High-intensity interval exercise increases humanin, a mitochondrial encoded peptide, in the plasma and muscle of men.
High-intensity interval exercise increases humanin, a mitochondrial encoded peptide, in the plasma and muscle of men.
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DOI：
10.1152/japplphysiol.00032.2020
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发表时间：
2020-04
影响因子：
3.3
通讯作者：
Jonathan S. T. Woodhead;R. D’Souza;C. Hedges;J. Wan;M. Berridge;D. Cameron-Smith;P. Cohen;A. Hickey;C. Mitchell;T. Merry
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文献类型：
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作者：
Jonathan S. T. Woodhead;R. D’Souza;C. Hedges;J. Wan;M. Berridge;D. Cameron-Smith;P. Cohen;A. Hickey;C. Mitchell;T. Merry
护脑素是线粒体基因组 16S 核糖体 RNA 基因 (MT-RNR2) 内编码的一种小调节肽，具有与有氧运动训练类似的细胞和代谢保护特性。在这里，我们研究了急性高强度间歇运动或短期高强度间歇训练（HIIT）是否影响骨骼肌和血浆护脑素水平。在 VO2peak 功率输出（未训练）完成 10 x 60 秒周期测力计训练之前、之后和之后 4 小时，从未经训练的年轻健康男性（n=10，24.5±3.7 岁）收集股外侧肌活检和血浆样本。在两周内完成六次 HIIT 课程（训练）后，还进行了休息和运动后采样。急性高强度运动后，肌肉和血浆中的护脑素蛋白丰度增加。 HIIT 倾向于降低 (p=0.063) 血浆绝对护脑素水平，而不影响肌肉或血浆对急性运动的反应。在血浆中观察到小护脑素样肽 6 (SHLP6) 的类似反应，但 SHLP2 没有，表明对 MT-RNR2 基因编码的肽进行选择性调节。肌肉和血浆护脑素水平之间存在微弱的正相关性，并且离体小鼠 EDL 肌肉的收缩使护脑素水平增加约 4 倍。急性运动时肌肉护脑素水平的增加与 MT-RNR2 mRNA 或护脑素 mRNA 水平（急性运动后下降）无关。总体而言，这些结果表明，护脑素是一种运动敏感的线粒体肽，肌肉中急性运动诱导的护脑素反应是非转录调节的，可能部分导致观察到的血浆浓度增加。
Humanin, a small regulatory peptide encoded within the 16S ribosomal RNA gene (MT-RNR2) of the mitochondrial genome, has cellular cyto- and metabolo-protective properties similar to that of aerobic exercise training. Here we investigated whether acute high-intensity interval exercise or short-term high-intensity interval training (HIIT) impacted skeletal muscle and plasma humanin levels. Vastus lateralis muscle biopsies and plasma samples were collected from young healthy untrained men (n=10, 24.5±3.7 y) before, immediately following, and 4 h following the completion of 10 x 60 s cycle ergometer bouts at VO2peak power output (untrained). Resting and post-exercise sampling was also performed after six HIIT sessions (trained) completed over 2 weeks. Humanin protein abundance in muscle and plasma were increased following an acute high-intensity exercise bout. HIIT trended (p=0.063) to lower absolute humanin plasma levels, without effecting the response in muscle or plasma to acute exercise. A similar response in the plasma was observed for the small humanin-like peptide 6 (SHLP6), but not SHLP2, indicating selective regulation of peptides encoded by MT-RNR2 gene. There was a weak positive correlation between muscle and plasma humanin levels, and contraction of isolated mouse EDL muscle increased humanin levels approximately 4-fold. The increase in muscle humanin levels with acute exercise was not associated with MT-RNR2 mRNA or humanin mRNA levels (which decreased following acute exercise). Overall, these results suggest that humanin is an exercise sensitive mitochondrial peptide and acute exercise-induced humanin responses in muscle are non-transcriptionally regulated and may partially contribute to the observed increase in plasma concentrations.