Swimming-based training ameliorates cardiac dysfunction and oxidative stress in chronically stressed rats

OBJECTIVE: The aim of this study is to evaluate the influence of swimming training on cardiac structure and function, and oxidative stress induced by the rat model of chronic restraint stress. METHODS: Young Wistar-UFES rats (n:40) were distributed in four groups: Control, Trained, Stressed, and Stressed and Trained. The training program consisted of 60 min per day, five times a week for 12 weeks, without additional load. The restraint stress was applied using an opaque PVC cylinder for 1 h per day, 5 days a week, for 12 weeks. Physical capacity, blood pressure, ventricular performance via echocardiogram, histological evaluations, and oxidative stress were assessed. RESULTS: After 12 weeks, only the trained groups improved physical capacity. Corticosterone levels (nmol/l) were higher than in the Trained group (174 ± 9) compared to Control (141 ± 8). Swimming training does not prevent the increase (Stressed and trained: 231 ± 17) but mitigate the effect of restraint stress on the corticosterone circulation (Stressed: 335 ± 24). SBP (mmHg) was similar in Trained (138 ± 14) and Control (135 ± 22). Chronic stress significantly increased SBP (180 ± 13), while swimming training prevented partially this increase (Stressed and Trained: 164 ± 16). Regarding ventricular performance, the A wave (mm/s) was lower in the Stressed group (268 ± 36) compared to Control (342 ± 63), Trained (355 ± 74), and Stressed and Trained (360 ± 80), and the E/A ratio was higher in the Stressed group (2.96 ± 0.70) compared to Control (1.66 ± 0.28), Trained (1.55 ± 0.30), and Stressed and Trained (1.75 ± 0.33). The values of DT, +dT/dtmax, and -dT/dtmax Trained group was high than Control, Stressed, and Stressed and Trained groups. For nuclear volume (μm3), no differences were observed between the Control (144 ± 7) and Trained (146 ± 7) groups, and both were smaller than the Stressed (175 ± 10) and Stressed and Trained (161 ± 2) groups, which differed from each other. Malondialdehyde (MDA, in μmol/l/mg) increased in the Stressed group (0.74 ± 0.07) beyond control levels (Control: 0.49 ± 0.09). This increase in MDA levels was prevented by swimming training (Stressed and trained: 0.43 ± 0.12). Oxidized proteins (μmol/l) also increased with restraint stress (Stressed: 1.4 ± 0.4 vs. Control: 0.76 ± 0.10, and Trained: 0.72 ± 0.04), but this increase was prevented by swimming training (Stressed and Trained: 0.69 ± 0.11). CONCLUSION: Restraint stress caused a significant increase in SBP, impairments in diastolic function, increase in nuclear volume, and oxidative stress. Swimming training in turn prevented these stress-evoked effects.