부산대학교 도서관

Objective: Diabetes is characterized by a comprehensive increase in apoptosis, mitochondrial dysfunction, and inflammation in skeletal muscle. Impaired mitochondrial function in skeletal muscle leads to an increase in Cytochrome C and Caspase-9, and muscle performance is reduced consequently. Exercise training through decreasing inflammatory factors and increasing anti-inflammatory elements prevents apoptosis pathways. Materials and Methods: Forty male Wistar rats (150±10 g, 8 weeks age) were assigned to 4 groups: control (C), diabetes (D), high-intensity interval training (HIIT), and diabetes high-intensity interval training (DHIIT). Diabetes was induced with intraperitoneal injections of Streptozotocin (STZ) and blood sugar higher than 250 was considered diabetic. The effects of six weeks of HIIT on soleus muscles, Cytochrome C, and Caspase-9 gene expression, as well as evaluation of tumor necrosis factor-alpha (TNF-a) in serum were evaluated using Real-Time PCR and ELISA techniques respectively. Results: In comparison with C group Diabetes has significantly increased the Cytochrome C (P= 0.001) and caspase-9 (P= 0.003). However, HIIT training in diabetic rats significantly decreased the Cytochrome C (P= 0.001) and caspase-9 (P= 0.008) in comparison of D group. Also, TNFa (P= 0.01) increased in the D group in comparison with C and DHIIT group (P= 0.001). In comparison between DHIIT groups in HIIT groups, has a significant increase in time to exhaustion post test than pretest (P= 0.001). Conclusion: It seems that HIIT training decreases intrinsic factors of the apoptosis pathway by decreasing inflammatory factors which leads to significant improvement in skeletal muscle function and overall health in diabetic rats. [ABSTRACT FROM AUTHOR]