Abstract
The myotendinous junction (MTJ) is the muscle-tendon interface and constitutes an integrated mechanical unit to force transmission. Joint immobilization promotes muscle atrophy via disuse, while physical exercise can be used as an adaptative stimulus. In this study, we aimed to investigate the components of the MTJ and their adaptations and the associated elements triggered with aquatic training after joint immobilization. Forty-four male Wistar rats were divided into sedentary (SD), aquatic training (AT), immobilization (IM), and immobilization/aquatic training (IMAT) groups. The samples were processed to measure fiber area, nuclear fractal dimension, MTJ nuclear density, identification of telocytes, sarcomeres, and MTJ perimeter length. In the AT group, the maintenance of ultrastructure and elements in the MTJ region were observed; the IM group presented muscle atrophy effects with reduced MTJ perimeter; the IMAT group demonstrated that aquatic training after joint immobilization promotes benefits in the muscle fiber area and fractal dimension, in the MTJ region shows longer sarcomeres and MTJ perimeter. We identified the presence of telocytes in the MTJ region in all experimental groups. We concluded that aquatic training is an effective rehabilitation method after joint immobilization due to reduced muscle atrophy and regeneration effects on MTJ in rats.
Highlights
IntroductionPublisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations
In the aquatic training (AT) group, we observed branched sarcoplasmatic invaginations, the presence of a telocyte in extracellular matrix (ECM) and their telopods, and a long sarcoplasmatic invagination connected to a vesicle cluster inside the muscle fiber
AT after joint immobilization did not lead to a higher organization complexity of the nucleus, a higher fiber area was observed than in the IM group. These results indicate that training contributes to muscle readaptation after joint immobilization and associated structures, without full return to its pre-immobilization morphology; these results were observed by Nascimento et al [19]
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. The myotendinous junction (MTJ) anchors the terminal sarcomeres to the extracellular matrix (ECM). The MTJ is the site of contractile force transmission from the muscle to the tendon, and the higher contact area between the muscle and tendon provides resistance to the muscle contractile force [1]. Joint immobilization promotes inactivity, which leads to muscle atrophy via disuse. Joint immobilization promotes diverse deleterious effects in the postimmobilization period in the form of impaired muscle performance [2] and reduced myotendinous interface [3,4]
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