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首页> 外文期刊>体力科学: Japanese journal of physical fitness and sports medicine >Recent development of research in exercise-induced muscle damage and plasticity of skeletal muscle
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Recent development of research in exercise-induced muscle damage and plasticity of skeletal muscle

机译:运动引起的肌肉损伤和骨骼肌可塑性的研究进展

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摘要

Skeletal muscles adapt structurally and physiologically to mechanical stimuli generated in muscle contractions, and two common consequences of such adaptation are strength gain and muscle hypertrophy, which are typical examples of skeletal muscle plasticity. Injurious physical, chemical, or biological stressors damage skeletal muscles. The severity of muscle damage varies from micro injury of a small number of muscle fibres to a disruption of a whole muscle depending on the cause of damage. Skeletal muscle fibres have a capability to regenerate, and satellite cells within the injured muscle fibres are activated, proliferate and differentiate to form myoblasts, which could fuse to form myotube in the regeneration process. Satellite cells are the source to maintain myonuclei to cytoplasmic volume ratio by adding myonuclei to the increasing area and length of muscle fibres, thus play a major role in muscle hypertrophy. It has been documented that activation of satellite cells is essential for skeletal muscle hypertrophy. Thus, it seems reasonable to assume that muscle damage increases hypertrophic responses. Several studies have reported superiority of resistance training consisting of eccentric contractions to concentric contractions for muscle hypertrophy. Since eccentric contractions, especially performed in "accustomed" exercise, result in muscle damage, one might think that muscle damage is responsible for muscle hypertrophy. However, it does not appear that muscle damage is a pre-requisite for muscle hypertrophy, although it is true that eccentric contractions are more potent stimulus for muscle hypertrophy than concentric contractions. It is important to note that protein synthesis should exceed protein degradation for a muscle to be hypertrophied, and muscle damage is the process of protein degradation. If a muscle is damaged regularly, muscle hypertrophy might not be induced. Therefore, damaging muscles does not necessarily induce muscle hypertrophy, and the benefit of eccentric contractions as stimulus for muscle hypertrophy should be considered separately from muscle damage. Muscles become less susceptible to muscle damage, when, the same or similar exercise is repeated, which is another example of plasticity. Because of this adaptation, it does not appear that muscle fibres are extensively damaged even in strenuous exercise training. The presentation will update the information about exercise-induced muscle damage, and discuss how muscle damage is associated with muscle plasticity.
机译:骨骼肌在结构上和生理上都适应肌肉收缩中产生的机械刺激,这种适应的两个常见后果是力量增加和肌肉肥大,这是骨骼肌可塑性的典型例子。有害的物理,化学或生物应激源会损害骨骼肌。肌肉损伤的严重程度从少量肌肉纤维的微损伤到整个肌肉的破坏,视损伤原因而定。骨骼肌纤维具有再生能力,受伤的肌纤维内的卫星细胞被激活,增殖和分化以形成成肌细胞,在再生过程中融合成肌管。卫星细胞是通过增加肌肉纤维的面积和长度来增加肌核来维持肌核与细胞质体积比的来源,因此在肌肉肥大中起主要作用。已有文献证明,卫星细胞的激活对于骨骼肌肥大至关重要。因此,假设肌肉损伤会增加肥大性反应似乎是合理的。几项研究报告了针对肌肉肥大的阻力训练由偏心收缩到同心收缩的优势。由于离心收缩,特别是在“习惯”运动中进行,会导致肌肉损伤,因此人们可能认为肌肉损伤是造成肌肉肥大的原因。然而,尽管确实存在偏心收缩比同心收缩对肌肉肥大更有效的刺激,但似乎肌肉损伤不是肌肉肥大的先决条件。重要的是要注意,蛋白质合成应超过蛋白质降解才能使肌肉肥大,而肌肉损伤是蛋白质降解的过程。如果肌肉定期受到损伤,则可能不会诱发肌肉肥大。因此,损害肌肉并不一定会诱发肌肉肥大,因此应该将离心收缩作为刺激肌肉肥大的好处与肌肉损害分开考虑。当重复相同或相似的运动时,肌肉变得不太容易受到肌肉损伤,这是可塑性的另一个例子。由于这种适应性,即使在剧烈的运动训练中,似乎也不会严重破坏肌肉纤维。该演讲将更新有关运动引起的肌肉损伤的信息,并讨论肌肉损伤如何与肌肉可塑性相关联。

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