Gaiad Thaís P, Oliveira Murilo X, Lobo Adalfredo R, Libório Lívia R, Pinto Priscilla A F, Fernandes Danielle C, Santos Ana Paula, Ambrósio Carlos Eduardo, Machado Alex Sander D
Department of Physical Therapy, Universidade Federal dos Vales do Jequitinhonha e Mucuri (UFVJM), Diamantina, Brazil.
Institute of Agriculture Scinces, Universidade Federal dos Vales do Jequitinhonha e Mucuri (UFVJM), Unaí, Brazil.
J Exerc Rehabil. 2017 Dec 27;13(6):693-703. doi: 10.12965/jer.1735094.547. eCollection 2017 Dec.
Recommendations of therapeutic exercise in Duchenne muscular dystrophy are still controversial. The hypothesis that a low-intensity training (LIT) protocol leads to muscle adaptations on mdx mice model was tested. Dystrophic male mice with 8 weeks old were separated in exercised (mdxE, n= 8) and sedentary (mdxC, n= 8) groups. Wild-type mice were used as control (WT, n= 8) group. Exercised group underwent a LIT protocol (9 m/min, 30 min, 3 days/wk, 60 days) on a horizontal treadmill. At day 60 all animals were analyzed regarding parameters of markers of muscle lesion and extracellular matrix turnover of muscle tissue by collagens fibers on tibial anterior muscle. Histomorphometry attested that centrally located nuclei fibers and the coefficient of variance of minimal Feret's diameter was similar in mdxE and mdxC groups (= 1.000) and both groups presented higher mean values than WT group (< 0.001). Fraction area of collagen fibers of mdxE group was lower than mdxC group (= 0,027) and similar to WT group (= 0,751). Intramuscular area of Col3 of the mdxE group was higher than mdxC and WT groups (<0.001). Intramuscular area of Col1 on the mdxE group was similar to the mdxC group (= 1.000) and both groups were higher than WT group (< 0.001). LIT protocol had not influenced muscle injuries resulting from the dystrophin-deficiency membrane fragility. Although, LIT had provoked adaptations on extracellular matrix bringing higher elastic feature to dystrophic muscle tissue.
杜氏肌营养不良症的治疗性运动建议仍存在争议。我们测试了低强度训练(LIT)方案能使mdx小鼠模型产生肌肉适应性变化的假说。将8周龄的营养不良雄性小鼠分为运动组(mdxE,n = 8)和久坐组(mdxC,n = 8)。野生型小鼠作为对照组(WT,n = 8)。运动组在水平跑步机上进行LIT方案(9米/分钟,30分钟,每周3天,共60天)。在第60天,通过对胫骨前肌胶原纤维分析所有动物的肌肉损伤标志物和肌肉组织细胞外基质更新参数。组织形态计量学证明,mdxE组和mdxC组中央核纤维以及最小费雷特直径的变异系数相似(= 1.000),且两组的平均值均高于WT组(< 0.001)。mdxE组胶原纤维的分数面积低于mdxC组(= 0.027),与WT组相似(= 0.751)。mdxE组Col3的肌内面积高于mdxC组和WT组(< <0.001)。mdxE组Col1的肌内面积与mdxC组相似(= 1.000),且两组均高于WT组(< 0.001)。LIT方案并未影响因肌营养不良蛋白缺乏导致的膜脆性引起的肌肉损伤。尽管如此,LIT引发了细胞外基质的适应性变化,使营养不良的肌肉组织具有更高的弹性特征。