白片段化。10周的阻力训练减弱了反应，在受过良好训练的男人中做出更精细的反应，认为这是一个适应性过程。鉴于无效的多泛素化IP发现，需要更多的研究来确定如何处理MyHC片段。此外，需要进一步的研究来确定衰老和疾病相关的肌肉萎缩如何影响这些结果，以及MyHC片段化是否是肌肉蛋白质转换率的可行替代品。
