The University of Queensland, NHMRC Centre of Clinical Research Excellence in Spinal Pain, Injury and Health, School of Health and Rehabilitation Sciences, Brisbane, Australia.
Alan Edwards Centre for Research on Pain, Faculty of Dentistry, McGill University, Montreal, Quebec, Canada.
Spine (Phila Pa 1976). 2021 Dec 1;46(23):1612-1620. doi: 10.1097/BRS.0000000000004105.
Case-controlled animal study.
The aim of this study was to investigate whether multifidus muscle fiber type distribution changes in models of interverbal disc (IVD) degeneration and whether this is resolved by physical activity (PA).
The loss of slow type I muscle fibers in the multifidus muscle in people with low back pain is contentious. Data from animal models of IVD degeneration suggest some discrepancies in human studies might be explained by the dependence of slow muscle fiber changes and their underlying mechanisms, on the time since injury and progression of IVD degeneration. It is not yet resolved what changes are apparent once the chronic phase is established. It is also not known whether muscle fiber changes can be resolved by whole body PA. This study aimed to examine slow fiber distribution in the multifidus muscle in models of IVD injury or spontaneous degeneration in animals with or without exposure to PA.
Two models of IVD degeneration were used. The first model used a genetically modified mouse (SPARC-null) that spontaneously develops IVD degeneration. The second model involved a surgically induced IVD lesion to induce degeneration. Mice in each study were allocated to housing with or without a running wheel for PA. At 12 months of age, the multifidus muscle was harvested. Slow muscle fiber distribution and the mRNA expression of genes associated with muscle fiber type transformation were examined.
The proportion and cross-sectional area of slow muscle fibers were reduced in both models of IVD degeneration compared to controls, without evidence of ongoing fiber transformation. Whole-body PA did not attenuate these alterations.
Results confirmed slow muscle fiber loss in the multifidus in the chronic phase of IVD degeneration induced spontaneously and by injury. Whole-body PA did not attenuate changes to muscle fiber distribution. More specific approaches to muscle activation might be required to achieve more complete reversal of muscle fiber changes, with potential implications for therapy in humans.Level of Evidence: N/A.
病例对照动物研究。
本研究旨在探讨椎间盘（IVD）退变模型中多裂肌纤维类型分布的变化，以及体力活动（PA）是否对此有影响。
腰痛患者多裂肌中慢型 I 型肌纤维的丧失存在争议。IVD 退变动物模型的数据表明，人类研究中的一些差异可能是由于慢肌纤维变化及其潜在机制对损伤时间和 IVD 退变进展的依赖性所致。一旦慢性阶段确立，哪些变化是明显的还没有定论。也不知道肌肉纤维的变化是否可以通过全身 PA 来解决。本研究旨在检查在有或没有暴露于 PA 的情况下，IVD 损伤或自发性退变动物模型中多裂肌中慢纤维的分布。
使用了两种 IVD 退变模型。第一种模型使用了一种自发发生 IVD 退变的基因修饰小鼠（SPARC-/-）。第二种模型涉及手术诱导的 IVD 损伤以诱导退变。每个研究中的小鼠被分配到有或没有跑步轮的环境中进行 PA。在 12 个月大时，采集多裂肌。检查慢肌纤维分布和与肌纤维类型转化相关的基因的 mRNA 表达。
与对照组相比，两种 IVD 退变模型中的慢肌纤维比例和横截面积均减少，没有证据表明存在持续的纤维转化。全身 PA 并没有减弱这些改变。
结果证实，自发性和损伤诱导的 IVD 退变慢性期多裂肌中慢肌纤维丢失。全身 PA 并不能减轻肌肉纤维分布的变化。可能需要更具体的肌肉激活方法来实现更完全的肌肉纤维变化逆转，这可能对人类治疗有影响。
N/A。
