限食8周对大鼠不同类型骨骼肌收缩功能及线粒体生物合成的影响

摘要

AIM:To investigate the influence of calorie restriction ( CR) on contractility and mitochondrial bi-osynthesis in different types of rat skeletal muscles .METHODS:CR rat model was set up by feeding 60%normal food in-take of control rat every day for 8 weeks.Soleus (SOL) and extensor digitorum longus (EDL) were isolated under anesthe-sia.The twitch tension, titanic tension and fatigue resistance of SOL and EDL in response to electrical stimulation were measured to reflect the contractile function of the muscles .The copy number ratio of mitochondrial gene cytochrome C oxi-dase subunit I ( COX I) to nuclear gene β-actin was determined to evaluate the mitochondrial biosynthesis .ATP content was measured to mirror mitochondrial function .RESULTS:Compared with control group , CR for 8 weeks significantly in-creased twitch tension and titanic tension of both SOL and EDL , but only improved fatigue resistance in SOL .Markedly in-crease in ATP content in both skeletal muscles by CR intervention was observed , especially in SOL .Although CR activated AMP-activated protein kinase (AMPK) in both 2 muscles, up-regulation of mitochondrial biosynthesis and transcription of mitochondrial regulatory genes peroxisome proliferator-activated receptor γcoactivator 1α( PGC-1α) and nuclear respirato-ry factor ( NRF) was only observed in SOL .CONCLUSION:CR for 8 weeks enhanced the contractility of both rat SOL and EDL in response to electrical stimulation , especially in SOL composed of slow-twitch fibers.The mechanisms may be related to the activation of AMPK and the promotion of mitochondrial biosynthesis in SOL .%目的：探讨限食对不同类型骨骼肌收缩功能和线粒体生物合成的影响，为阐明限食的有益作用及机制提供实验依据。方法：每天按正常大鼠摄食量的60％饲养动物以制备限食8周大鼠模型，麻醉下分离比目鱼肌和趾长伸肌，记录电刺激诱导骨骼肌单次、强直和疲劳收缩，观测线粒体基因细胞色素C氧化酶I亚基（ COX I）和核基因β－actin拷贝数的比值以反映线粒体生物合成，检测骨骼肌ATP含量以反映线粒体功能。结果：限食8周对电刺激诱导的比目鱼肌和趾长伸肌的单次和强直收缩均有增强作用，但仅提高比目鱼肌的抗疲劳作用；限食也增加两种肌肉的ATP含量，但对比目鱼肌更明显；限食虽对2种肌肉腺苷酸活化蛋白激酶（ AMPK）的磷酸化具有增加作用，但只上调比目鱼肌内线粒体生物合成及其调节基因PGC－1α和NRF的转录。结论：限食8周增强大鼠比目鱼肌和趾长伸肌对电刺激的收缩反应，尤其对富含氧化型肌纤维的比目鱼肌更明显；其机制除与限食促进这2种肌肉AMPK活化、增加ATP供应以外，还与上调比目鱼肌线粒体生物合成及其调控因子有关。