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Does skeletal muscle fiber branching play a role in the inability of old EDL dystrophic muscle to resist large passive stretches?

机译:骨骼肌纤维分支在老年EDL营养不良性肌肉无力抵抗较大的被动拉伸中是否起作用?

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Hakim et al. (3) examined the passive mechanical properties of fast-twitch extensor digitorum longus (EDL) muscles from young and old mdx dystrophic mice. They elegantly showed that by increasing passive strain on the dystrophic muscle from 110% of optimal length (Lo) to 160% of Lo, the muscle physically ruptured in a manner that got progressively worse with age. At the oldest age points tested, 14 and 20 mo, the dystrophic muscles pulled apart. Importantly, in age matched dystrophin positive controls, this pulling apart of the muscle did not occur. The authors (3) propose that one reason for this dramatic tearing of the dystrophic muscle with age is due to increased fibrosis and muscle stiffness. Undoubtedly, increasing stiffness with age would play a role in dystrophic damage. However, I suggest that the widely reported age-related increase in the number of branched skeletal muscle fibers present within the dystrophic muscle will also make a significant contribution (1,2,4-6).
机译:Hakim等。 (3)研究了年轻和年老的mdx营养不良小鼠的快速抽搐指长肌(EDL)肌肉的被动力学性能。他们优雅地表明,通过将营养不良性肌肉的被动张力从最佳长度(Lo)的110%增加到Lo的160%,肌肉会随着年龄的增长而逐渐破裂。在测试的最高年龄点(14和20个月),营养不良的肌肉会分开。重要的是,在年龄匹配的肌营养不良蛋白阳性对照中,这种拉开肌肉没有发生。作者(3)提出,随着年龄的增长,营养不良性肌肉急剧撕裂的原因之一是由于纤维化和肌肉僵硬的增加。毫无疑问,随着年龄增长而增加的僵硬度将在营养不良性损害中起作用。但是,我建议营养不良性肌肉中存在的与年龄相关的广为报道的分支骨骼肌纤维数量的增加也将做出重大贡献(1、2、4-6)。

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