Kwon Insu, Kim Kyoung Soo, Lee Youngil
Physical Activity & Performance Institute, Konkuk University, Seoul, Republic of Korea.
Department of Clinical Pharmacology and Therapeutics, College of Medicine, Kyung Hee University, Seoul, Republic of Korea.
Phys Act Nutr. 2024 Jun;28(2):23-34. doi: 10.20463/pan.2024.0013. Epub 2024 Jun 30.
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.
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.
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.
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.
耐力运动可诱导肌纤维类型转变和自噬;然而,自噬在肌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)和趾长伸肌(EDL)中肌纤维类型转变与自噬之间的关系,这两块肌肉在代谢上有所不同。
将雄性C57BL/6J小鼠随机分为久坐对照组(CON)和运动组(EXE)。在适应跑步机跑步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。在最后一次运动后90分钟处死所有小鼠,并迅速解剖目标组织。组织的右侧用于蛋白质免疫印迹分析,而左侧进行免疫组织化学分析。
耐力运动导致SOL肌肉出现肌纤维类型转变(从IIa型转变为I型)和自噬(LC3-II增加)。然而,SOL和EDL肌肉中的肌纤维类型转变与自噬并无相关性。有趣的是,与经典的自噬信号通路不同,我们的研究表明运动诱导的自噬伴随着合成代谢增强(p-AKTSer473/AKT和p-mTOR/mTORSer2448比值增加)和分解代谢抑制(p-AMPKThr172/AMPK比值降低)状态。
我们的研究结果表明,慢性耐力运动诱导的肌纤维类型转变和自噬以肌肉特异性方式发生(例如在SOL中)。更重要的是,我们的研究表明耐力训练诱导的SOL肌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。