Maintenance of contractile force and increased fatigue resistance in slow‐twitch skeletal muscle of long‐term high‐fat‐fed mice
Maintenance of contractile force and increased fatigue resistance in slow‐twitch skeletal muscle of long‐term high‐fat‐fed mice
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长期高脂喂养小鼠慢肌骨骼肌的收缩力维持和抗疲劳能力增强
DOI：
10.1096/fasebj.31.1_supplement.1081.2
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发表时间：
2017
期刊：
影响因子：
--
通讯作者：
H. Watada
中科院分区：
文献类型：
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作者：
Hiroaki Eshima;Y. Tamura;Saori Kakehi;R. Kawamori;H. Watada
高脂肪饮食（HFD）已被证明可以显着提高肌肉线粒体酶活性和耐力表现。我们最近证明，长期高脂饮食会损害快肌纤维的收缩力并转变为氧化纤维成分。然而，长期HFD对慢肌优势肌的肌肉功能（即收缩力和抗疲劳能力）的影响尚未阐明。雄性 C57BL/6J 小鼠的离体慢肌比目鱼肌 (SOL) 被喂食 HFD（60% kcal：脂肪）12 周。在静息条件下和重复破伤风引起的疲劳期间测量肌肉收缩力（100 Hz，50 次收缩，2 s 间隔）。 HFD 和对照之间的肌肉抽搐和强直力没有明显差异，而 HFD 的整个末期疲劳抵抗力均有所提高（初始相对力；CONT，26.6±1.6 vs HFD，37.6±1.6%，P < 0.05）。与对照组相比，即使在 HFD 中，SOL 肌肉重量和横截面积也没有变化（P>0.05）。 HFD 喂养小鼠的 SOL 肌肉显示出琥珀酸脱氢酶活性增加，以及线粒体生物发生触发因素（PGC-1α 和 COX IV）的表达增加。因此，与对照相比，HFD 中的线粒体融合指数（Mfn2 与 Drp1 比率）显着增加（+ 76±4% 与对照相比，P < 0.05）。这些发现表明，长期高脂饮食会导致慢肌优势肌纤维的肌肉抗疲劳能力提高。后者可能与线粒体数量和/或质量升高有关。
High-fat diet (HFD) has been shown to significantly raise muscle mitochondrial enzyme activity and endurance performance. We recently demonstrated that long-term HFD impairs contractile force and shift to oxidative fiber composition in fast-twitch muscle fibers. However, the effects of long-term HFD on the muscle function (ie, contractile force and fatigue resistance) of slow-twitch dominant muscles have not yet been elucidated. Isolated slow-twitch soleus (SOL) from male C57BL/6J mice was fed a HFD (60% kcal: fat) for 12 weeks. Muscle contractile force were measured under resting conditions and during fatigue induced by repeated tetanus (100 Hz, 50 contraction, 2 s interval). No differences in muscle twitch and tetanic force were evident between HFD and control, whereas fatigue resistance elevated for the entire end-stage period in HFD (relative force for the initial; CONT, 26.6±1.6 vs HFD, 37.6±1.6%, P< 0.05). SOL muscle weights and cross-sectional area were unchanged even in HFD compared with the control (P> 0.05). SOL muscles of HFD fed mice showed increased activities of succinate dehydrogenase, and expression of triggers of mitochondrial biogenesis (PGC-1α and COX IV). Accordingly, mitochondrial fusion index (Mfn2-to-Drp1 ratio) was significantly increased in HFD compared to control (+ 76±4% vs control, P< 0.05). These findings indicate that long-term HFD induces elevated muscle fatigue resistance in slow-twitch dominant muscle fiber. The latter may be associated with elevated quantity and/or quality of mitochondria.