Schleip Robert, Duerselen Lutz, Vleeming Andry, Naylor Ian L, Lehmann-Horn Frank, Zorn Adjo, Jaeger Heike, Klingler Werner
Fascia Research Group, Division of Neurophysiology, Ulm University, Albert-Einstein-Allee 11, 89081 Ulm, Germany.
J Bodyw Mov Ther. 2012 Jan;16(1):94-100. doi: 10.1016/j.jbmt.2011.09.003. Epub 2011 Dec 5.
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.
拉伸及随后的休息所诱导的刚度增加。将小鼠腰背部筋膜等长拉伸15分钟，随后休息30分钟（n = 16）。在大多数样本中观察到刚度增加，包括无活力的对照样本。对猪腰部筋膜进行的研究探讨了水化变化作为一种解释（n = 24）。在经历相似加载程序时，组织在拉伸后即刻显示出液体含量减少，而在休息阶段增加。当给予足够的休息时间时，观察到一种超补偿现象，其特征为基质水化高于初始水平且组织刚度增加。因此，筋膜应变硬化似乎并不依赖于细胞收缩，而是依赖于这种超补偿。鉴于这种行为在体内有类似发生情况，预防损伤常规方法的临床应用值得探索。
