耐力运动训练诱导的肌肉纤维类型转变与小鼠慢速和快速肌骨骼肌自噬之间的关系

Physical activity and nutrition Pub Date : 2024-06-01 Epub Date: 2024-06-30 DOI:10.20463/pan.2024.0013
Insu Kwon, Kyoung Soo Kim, Youngil Lee
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引用次数: 0

摘要

目的:耐力锻炼可诱导肌肉纤维类型转变和自噬;然而,自噬在肌肉纤维类型转变中的潜在作用仍不清楚。本研究探讨了比目鱼肌(SOL)和伸肌(EDL)肌肉纤维类型转变与自噬之间的关系:雄性 C57BL/6J 小鼠被随机分配到静坐对照组(CON)和运动组(EXE)。适应跑步机跑步 1 周后,EXE 组小鼠以 12-15 米/分钟的速度跑步,每天 60 分钟,每周 5 天,持续 6 周。所有小鼠在最后一次运动后 90 分钟处死,并迅速解剖目标组织。右侧组织用于 Western 印迹分析,左侧组织用于免疫组化分析:结果:耐力锻炼导致 SOL 肌肉的肌纤维类型转变(从 IIa 型转变为 I 型)和自噬(LC3-II 增加)。然而,在 SOL 和 EDL 肌肉中,肌肉纤维类型转换和自噬并不相关。有趣的是,与典型的自噬信号通路相反,我们的研究表明,运动诱导的自噬与增强的合成代谢(p-AKTSer473/AKT 和 p-mTOR/mTORSer2448 比率增加)和抑制的分解代谢(p-AMPKThr172/AMPK 比率降低)状态一致:我们的研究结果表明,慢性耐力运动诱导的肌肉纤维类型转变和自噬是以肌肉特异性的方式发生的(例如,SOL)。更重要的是,我们的研究表明,耐力训练诱导的 SOL 肌肉纤维类型转变可能是由 AMPK 和 AKT/mTOR 信号通路而非自噬引起的代谢调节的基础。
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Relationships between endurance exercise training-induced muscle fiber-type shifting and autophagy in slow- and fast-twitch skeletal muscles of mice.

Purpose: Endurance exercise induces muscle fiber-type shifting and autophagy; however, the potential role of autophagy in muscle fiber-type transformation remains unclear. This study examined the relationship between muscle fiber-type shifting and autophagy in the soleus (SOL) and extensor digitorum longus (EDL) muscles, which are metabolically discrete muscles.

Methods: Male C57BL/6J mice were randomly assigned to sedentary control (CON) and exercise (EXE) groups. After 1 week of acclimation to treadmill running, the mice in the EXE group ran at 12-15 m/min, 60 min/day, 5 days/week for 6 weeks. All mice were sacrificed 90 min after the last exercise session, and the targeted tissues were rapidly dissected. The right side of the tissues was used for western blot analysis, whereas the left side was subjected to immunohistochemical analysis.

Results: Endurance exercise resulted in muscle fiber-type shifting (from type IIa to type I) and autophagy (an increase in LC3-II) in the SOL muscle. However, muscle fiber-type transformation and autophagy were not correlated in the SOL and EDL muscles. Interestingly, in contrast to the canonical autophagy signaling pathways, our study showed that exercise-induced autophagy concurs with enhanced anabolic (increased p-AKTSer473/AKT and p-mTOR/mTORSer2448 ratios) and suppressed catabolic (reduced p-AMPKThr172/AMPK ratio) states.

Conclusion: Our findings demonstrate that chronic endurance exercise-induced muscle fiber-type transformation and autophagy occur in a muscle-specific manner (e.g., SOL). More importantly, our study suggests that endurance training-induced SOL muscle fiber-type transition may underlie metabolic modulations caused by the AMPK and AKT/mTOR signaling pathways rather than autophagy.

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