Functional, structural, and molecular response to preventive high-intensity resistance training in CFA-induced arthritis rat model
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Flávia Heloísa da Silva1, Gabriella Lopes Cappellaro2, Mustafa Munir Mustafa Dahleh3
1Laboratory of Structural and Functional Biology, Center for Biological and Health Sciences, State University of Western Paraná. Cascavel, Cascavel, Paraná, Brazil.
Objective And Design:
Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by autoimmune dysregulation and persistent inflammation, leading to impaired functional capacity and reduced quality of life. Resistance training (RT) has been proposed as a non-pharmacological strategy to modulate inflammatory, oxidative, and morphological responses in skeletal muscle. However, the preventive effects of high-intensity RT prior to arthritis onset remain unclear. This study investigated whether preventive high-intensity resistance training (RT) attenuates the decline in grip strength (primary outcome) and improves secondary functional, morphological, and molecular parameters in a CFA-induced arthritis model.
Methods:
Twenty Wistar rats were divided into four groups: control (CG), arthritic (AG), exercised (EG), and exercised arthritic (EAG). Animals performed 31 RT sessions on a vertical ladder with progressive overload before arthritis induction. Grip strength (primary endpoint) and motor function were assessed longitudinally. Muscle samples were analyzed for histomorphometry, connective tissue, neuromuscular junctions, and molecular markers (inflammatory, apoptotic, mitochondrial, and redox).
Results:
The AG group showed reduced functional performance, muscle fiber atrophy, inflammatory infiltrate, structural disorganization, increased connective tissue, decreased neuromuscular junction area, and molecular alterations. In contrast, the EAG group demonstrated preservation of muscle morphology and junctions, improved functional recovery, and reduced inflammatory and apoptotic markers.
Conclusion:
Preventive RT attenuated functional, structural, and molecular impairments induced by arthritis, with preservation of grip strength as the primary observed benefit.