Abstract

Background Type 2 diabetes (T2D) leads to serious respiratory problems. This study investigated the efectiveness of high-intensity interval training (HIIT) on T2D-induced lung injuries at histopathological and molecular levels. Methods Forty-eight male Wistar rats were randomly allocated into control (CTL), Diabetes (Db), exercise (Ex), and Diabetes+exercise (Db+Ex) groups. T2D was induced by a high-fat diet plus (35 mg/kg) of streptozotocin (STZ) administration. Rats in Ex and Db+Ex performed HIIT for eight weeks. Tumor necrosis factor-alpha (TNFα), Interleukin 10 (IL-10), BAX, Bcl2, Lecithin, Sphingomyelin (SPM) and Surfactant protein D (SPD) levels were measured in the bron‑ choalveolar lavage fuid (BALF) and malondialdehyde (MDA) and total antioxidant capacity (TAC) levels were meas‑ ured in lung tissue. Lung histopathological alterations were assessed by using H&E and trichrome mason staining. Results Diabetes was signifcantly associated with imbalance in pro/anti-infammatory, pro/anti-apoptosis and redox systems, and reduced the SPD, lecithin sphingomyelin and alveolar number. Performing HIIT by diabetic animals increased Bcl2 (P<0.05) and IL10 (P<0.01) levels as well as surfactants components and TAC (P<0.05) but decreased fasting blood glucose (P<0.001), TNFα (P<0.05), BAX (P<0.05) and BAX/Bcl2 (P<0.001) levels as well as MDA (P<0.01) and MDA/TAC (P<0.01) compared to the diabetic group. Furthermore, lung injury and fbrosis scores were increased by T2D and recovered in presence of HIIT. Conclusion These fndings suggested that the attenuating efect of HIIT on diabetic lung injury mediated by reducing blood sugar, infammation, oxidative stress, and apoptosis as well as improving pulmonary surfactants components.