首页> 外文期刊>Journal of bodywork and movement therapies >Strain hardening of fascia: static stretching of dense fibrous connective tissues can induce a temporary stiffness increase accompanied by enhanced matrix hydration.
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Strain hardening of fascia: static stretching of dense fibrous connective tissues can induce a temporary stiffness increase accompanied by enhanced matrix hydration.

机译:筋膜的应变硬化:致密的纤维结缔组织的静态拉伸会导致暂时的硬度增加,并伴随基质水化增强。

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This study examined a potential cellular basis for strain hardening of fascial tissues: an increase in stiffness induced by stretch and subsequent rest. Mice lumbodorsal fascia were isometrically stretched for 15 min followed by 30 min rest (n=16). An increase in stiffness was observed in the majority of samples, including the nonviable control samples. Investigations with porcine lumbar fascia explored hydration changes as an explanation (n=24). Subject to similar loading procedures, tissues showed decreases in fluid content immediately post-stretch and increases during rest phases. When allowed sufficient resting time, a super-compensation phenomenon was observed, characterised by matrix hydration higher than initial levels and increases in tissue stiffness. Therefore, fascial strain hardening does not seem to rely on cellular contraction, but rather on this super-compensation. Given a comparable occurrence of this behaviour in vivo, clinical application of routines for injury prevention merit exploration.
机译:这项研究检查了筋膜组织应变硬化的潜在细胞基础:拉伸和随后的休息引起的僵硬度增加。等距拉伸小鼠腰背部筋膜15分钟,然后休息30分钟(n = 16)。在大多数样品(包括不可行的对照样品)中观察到刚度增加。猪腰椎筋膜的调查探讨了水化变化作为解释(n = 24)。遵循类似的加载程序,组织在拉伸后立即显示出液体含量减少,而在休息阶段则显示增加。当允许足够的休息时间时,观察到超补偿现象,其特征在于基质水合作用高于初始水平并增加了组织刚度。因此,筋膜应变硬化似乎并不依赖于细胞的收缩,而是依赖于这种超补偿。鉴于这种行为在体内的发生率相当,预防损伤的常规临床应用值得探索。

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