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被动拉伸对去神经支配的趾长伸肌生长和蛋白质周转的影响。

The influence of passive stretch on the growth and protein turnover of the denervated extensor digitorum longus muscle.

作者信息

Goldspink D F

出版信息

Biochem J. 1978 Aug 15;174(2):595-602. doi: 10.1042/bj1740595.

Abstract

At 7 days after cutting the sciatic nerve, the extensor digitorum longus muscle was smaller and contained less protein than its innervated control. Correlating with these changes was the finding of elevated rates of protein degradation (measured in vitro) in the denervated tissue. However, at this time, rates of protein synthesis (measured in vitro) and nucleic acid concentrations were also higher in the denervated tissue, changes more usually associated with an active muscle rather than a disused one. These anabolic trends have, at least in part, been explained by the possible greater exposure of the denervated extensor digitorum longus to passive stretch. When immobilized under a maintained influence of stretch the denervated muscle grew to a greater extent. Although this stretch-induced growth appeared to occur predominantly through a stimulation of protein synthesis, it was opposed by smaller increases in degradative rates. Nucleic acids increased at a similar rate to the increase in muscle mass when a continuous influence of stretch was imposed on the denervated tissue. In contrast, immobilization of the denervated extensor digitorum longus in a shortened unstretched state reversed most of the stretch-induced changes; that is, the muscle became even smaller, with protein synthesis decreasing to a greater extent than breakdown after the removal of passive stretch. The present investigation suggests that stretch will promote protein synthesis and hence growth of the extensor digitorum longus even in the absence of an intact nerve supply. However, some factor(s), in addition to passive stretch, must contribute to the anabolic trends in this denervated muscle.

摘要

切断坐骨神经7天后,与受神经支配的对照肌肉相比,趾长伸肌体积变小,蛋白质含量减少。与这些变化相关的是,在失神经支配的组织中发现蛋白质降解率(体外测量)升高。然而,此时失神经支配组织中的蛋白质合成率(体外测量)和核酸浓度也较高,这些变化通常与活跃的肌肉而非废用的肌肉相关。这些合成代谢趋势至少部分可以通过失神经支配的趾长伸肌可能更多地受到被动拉伸来解释。当在持续的拉伸影响下固定时,失神经支配的肌肉生长程度更大。尽管这种拉伸诱导的生长似乎主要通过刺激蛋白质合成而发生,但它受到降解率较小增加的对抗。当对失神经支配的组织施加持续的拉伸影响时,核酸的增加速率与肌肉质量的增加速率相似。相反,将失神经支配的趾长伸肌固定在缩短的未拉伸状态会逆转大部分拉伸诱导的变化;也就是说,肌肉变得更小,在去除被动拉伸后蛋白质合成的减少程度大于分解程度。本研究表明,即使在没有完整神经供应的情况下,拉伸也会促进趾长伸肌的蛋白质合成,从而促进其生长。然而,除了被动拉伸之外,一些因素必定促成了这种失神经支配肌肉的合成代谢趋势。

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