# Changes in the Structure of the Neuromuscular Junction and Muscle Fiber Types Following an Acute Injury Model Induced by Eccentric Contraction

**Authors:** Mariana Baptista, Jurandyr Pimentel Neto, Matheus Bertanha Fior, Isabella Gomes, Adriano Polican Ciena

PMC · DOI: 10.3390/cimb48030325 · 2026-03-19

## TL;DR

This study examines how muscle injury from eccentric contractions affects neuromuscular junctions and muscle fiber types in rats.

## Contribution

The paper introduces a novel experimental model using eccentric contractions to study acute muscle injury effects on neuromuscular junction structure.

## Key findings

- Injury group showed presynaptic region alterations and increased Type I fibers at 0 hours.
- Postsynaptic region disorganization was observed 24 hours after injury.
- By 7 days, increased Type II fiber density and cross-sectional area indicated recovery.

## Abstract

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.

## Full-text entities

- **Genes:** Chrna2 (cholinergic receptor nicotinic alpha 2 subunit) [NCBI Gene 170945] {aka ACHR}, Syp (synaptophysin) [NCBI Gene 24804] {aka Syp1}
- **Diseases:** Muscle injuries (MESH:D009135), overdose (MESH:D062787), neuronal lesions (MESH:D009410), inflammation (MESH:D007249), adipose (MESH:D018205), fatigue (MESH:D005221), contusions (MESH:D003288), sarcopenia (MESH:D055948), atrophy (MESH:D001284), obesity (MESH:D009765), degeneration of the neuromuscular system (MESH:D020879), death (MESH:D003643), disuse muscle atrophy (MESH:D020966), Injury (MESH:D014947), NMJ (MESH:D020511)
- **Chemicals:** ACh (MESH:D000109), Xylazine (MESH:D014991), glycine (MESH:D005998), water (MESH:D014867), DTT (MESH:D004229), nitrogen (MESH:D009584), NaCl (MESH:D012965), sodium acetate (MESH:D019346), cobalt chloride (MESH:C018021), ATP (MESH:D000255), Triton X-100 (MESH:D017830), Ketamine (MESH:D007649), C (MESH:D002244), Calcium (MESH:D002118), 24H (-), EDTA (MESH:D004492), Alexa Fluor 488 (MESH:C000711379), isopentane (MESH:C067038), CaCl2 (MESH:D002122), xylene (MESH:D014992), alcohols (MESH:D000438)
- **Species:** Rattus norvegicus (brown rat, species) [taxon 10116], Homo sapiens (human, species) [taxon 9606]

## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC13025536/full.md

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Source: https://tomesphere.com/paper/PMC13025536