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核糖体生物发生适应在抗阻训练诱导的人体骨骼肌肥大中的作用。

Ribosome biogenesis adaptation in resistance training-induced human skeletal muscle hypertrophy.

机构信息

Liggins Institute, University of Auckland, Auckland, New Zealand;

Department of Physiology, University of Melbourne, Melbourne, Victoria, Australia; and.

出版信息

Am J Physiol Endocrinol Metab. 2015 Jul 1;309(1):E72-83. doi: 10.1152/ajpendo.00050.2015. Epub 2015 May 12.

DOI:10.1152/ajpendo.00050.2015
PMID:25968575
Abstract

Resistance training (RT) has the capacity to increase skeletal muscle mass, which is due in part to transient increases in the rate of muscle protein synthesis during postexercise recovery. The role of ribosome biogenesis in supporting the increased muscle protein synthetic demands is not known. This study examined the effect of both a single acute bout of resistance exercise (RE) and a chronic RT program on the muscle ribosome biogenesis response. Fourteen healthy young men performed a single bout of RE both before and after 8 wk of chronic RT. Muscle cross-sectional area was increased by 6 ± 4.5% in response to 8 wk of RT. Acute RE-induced activation of the ERK and mTOR pathways were similar before and after RT, as assessed by phosphorylation of ERK, MNK1, p70S6K, and S6 ribosomal protein 1 h postexercise. Phosphorylation of TIF-IA was also similarly elevated following both RE sessions. Cyclin D1 protein levels, which appeared to be regulated at the translational rather than transcriptional level, were acutely increased after RE. UBF was the only protein found to be highly phosphorylated at rest after 8 wk of training. Also, muscle levels of the rRNAs, including the precursor 45S and the mature transcripts (28S, 18S, and 5.8S), were increased in response to RT. We propose that ribosome biogenesis is an important yet overlooked event in RE-induced muscle hypertrophy that warrants further investigation.

摘要

抗阻训练(RT)有增加骨骼肌质量的能力,这部分归因于运动后恢复过程中肌肉蛋白合成率的短暂增加。核糖体生物发生在支持增加的肌肉蛋白合成需求中的作用尚不清楚。本研究检查了单次急性抗阻运动(RE)和慢性 RT 方案对肌肉核糖体生物发生反应的影响。14 名健康年轻男性在进行 8 周慢性 RT 前后均进行了一次 RE。肌肉横截面积增加了 6±4.5%,以响应 8 周的 RT。ERK 和 mTOR 途径的急性 RE 诱导激活在 RT 前后相似,通过 ERK、MNK1、p70S6K 和 S6 核糖体蛋白的磷酸化在运动后 1 小时进行评估。在两次 RE 后,TIF-IA 的磷酸化也明显升高。细胞周期蛋白 D1 蛋白水平似乎在转录水平而非翻译水平受到调节,在 RE 后急性增加。UBF 是在训练 8 周后休息时唯一发现高度磷酸化的蛋白质。此外,核糖体 RNA 的肌肉水平增加,包括前体 45S 和成熟转录物(28S、18S 和 5.8S),以响应 RT。我们提出核糖体生物发生是 RE 诱导肌肉肥大中的一个重要但被忽视的事件,值得进一步研究。

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