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肌生成抑制素基因敲除小鼠的耐力运动训练。

Endurance exercise training in myostatin null mice.

机构信息

Genetics of Development and Disease Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.

出版信息

Muscle Nerve. 2010 Sep;42(3):355-62. doi: 10.1002/mus.21688.

DOI:10.1002/mus.21688
PMID:20544938
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2976492/
Abstract

The growth factor myostatin (Mstn) is a negative regulator of skeletal muscle mass. Mstn(-/-) muscles are hypertrophied, stronger, and more glycolytic than Mstn(+/+) muscles, suggesting that they might not perform endurance exercise as well as Mstn(+/+) mice. Indeed, it has previously been shown that treadmill exercise training reduces triceps weight in Mstn(-/-) mice. To analyze the response of Mstn(-/-) muscle to endurance exercise in detail, we carried out endurance training over 4 weeks to examine muscle mass, histology, and oxidative enzyme activity. We found that muscle mass was reduced with training in several muscles from both genotypes, with no evidence of muscle damage. Citrate synthase activity was increased with training in control and mutant mice. Non-trained Mstn(-/-) mice did, however, have lower maximal exercise capacity compared with Mstn(+/+) mice. These results show that Mstn(-/-) muscle retains the metabolic plasticity necessary to adapt normally to endurance training.

摘要

生长因子肌肉生长抑制素 (Mstn) 是骨骼肌质量的负调节剂。Mstn(-/-)肌肉比 Mstn(+/+)肌肉肥大、更强壮、更具糖酵解特性,这表明它们可能不如 Mstn(+/+)小鼠适合进行耐力运动。事实上,之前已经表明,跑步机运动训练会降低 Mstn(-/-)小鼠的三头肌重量。为了详细分析 Mstn(-/-)肌肉对耐力运动的反应,我们进行了 4 周的耐力训练,以检查肌肉质量、组织学和氧化酶活性。我们发现,两种基因型的几种肌肉的肌肉质量都随着训练而减少,没有肌肉损伤的证据。柠檬酸合酶活性在对照和突变小鼠中随训练而增加。然而,未经训练的 Mstn(-/-)小鼠的最大运动能力确实低于 Mstn(+/+)小鼠。这些结果表明,Mstn(-/-)肌肉保留了适应耐力训练所需的代谢可塑性。

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Endurance exercise training in myostatin null mice.肌生成抑制素基因敲除小鼠的耐力运动训练。
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本文引用的文献

1
Myostatin inhibition enhances the effects of exercise on performance and metabolic outcomes in aged mice.肌生成抑制蛋白抑制增强了运动对老年小鼠运动能力和代谢结果的影响。
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Muscle hypertrophy driven by myostatin blockade does not require stem/precursor-cell activity.由肌肉生长抑制素阻断驱动的肌肉肥大并不需要干细胞/前体细胞的活性。
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Redundancy of myostatin and growth/differentiation factor 11 function.肌生成抑制蛋白与生长/分化因子11功能的冗余性。
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Myostatin inhibition in muscle, but not adipose tissue, decreases fat mass and improves insulin sensitivity.肌肉而非脂肪组织中的肌生成抑制素抑制作用可减少脂肪量并改善胰岛素敏感性。
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A soluble activin type IIB receptor improves function in a mouse model of amyotrophic lateral sclerosis.可溶性激活素IIB型受体可改善肌萎缩侧索硬化小鼠模型的功能。
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A phase I/IItrial of MYO-029 in adult subjects with muscular dystrophy.一项针对成年肌肉萎缩症患者的MYO-029 I/II期试验。
Ann Neurol. 2008 May;63(5):561-71. doi: 10.1002/ana.21338.
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Long-term enhancement of skeletal muscle mass and strength by single gene administration of myostatin inhibitors.通过单基因施用肌肉生长抑制素抑制剂长期增强骨骼肌质量和力量。
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