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大小和部位很重要:胼胝体亚区域病变对力量交叉训练程度的影响。

Size and site matter: the influence of corpus callosum subregional lesions on the magnitude of cross-education of strength.

作者信息

Morrone Marco, Martinez Gianluca, Achene Antonio, Scaglione Mariano, Masala Salvatore, Manca Andrea, Deriu Franca

机构信息

Department of Biomedical Sciences, University of Sassari, Sassari, Italy.

Department of Medicine, Surgery and Pharmacy, University of Sassari, Sassari, Italy.

出版信息

Front Physiol. 2025 Feb 24;16:1554742. doi: 10.3389/fphys.2025.1554742. eCollection 2025.

DOI:10.3389/fphys.2025.1554742
PMID:40066282
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11891228/
Abstract

INTRODUCTION

Cross-education is an established yet not fully understood phenomenon involving interhemispheric processes within the corpus callosum (CC) that result in strength gains in the untraining limb following training of the contralateral homologous muscles. There is a substantial lack of cross-education studies employing lesional models. This study employed the model of multiple sclerosis, a condition typically featuring demyelinating callosal lesions, to pinpoint CC subregions that mediate cross-education, potentially fostering the mechanistic understanding of the interlimb transfer.

METHODS

Nine individuals with relapsing-remitting multiple sclerosis (median Expanded Disability Status Scale: 3.5) and focal CC lesions underwent a 6-week, high-intensity isokinetic training program (≥80% maximal effort at 10°/s) targeting their stronger ankle dorsiflexors. Sagittal FLAIR MRI scans were segmented into five CC subregions (CC1-CC5), with lesion volumes quantified for each subregion. Strength (peak concentric torque at 10°/s) was measured bilaterally before (PRE) and after (POST) training to determine cross-education, defined as the percentage increase in torque of the untrained, weaker limb. Correlations between lesion volumes in CC subregions and cross-education were analyzed.

RESULTS

Both the trained (+21.5 ± 15.8%, p = 0.002) and untrained (+35.2 ± 24.9%, p = 0.003) limbs demonstrated post-training strength gains, reducing but not eliminating inter-limb asymmetry. Lesions specifically in the rostral body (CC2) correlated with reduced cross-education magnitude (rs = -0.670, p = 0.048) and smaller improvements in strength asymmetry (rs = 0.809, p = 0.008). No associations were detected in other CC subregions.

CONCLUSION

These findings highlight the pivotal role of specific CC subregions, particularly the rostral body, in mediating cross-education of strength. These findings advance our understanding of CC role in the interhemispheric dynamics underpinning cross-education. Routine MRI can identify patients without CC2 lesions who may benefit from cross-education, providing a practical approach to improving muscle strength when weaker muscles cannot be directly trained.

CLINICAL TRIAL REGISTRATION

ClinicaTrials.Gov, identifier NCT02010398.

摘要

引言

交叉训练效应是一种已被证实但尚未完全理解的现象,涉及胼胝体(CC)内的半球间过程,导致对侧同源肌肉训练后未训练肢体力量增加。目前严重缺乏采用损伤模型的交叉训练效应研究。本研究采用多发性硬化症模型(一种典型的以胼胝体脱髓鞘病变为特征的疾病)来确定介导交叉训练效应的CC亚区,这可能有助于对肢体间转移的机制理解。

方法

9名复发缓解型多发性硬化症患者(扩展残疾状态量表中位数:3.5)和局灶性CC病变患者接受了为期6周的高强度等速训练计划(在10°/s时≥80%最大努力),目标是他们较强的踝背屈肌。矢状面液体衰减反转恢复(FLAIR)MRI扫描被分割为五个CC亚区(CC1 - CC5),每个亚区的病变体积被量化。在训练前(PRE)和训练后(POST)双侧测量力量(10°/s时的峰值向心扭矩)以确定交叉训练效应,交叉训练效应定义为未训练的较弱肢体扭矩增加的百分比。分析CC亚区病变体积与交叉训练效应之间的相关性。

结果

训练肢体(+21.5 ± 15.8%,p = 0.002)和未训练肢体(+35.2 ± 24.9%,p = 0.003)训练后力量均增加,减少但未消除肢体间不对称。特别是胼胝体嘴部(CC2)的病变与交叉训练效应幅度降低相关(rs = -0.670,p = 0.048)以及力量不对称改善较小相关(rs = 0.809,p = 0.008)。在其他CC亚区未检测到相关性。

结论

这些发现突出了特定CC亚区,特别是胼胝体嘴部,在介导力量交叉训练效应中的关键作用。这些发现推进了我们对CC在支撑交叉训练效应的半球间动力学中作用的理解。常规MRI可以识别没有CC2病变且可能从交叉训练效应中受益的患者,当较弱肌肉无法直接训练时,提供了一种改善肌肉力量的实用方法。

临床试验注册

ClinicalTrials.Gov,标识符NCT02010398。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fc7/11891228/6ff5ddbef38a/fphys-16-1554742-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fc7/11891228/b86714431bbb/fphys-16-1554742-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fc7/11891228/6ff5ddbef38a/fphys-16-1554742-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fc7/11891228/b86714431bbb/fphys-16-1554742-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fc7/11891228/6ff5ddbef38a/fphys-16-1554742-g002.jpg

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