The purpose of this study is to determine whether moderate aerobic exercise training improves high-fat diet-induced alterations in mitochondrial function and structure in the skeletal muscle. Male 4-week-old C57BL/6 mice were randomly divided into four groups: control (CON), control plus exercise (CON + EX), high-fat diet (HFD), and high-fat diet plus exercise (HFD + EX). After obesity was induced by 20 weeks of 60% HFD, treadmill exercise training was performed at 13-16 m/min, 40-50 min/day, and 6 days/week for 12 weeks. Mitochondrial structure, function, and dynamics, and mitophagy were analyzed in the skeletal muscle fibers from the red gastrocnemius. Exercise training increased mitochondrial number and area and reduced high-fat diet-induced obesity and hyperglycemia. In addition, exercise training attenuated mitochondrial dysfunction in the permeabilized myofibers, indicating that HFD-induced decrease of mitochondrial O2 respiration and Ca2+ retention capacity and increase of mitochondrial H2 O2 emission were attenuated in the HFD + EX group compared to the HFD group. Exercise also ameliorated HFD-induced imbalance of mitochondrial fusion and fission, demonstrating that HFD-induced decrease in fusion protein levels was elevated, and increase in fission protein levels was reduced in the HFD + EX groups compared with the HFD group. Moreover, dysregulation of mitophagy induced by HFD was mitigated in the HFD + EX group, indicating a decrease in PINK1 protein level. Our findings demonstrated that moderate aerobic exercise training mitigated obesity-induced insulin resistance by improving mitochondrial function, and reversed obesity-induced mitochondrial structural damage by improving mitochondrial dynamics and mitophagy, suggesting that moderate aerobic exercise training may play a therapeutic role in protecting the skeletal muscle against mitochondrial impairments and insulin resistance induced by obesity.

中文翻译：

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适度有氧运动训练改善高脂饮食诱导肥胖小鼠骨骼肌线粒体功能和动力学损伤

本研究的目的是确定适度的有氧运动训练是否能改善高脂肪饮食引起的骨骼肌线粒体功能和结构的改变。4 周龄雄性 C57BL/6 小鼠随机分为四组：对照组（CON）、对照组加运动（CON+EX）、高脂饮食（HFD）、高脂饮食加运动（HFD+EX） ）。在 20 周 60% HFD 诱导肥胖后，以 13-16 m/min、40-50 min/天和 6 天/周的速度进行跑步机运动训练，持续 12 周。在来自红色腓肠肌的骨骼肌纤维中分析了线粒体结构、功能和动力学以及线粒体自噬。运动训练增加了线粒体数量和面积，减少了高脂肪饮食引起的肥胖和高血糖。此外，运动训练减轻了透化肌纤维中的线粒体功能障碍，表明与 HFD 组相比，HFD + EX 组中 HFD 诱导的线粒体 O2 呼吸和 Ca2+ 保留能力的降低以及线粒体 H2 O2 排放的增加有所减弱。运动还改善了 HFD 诱导的线粒体融合和裂变失衡，表明 HFD 诱导的融合蛋白水平降低升高，与 HFD 组相比，HFD + EX 组中裂变蛋白水平的增加减少。此外，HFD 诱导的线粒体自噬失调在 HFD + EX 组中得到缓解，表明 PINK1 蛋白水平降低。我们的研究结果表明，适度的有氧运动训练通过改善线粒体功能来减轻肥胖引起的胰岛素抵抗，