Effects of aquatic exercise on nociceptive behavior, systemic inflammation, and skeletal muscle redox status in healthy and reserpine-treated rats.

Abstract

This study investigated whether a 21-day swimming exercise protocol administered concurrently with reserpine exposure modifies nociceptive behavior, serum serotonin and TNF-α levels, and skeletal muscle redox markers in a reserpine-induced fibromyalgia (FM) model. Twenty-four female rats were randomly allocated into Control (CON), Reserpine (RES), Exercise (EX), and RES + EX groups. FM was induced via subcutaneous reserpine administration (1 mg kg^-1 day^-1 for 3 days). Swimming groups exercised for 60 min day^-1 over 21 days. Behavioral hyperalgesia was evaluated using the cold-plate test. Serum tumor necrosis factor-alpha (TNF-α) and serotonin, alongside skeletal muscle malondialdehyde (MDA), protein carbonyl (PC), superoxide dismutase (SOD), glutathione (GSH), and total antioxidant capacity (TAC) were quantified using ELISA. Compared with CON, the RES group showed shorter cold-plate latency, lower serum serotonin, higher serum TNF-α, higher muscle PC, and lower muscle SOD and GSH (p ≤ 0.05). MDA was higher in RES than in EX and RES + EX, but a significant difference between RES and CON was not reported. Swimming increased cold-plate latency in RES + EX compared with RES on days 7, 14, and 21 (all p < 0.001). RES + EX also showed higher serotonin and lower TNF-α than RES (p ≤ 0.05). Muscle PC was lower and SOD/GSH were higher in RES + EX than in RES for the reported comparisons; however, GSH remained lower in RES + EX than in EX. TAC did not differ significantly among groups (p = 0.228). Swimming exercise attenuated reserpine-associated cold allodynia and was associated with more favorable serum serotonin/TNF-α profiles and skeletal muscle redox markers.