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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.

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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