Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada.
Department of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, University of Western Ontario, London, Ontario, Canada.
Spine (Phila Pa 1976). 2021 Jul 1;46(13):E710-E718. doi: 10.1097/BRS.0000000000003882.
Basic science study of the relationship between spine pathology and the contractile ability of the surrounding muscles.
The aim of this study was to investigate single muscle fiber contractile function in a model of progressive spine mineralization (ENT1-/- mice).
Altered muscle structure and function have been associated with various spine pathologies; however, studies to date have provided limited insight into the fundamental ability of spine muscles to actively contract and generate force, and how this may change in response to spine pathology.
Experiments were performed on two groups (ENT1-/- [KO] and ENT1+/+ [WT]) of mice at 8 months of age (n = 12 mice/group). Single muscle fibers were isolated from lumbar multifidus and erector spinae, as well as tibialis anterior (a non-spine-related control) and tested to determine their active contractile characteristics.
The multifidus demonstrated decreases in specific force (type IIax fibers: 36% decrease; type IIb fibers: 29% decrease), active modulus (type IIax: 35% decrease; type IIb: 30% decrease), and unloaded shortening velocity (Vo) (type IIax: 31% decrease) in the ENT1-/- group when compared to WT controls. The erector spinae specific force was reduced in the ENT1-/- mice when compared to WT (type IIax: 29% decrease), but active modulus and Vo were unchanged. There were no differences in any of the active contractile properties of the lower limb TA muscle, validating that impairments observed in the spine muscles were specific to the underlying spine pathology and not the global loss of ENT1.
These results provide the first direct evidence of cellular level impairments in the active contractile force generating properties of spine muscles in response to chronic spine pathology.Level of Evidence: N/A.
脊柱病理学与周围肌肉收缩能力关系的基础科学研究。
本研究旨在研究进行性脊柱矿化（ENT1-/- 小鼠）模型中单个肌纤维收缩功能。
脊柱病变与肌肉结构和功能改变有关；然而，迄今为止的研究仅提供了对脊柱肌肉主动收缩和产生力的基本能力的有限了解，以及这种能力如何因脊柱病变而改变。
在 8 月龄的两组（ENT1-/- [KO]和 ENT1+/+ [WT]）小鼠中进行实验（每组 12 只小鼠）。从腰椎多裂肌和竖脊肌以及胫骨前肌（与脊柱无关的对照）中分离出单个肌纤维，并对其进行测试以确定其主动收缩特性。
与 WT 对照组相比，ENT1-/- 组的多裂肌的比力（IIax 型纤维：减少 36%；IIb 型纤维：减少 29%）、主动模量（IIax 型：减少 35%；IIb 型：减少 30%）和空载缩短速度（Vo）（IIax 型：减少 31%）降低。与 WT 相比，ENT1-/- 小鼠的竖脊肌比力降低（IIax 型：减少 29%），但主动模量和 Vo 不变。下肢 TA 肌肉的任何主动收缩特性均无差异，证实了脊柱肌肉观察到的损伤是脊柱潜在病理的特异性，而不是 ENT1 的整体缺失。
这些结果首次提供了慢性脊柱病变时脊柱肌肉主动收缩力产生特性的细胞水平损伤的直接证据。
N/A。
