Tsai Liang-Ching, Wu Yi-Ning, Liu Shu Q, Zhang Li-Qun
Department of Physical Therapy, Georgia State University, Atlanta, GA, United States.
Department of Physical Therapy and Kinesiology, University of Massachusetts Lowell, Lowell, MA, United States.
Front Physiol. 2020 Dec 17;11:581846. doi: 10.3389/fphys.2020.581846. eCollection 2020.
While abnormal muscle tone has been observed in people with stroke, how these changes in muscle tension affect sarcomere morphology remains unclear. The purpose of this study was to examine time-course changes in passive muscle fiber tension and sarcomeric adaptation to these changes post-ischemic stroke in a mouse model by using a novel force microscope. Twenty-one mice were evenly divided into three groups based on the time point of testing: 3 days (D3), 10 days (D10), and 20 days (D20) following right middle cerebral artery ligation. At each testing time, the muscle length, width, and estimated volume of the isolated soleus muscle were recorded, subsequently followed by muscle tension and sarcomere length measurement. The mass of the soleus muscle was measured at the end of testing to calculate muscle density. Two-way ANOVA with repeated measures was used to examine the differences in each of the dependent variable among the three time-point groups and between the two legs. The passive muscle stress of the impaired limbs in the D3 group (27.65 ± 8.37 kPa) was significantly lower than the less involved limbs (42.03 ± 18.61 kPa; = 0.05) and the impaired limbs of the D10 (48.92 ± 14.73; = 0.03) and D20 (53.28 ± 20.54 kPa; = 0.01) groups. The soleus muscle density of the impaired limbs in the D3 group (0.69 ± 0.12 g/cm) was significantly lower than the less involved limbs (0.80 ± 0.09 g/cm; = 0.04) and the impaired limbs of the D10 (0.87 ± 0.12 g/cm; = 0.02) and D20 (1.00 ± 0.14 g/cm; < 0.01) groups. The D3 group had a shorter sarcomere length (2.55 ± 0.26 μm) than the D10 (2.83 ± 0.20 μm; = 0.03) and D20 group (2.81 ± 0.15 μm; = 0.04). These results suggest that, while ischemic stroke may cause considerable changes in muscle tension and stress, sarcomere additions under increased mechanical loadings may be absent or disrupted post-stroke, which may contribute to muscle spasticity and/or joint contracture commonly observed in patients following stroke.
虽然在中风患者中观察到了异常肌张力，但这些肌肉张力变化如何影响肌节形态仍不清楚。本研究的目的是通过使用一种新型力显微镜，在小鼠模型中研究缺血性中风后被动肌纤维张力的时间进程变化以及肌节对这些变化的适应性。根据测试时间点，将21只小鼠平均分为三组：右侧大脑中动脉结扎后3天（D3）、10天（D10）和20天（D20）。在每个测试时间，记录分离的比目鱼肌的肌肉长度、宽度和估计体积，随后进行肌肉张力和肌节长度测量。在测试结束时测量比目鱼肌的质量以计算肌肉密度。使用重复测量的双向方差分析来检验三个时间点组之间以及两条腿之间每个因变量的差异。D3组受损肢体的被动肌肉应力（27.65±8.37 kPa）显著低于受累较轻的肢体（42.03±18.61 kPa；P = 0.05）以及D10组（48.92±14.73；P = 0.03）和D20组（53.28±20.54 kPa；P = 0.01）的受损肢体。D3组受损肢体的比目鱼肌密度（0.69±0.12 g/cm）显著低于受累较轻的肢体（0.80±0.09 g/cm；P = 0.04）以及D10组（0.87±0.12 g/cm；P = 0.02）和D20组（1.00±0.14 g/cm；P < 0.01）的受损肢体。D3组的肌节长度（2.55±0.26μm）比D10组（2.83±0.20μm；P = 0.03）和D20组（2.81±0.15μm；P = 0.04）短。这些结果表明，虽然缺血性中风可能会导致肌肉张力和应力发生相当大的变化，但中风后增加机械负荷下的肌节增加可能不存在或受到破坏，这可能导致中风患者中常见的肌肉痉挛和/或关节挛缩。
