The Laboratory of Physiological Hygiene and Exercise Science, University of Minnesota Twin Cities, Minneapolis, Minnesota, USA; Department of Orthopedic Surgery, Mayo Clinic, Rochester, Minnesota, USA.
Laboratory of Exercise and Sports Nutrition, Department of Kinesiology, The University of Texas at San Antonio, Texas, USA.
J Nutr Biochem. 2022 Feb;100:108902. doi: 10.1016/j.jnutbio.2021.108902. Epub 2021 Nov 5.
A diet high in saturated fat leads to skeletal muscle deteriorations including insulin resistance, mitochondrial dysfunction and muscle fiber atrophy. Consumption of long-chain polyunsaturated fatty acids and exercise have shown promise in ameliorating high-fat diet (HFD)-induced oxidative stress and inflammation. However, the impact of extra virgin olive oil (EVOO) on mitochondrial homeostasis in muscle is largely unknown. This study aimed to investigate whether 12 wks of EVOO feeding alone and in conjunction with endurance training could protect against metabolic and mitochondrial dysfunction rat muscle with HFD. Female Sprague-Dawley rats were divided into 4 groups fed a control diet (C), HFD, EVOO diet, and EVOO diet with training (EVOO+T). Mitochondrial enzyme activity and protein content decreased with HFD compared to C, but were restored with EVOO and EVOO+T. EVOO+T elevated muscle cytochrome c and PGC-1α levels. HFD increased muscle proteolytic markers and protein ubiquitination, whereas these effects were not seen in EVOO and EVOO+T. HFD suppressed mitochondrial fusion protein level while increasing fission protein levels, but were restored with EVOO and EVOO+T. Mitophagy marker PINK1 content decreased with HFD, but was unchanged in EVOO and EVOO+T. EVOO+T upregulated autophagy markers, along with decreased phosphorylated/dephosphorylated FoxO3 ratio. Antioxidants enzyme levels were upregulated by EVOO and EVOO+T, and EVOO+T reduced HFD-induced lipid peroxidation. In conclusion, HFD impaired muscle oxidative capacity, promoted protein ubiquitination and mitochondrial fission, and upregulated autophagy markers. Replacement of HFD with EVOO corrected the observed adverse effects, while exercise training in conjunction with EVOO provided additional protection to the muscle.
高脂肪饮食会导致骨骼肌恶化，包括胰岛素抵抗、线粒体功能障碍和肌纤维萎缩。长链多不饱和脂肪酸的消耗和运动已被证明可以改善高脂肪饮食（HFD）引起的氧化应激和炎症。然而，特级初榨橄榄油（EVOO）对肌肉中线粒体动态平衡的影响在很大程度上尚不清楚。本研究旨在探讨单独使用 EVOO 喂养 12 周以及与耐力训练相结合是否可以预防 HFD 引起的代谢和线粒体功能障碍大鼠肌肉。将雌性 Sprague-Dawley 大鼠分为 4 组，分别喂食对照饮食（C）、HFD、EVOO 饮食和 EVOO 饮食加训练（EVOO+T）。与 C 相比，HFD 降低了肌肉中线粒体酶活性和蛋白含量，但 EVOO 和 EVOO+T 恢复了这些水平。EVOO+T 增加了肌肉细胞色素 c 和 PGC-1α 水平。HFD 增加了肌肉蛋白水解标志物和蛋白泛素化，而 EVOO 和 EVOO+T 则没有出现这种情况。HFD 抑制了线粒体融合蛋白水平，增加了分裂蛋白水平，但 EVOO 和 EVOO+T 恢复了这些水平。HFD 降低了线粒体自噬标志物 PINK1 的含量，但 EVOO 和 EVOO+T 没有改变。EVOO+T 上调了自噬标志物，同时降低了磷酸化/去磷酸化 FoxO3 的比例。抗氧化酶水平被 EVOO 和 EVOO+T 上调，EVOO+T 降低了 HFD 引起的脂质过氧化。综上所述，HFD 损害了肌肉的氧化能力，促进了蛋白泛素化和线粒体分裂，并上调了自噬标志物。用 EVOO 替代 HFD 纠正了观察到的不良反应，而 EVOO 与运动训练相结合为肌肉提供了额外的保护。
