Herzog W, Longino D, Clark A
University of Calgary, 2500 University Drive N.W., Calgary, Alberta, T2N 1N4, Canada.
Langenbecks Arch Surg. 2003 Oct;388(5):305-15. doi: 10.1007/s00423-003-0402-6. Epub 2003 Sep 20.
Muscles are the primary contributors to joint loading. Loading is typically associated with the onset and progression of joint degeneration, and in turn, joint degeneration is known to affect negatively the control of muscle forces and co-ordination patterns. Nevertheless, the role of muscles in joint adaptation and degeneration has been largely ignored. Here, we review some of our research on the in vivo changes in muscular forces and joint loading in animal models of osteoarthritis and in patients with joint injury and disease. We attempt to emphasize the close dependence of muscle forces, joint loading and degeneration and, vice versa, try to point out how joint degeneration affects muscle forces and joint loading.
We measured the forces and electromyographic signals in normal and anterior cruciate ligament transected feline knees and measured (1) a consistent decrease in the knee extensor and ankle extensor muscle forces for weeks following intervention; (2) a corresponding decrease in the static and dynamic external ground reaction forces; and (3) a change in the electromyographic signals (in terms of the firing patterns of individual muscles and of the co-ordination of extensors and flexors during locomotion). We introduced results on the biosynthetic response of articular cartilage to controlled, in vivo, loading and discuss preliminary results from an experimental animal model of muscle weakness. In contrast to much of the published literature, loading, in our case, is introduced by controlled nerve stimulation and the corresponding muscular forces that load the joint in its in vivo configuration.
We found that short-term loading (30-60 min) in the cat knee produces distinct up-regulation of mRNA of specific metalloproteinases (MMPs) and some of the MMP inhibitors. In our newly developed muscle-weakness model, we confirmed that controlled Botox injections in the rabbit knee extensor muscles cause a 60-80% decrease in muscle force, and that these changes in muscle force are associated with changes in the external ground reaction forces, and most importantly, that muscle weakness seems to be associated with degeneration of the knee in the absence of joint instability or any other intervention.
From the results of our research, we conclude that muscle health and muscle rehabilitation are key components for the successful prevention of, and recovery from, joint injury and disease.
肌肉是关节负荷的主要贡献者。负荷通常与关节退变的发生和进展相关,反过来,已知关节退变会对肌肉力量控制和协调模式产生负面影响。然而,肌肉在关节适应和退变中的作用在很大程度上被忽视了。在此,我们回顾一些关于骨关节炎动物模型以及关节损伤和疾病患者体内肌肉力量和关节负荷变化的研究。我们试图强调肌肉力量、关节负荷和退变之间的紧密依赖关系,反之,指出关节退变如何影响肌肉力量和关节负荷。
我们测量了正常和前交叉韧带切断的猫膝关节的力量和肌电信号,并测量了:(1)干预后数周膝关节伸肌和踝关节伸肌力量持续下降;(2)静态和动态地面外力反作用力相应下降;(3)肌电信号的变化(就个体肌肉的放电模式以及运动过程中伸肌和屈肌的协调而言)。我们介绍了关节软骨对体内可控负荷的生物合成反应的结果,并讨论了肌肉无力实验动物模型的初步结果。与许多已发表的文献不同,在我们的研究中,负荷是通过可控的神经刺激以及在体内构型下加载关节的相应肌肉力量引入的。
我们发现猫膝关节的短期负荷(30 - 60分钟)会使特定金属蛋白酶(MMPs)及其一些抑制剂的mRNA明显上调。在我们新开发的肌肉无力模型中,我们证实对兔膝关节伸肌进行可控的肉毒杆菌毒素注射会使肌肉力量下降60 - 80%,并且这些肌肉力量的变化与地面外力反作用力的变化相关,最重要的是,在没有关节不稳定或任何其他干预的情况下,肌肉无力似乎与膝关节退变有关。
从我们的研究结果得出结论,肌肉健康和肌肉康复是成功预防关节损伤和疾病以及从关节损伤和疾病中恢复的关键组成部分。