The neuromuscular junction (NMJ) is responsible for transmitting neural signals that trigger muscle contraction. Muscle injuries cause damage to cellular structures and trigger local inflammatory processes. In this context, eccentric contraction was used as an experimental model because it involves excessive stretching, generating mechanical stress. Twenty-five adult male Wistar rats were distributed into groups: Control (C) (n = 5) and Injury (I) (n = 20). The protocol was performed on a treadmill and consisted of 18 sets/5 min/16 m/min speed, with intervals, and with a negative incline (−16º). The analyses consisted of histochemical techniques, such as myofibrillar ATPase and immunofluorescence (calcium channels, synaptophysin and α-bungarotoxin). Group I-0H showed alterations in the presynaptic region and an increase in Type I fibers. I-24H presented disorganization in the postsynaptic region. In I-4D, we observed the reorganization of neuromuscular activity, while I-7D presented greater density and cross-sectional area (CSA) of Type II fibers. It is concluded that the protocol promotes changes in NMJ structure and fiber distribution, mainly in I-24H. In I-4d, a reorganization of neuromuscular activity is observed, and in I-7D, a structural indicator consistent with recovery demonstrates the skeletal muscle’s ability to adapt to injury.
Baptista et al. (Thu,) studied this question.
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