The study was aimed at investigating the mechanisms and structures which determine mechanical properties of skeletal muscles under gravitational unloading and plantar mechanical stimulation (PMS). We hypothesized that PMS would increase NO production and prevent an unloading-induced reduction in skeletal muscle passive stiffness. Wistar rats were hindlimb suspended and subjected to a daily PMS and one group of stimulated animals was also treated with nitric oxide synthase (NOS) inhibitor (L-NAME). Animals received mechanical stimulation of the feet for 4 h a day throughout 7-day hindlimb suspension (HS) according to a scheme that mimics the normal walking of the animal. Seven-day HS led to a significant reduction in soleus muscle weight by 25%. However, PMS did not prevent the atrophic effect induced by HS. Gravitational unloading led to a significant decrease in maximum isometric force and passive stiffness by 38% and 31%, respectively. The use of PMS prevented a decrease in the maximum isometric strength of the soleus muscle. At the same time, the passive stiffness of the soleus in the PMS group significantly exceeded the control values by 40%. L-NAME (NOS inhibitor) administration attenuated the effect of PMS on passive stiffness and maximum force of the soleus muscle. The content of the studied cytoskeletal proteins (α-actinin-2, α-actinin-3, desmin, titin, nebulin) decreased after 7-day HS, but this decrease was successfully prevented by PMS in a NOS-dependent manner. We also observed significant decreases in mRNA expression levels of α-actinin-2, desmin, and titin after HS, which was prevented by PMS. The study also revealed a significant NOS-dependent effect of PMS on the content of collagen-1a, but not collagen-3a. Thus, PMS during mechanical unloading is able to maintain soleus muscle passive tension and force as well as mRNA transcription and protein contents of cytoskeletal proteins in a NOS-dependent manner.

中文翻译：

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足底机械刺激对大鼠比目鱼肌后肢悬吊力学特性和细胞骨架蛋白的 NOS 依赖性影响

该研究旨在研究在重力卸载和足底机械刺激 (PMS) 下决定骨骼肌机械特性的机制和结构。我们假设 PMS 会增加 NO 的产生并防止卸载引起的骨骼肌被动僵硬度降低。Wistar 大鼠后肢悬吊并进行每日 PMS，一组受刺激的动物也用一氧化氮合酶 (NOS) 抑制剂 (L-NAME) 治疗。根据模拟动物正常行走的方案，动物在整个 7 天后肢悬吊 (HS) 期间接受足部机械刺激 4 小时。7 天 HS 导致比目鱼肌重量显着减少 25%。然而，PMS 并不能阻止 HS 引起的萎缩效应。重力卸载导致最大等长力和被动刚度分别显着降低 38% 和 31%。PMS 的使用防止了比目鱼肌最大等长肌力的降低。同时，PMS组比目鱼肌被动刚度明显超过对照值40%。L-NAME（NOS 抑制剂）给药减弱了 PMS 对比目鱼肌被动僵硬和最大力量的影响。研究的细胞骨架蛋白（α-actinin-2、α-actinin-3、desmin、titin、nebulin）的含量在 HS 7 天后下降，但 PMS 以 NOS 依赖性方式成功阻止了这种下降。我们还观察到 HS 后 α-actinin-2、desmin 和titin 的 mRNA 表达水平显着降低，这被 PMS 阻止。该研究还揭示了 PMS 对胶原蛋白 1a 的含量有显着的 NOS 依赖性影响，但对胶原蛋白 3a 的含量没有影响。因此，机械卸载期间的 PMS 能够以 NOS 依赖性方式维持比目鱼肌被动张力和力以及细胞骨架蛋白的 mRNA 转录和蛋白质含量。