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肌外肌筋膜负荷导致沿肌纤维方向非均匀应变分布的机制原理:有限元建模

Principles of the Mechanism for Epimuscular Myofascial Loads Leading to Non-uniform Strain Distributions Along Muscle Fiber Direction: Finite Element Modeling.

作者信息

Pamuk Uluç, Cankaya Alican Onur, Yucesoy Can A

机构信息

Biomechanica Laboratory, Institute of Biomedical Engineering, Boğaziçi University, Istanbul, Turkey.

出版信息

Front Physiol. 2020 Jul 3;11:789. doi: 10.3389/fphys.2020.00789. eCollection 2020.

DOI:10.3389/fphys.2020.00789
PMID:32714211
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7351515/
Abstract

Sarcomere lengths and their changes are key determinants of muscle active force production. Recent studies indicate inhomogeneity of sarcomere lengths within the muscle. Studies utilizing magnetic resonance imaging (MRI) analyses for quantifying local muscle tissue strains and diffusion tensor imaging (DTI) analyses allowing for determination of their components along muscle fascicles show that those length changes can be non-uniform. Specifically, two questions arise regarding the muscle's length change heterogeneities along the muscle fiber direction: (1) How can a passively lengthened muscle show shortened regions? (2) How can an isometric contracting muscle show lengthened parts? Using finite element modeling and studying principles of the mechanism of strain heterogeneity along the muscle fiber direction, the aim was to test the following hypothesis: epimuscular myofascial loads can lead locally to strains opposing those elsewhere within the muscle that are determined by the globally imposed conditions. The geometry of the model was defined by the contour of a longitudinal slice of the rat extensor digitorum longus (EDL) muscle belly. Three models were studied: (1) isolated muscle (muscle modeled fully isolated from its surroundings) and models aiming at representing the principles of a muscle in its context including (2) extramuscularly connected muscle (muscle's connections to non-muscular structures are modeled exclusively) and (3) epimuscularly connected muscle (additionally muscle's connections to neighboring muscle are modeled). Three cases were studied: passive isometric muscle with imposed relative position change (Case I), passive lengthened muscle (Case II), and active isometric muscle with imposed relative position change (Case III). The findings indicated non-uniform strains for all models except for zero strain in model (1) in Case I, but models (2) and (3) also showed strains opposing the imposed effect. Case I: model (3) showed shortened and lengthened sections (up to 35.3%), caused exclusively by imposed relative position change. Case II: models (2) and (3) showed shortened sections (up to 12.7 and 19.5%, respectively) in addition to lengthened sections. Case III: models (2) and (3) showed lengthened sections (up to 5 and 23.4%, respectively) in addition to shortened sections. These effects get more pronounced with stiffer epimuscular connections. Assessments of forces exerted on the muscle by the epimuscular connections showed that such strain heterogeneities are ascribed to epimuscular myofascial loads determined by muscle relative position changes.

摘要

肌节长度及其变化是肌肉主动力产生的关键决定因素。最近的研究表明肌肉内肌节长度存在不均匀性。利用磁共振成像(MRI)分析来量化局部肌肉组织应变以及利用扩散张量成像(DTI)分析来确定其沿肌束的组成部分的研究表明,这些长度变化可能是不均匀的。具体而言,关于肌肉沿肌纤维方向的长度变化异质性出现了两个问题:(1)被动拉长的肌肉如何会出现缩短区域?(2)等长收缩的肌肉如何会出现拉长部分?通过有限元建模并研究沿肌纤维方向应变异质性机制的原理,目的是检验以下假设:肌外肌筋膜负荷可局部导致与肌肉其他部位由整体施加条件所决定的应变相反的应变。模型的几何形状由大鼠趾长伸肌(EDL)肌腹纵向切片的轮廓定义。研究了三种模型:(1)孤立肌肉(将肌肉建模为完全与其周围环境隔离)以及旨在表示处于其环境中的肌肉原理的模型,包括(2)肌外连接肌肉(仅对肌肉与非肌肉结构的连接进行建模)和(3)肌外膜连接肌肉(此外还对肌肉与相邻肌肉的连接进行建模)。研究了三种情况:施加相对位置变化的被动等长肌肉(情况I)、被动拉长肌肉(情况II)以及施加相对位置变化的主动等长肌肉(情况III)。研究结果表明,除情况I中模型(1)的应变为零外,所有模型的应变都是不均匀的,但模型(2)和(3)也显示出与施加效应相反的应变。情况I:模型(3)显示出缩短和拉长的部分(高达35.3%),这完全是由施加的相对位置变化引起的。情况II:模型(2)和(3)除了有拉长部分外,还显示出缩短部分(分别高达12.7%和19.5%)。情况III:模型(2)和(3)除了有缩短部分外,还显示出拉长部分(分别高达5%和23.4%)。随着肌外膜连接更僵硬,这些效应会更加明显。对肌外膜连接施加在肌肉上的力的评估表明,这种应变异质性归因于由肌肉相对位置变化所决定的肌外肌筋膜负荷。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/577f/7351515/4837ae64a311/fphys-11-00789-g006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/577f/7351515/7084d671bec5/fphys-11-00789-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/577f/7351515/85ff864c3841/fphys-11-00789-g003.jpg
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