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Diabetes mellitus (DM) causes significant lung alterations whereas moderate exercise reduces inflammation and oxidative stress. We evaluated lung functional, biochemical, and histological impairments in streptozotocin-induced diabetic rats and the preventive effect of moderate aerobic exercise (CEUA-UECE/31032.011205/2024-52). Wistar rats were divided into control (C, n = 8), exercise (C+EXE, n = 8), diabetic (D, n = 7), and diabetic with exercise (D+EXE, n = 7) groups. DM was induced by streptozotocin. Exercise groups were trained on a treadmill 5 days/week for 8 weeks. Blood glucose, body weight, exercise capacity, lung mechanics, bronchoconstriction index (BCI), polymorphonuclear cells (PMN), catalase (CAT), superoxide dismutase (SOD), TNF-α, and IL-1β levels were analysed (One-way ANOVA/Holm-Sidak test, p < 0.05). Post-prandial glycemia of D (436 ± 38.08 mg/dL) and D+EXE (445 ± 39.90 mg/dL) was higher than C (104 ± 1.16 mg/dL) and C+EXE (107 ± 2.53 mg/dL). Exercise capacity in C+EXE (1.242 ± 0.03 km/h) and D+EXE (1.160 ± 0.05 km/h) exceeded C (0.918 ± 0.12 km/h) and D (0.633 ± 0.15 km/h). At 1 Hz, D exhibited higher elastance (65.271 ± 0.97 × 10⁴ N/m²), and hysteresis (0.152 ± 0.003) than C (46.814 ± 1.74; 0.090 ± 0.006), C+EXE (44.244 ± 6.73; 0.098 ± 0.008), and D+EXE (51.897 ± 4.49; 0.119 ± 0.010), respectively. BCI and PMN cells were higher in D group (2.565 ± 0.18; 0.82 ± 0.01 cells-2/µm-2) versus C (2.130 ± 0.20; 0.50 ± 0.01 cells-2/µm-2), C+EXE (2.199 ± 0.16; 0.55 ± 0.11 cells-2/µm-2) and D+EXE (2.376 ± 0.13; 0.55 ± 0.01 cells-2/µm-2). CAT in D group (0.394 ± 0.09 U/mg ptn) was higher than C (0.225 ± 0.09 U/mg ptn) and D+EXE (0.169 ± 0.03 U/mg ptn). SOD was lower in D group (0.063 ± 0.008 U/mg ptn) than C (0.133 ± 0.02 U/mg ptn), C+EXE (0.1137 ± 0.03 U/mg ptn) and D+EXE (0.119 ± 0.04 U/mg ptn). TNF-α levels in D group (3.145 ± 1.50 pg/mL) were elevated compared to C (0.896 ± 0.48 pg/mL), C+EXE (0.814 ± 0.49 pg/mL) and D+EXE (1.469 ± 0.79 pg/mL). In conclusion, moderate aerobic exercise prevents diabetes-induced lung mechanical, morphological, and biochemical deterioration.
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