School of Biomedical, Biomolecular and Chemical Sciences, University of Western Australia, Crawley, Western Australia, Australia.
Muscle Nerve. 2010 Nov;42(5):769-77. doi: 10.1002/mus.21744.
When an active muscle is stretched, the force increases due to strain of contractile and noncontractile proteins. We examined this force enhancement in rat extensor digitorum longus (EDL) and soleus muscles, which differ in their composition of these proteins, and their susceptibility to damage. Small stretches were applied at different velocities during isometric contractions from which we quantified the velocity-dependent contractile and velocity-independent noncontractile contributions to force enhancement. Whereas the contractile contribution was significantly greater in soleus than EDL, the noncontractile force enhancement was significantly greater in EDL than soleus, and increased ≈6-fold after damaging eccentric contractions. The increased contractile stiffness may be functionally beneficial in slow muscle, as resistance to lengthening is fundamental to maintaining posture. Following stretch-induced muscle damage this capacity is compromised, leading to increased strain of noncontractile proteins that may facilitate the activation of signaling pathways involved in muscle adaptation to injury.
当活跃的肌肉被拉伸时，由于收缩蛋白和非收缩蛋白的应变，力会增加。我们研究了这些蛋白质组成不同、易受损伤的大鼠伸趾长肌 (EDL) 和比目鱼肌中的这种力增强现象。在等长收缩过程中以不同速度施加小拉伸，我们从这些拉伸中量化了速度依赖性收缩和速度非依赖性非收缩对力增强的贡献。尽管比目鱼肌中的收缩贡献明显大于 EDL，但 EDL 中非收缩力增强的贡献明显大于比目鱼肌，并且在损伤性离心收缩后增加了约 6 倍。增加的收缩刚度在慢肌中可能具有功能上的益处，因为抵抗伸长是维持姿势的基础。在拉伸引起的肌肉损伤后，这种能力会受到损害，导致非收缩蛋白的应变增加，这可能有助于激活参与肌肉对损伤适应的信号通路。
