نوع مقاله : مقاله پژوهشی
نویسندگان
1 محقق دانشکده علوم ورزشی، گروه فیزیولوژی ورزش، دانشگاه اصفهان، اصفهان، ایران
2 استاد دانشکده علوم ورزشی، گروه فیزیولوژی ورزش، دانشگاه اصفهان، اصفهان، ایران
چکیده
کلیدواژهها
عنوان مقاله [English]
نویسندگان [English]
Background and Objective: Diabetes impairs hippocampal synaptic plasticity by reducing brain-derived neurotrophic factor (BDNF) and its associated cellular pathways. Exercise is an effective intervention in improving this process, but its molecular mechanisms are not well understood. This study aimed to compare the effects of endurance training and high-intensity interval training (HIIT) on the AMP-activated protein kinase (CaMKII)/cAMP response element binding protein (CREB)/mechanistic target of rapamycin (mTOR) signaling pathway and BDNF expression in the hippocampus of diabetic rats. Materials and Methods: In this experimental study, 40 male Wistar rats were randomly divided into healthy control (NC), diabetic control (DC), diabetic + endurance training (DE), and diabetic + high-intensity interval training (DHIIT) groups. Endurance and HIIT training programs were performed for 8 weeks, 5 days a week for the respective groups. In both protocols, the intensity and duration of exercise gradually increased during the course, so that at the end of 8 weeks, the total time of exercise sessions significantly increased compared to the beginning of the course. Diabetes was induced by injection of streptozotocin (55 mg/kg body weight). At the end, the expression of BDNF, CaMKII, CREB and mTOR genes in hippocampal tissue was measured by Real-time PCR. Differences between groups were examined using two-way analysis of variance and Tukey's post hoc test at the p < 0.05 level. Results: Diabetes caused a significant decrease in the expression of BDNF (p < 0.009), CaMKII (p < 0.0001), CREB (p < 0.009) and mTOR (p < 0.0001) genes in the hippocampus of rats. Both types of exercise training significantly compensated for these decreases and resulted in increased expression of BDNF (p<0.0001), CaMKII (p<0.001), CREB (p<0.0001), and mTOR (p<0.0001) genes compared to the diabetic control group. However, the HIIT group showed a more pronounced increase in the expression of CREB (p<0.0001) and mTOR (p<0.0001) genes compared to the endurance training group. Conclusion: Both endurance training and HIIT are able to restore the mTOR/CREB/CaMKII signaling pathway and increase BDNF gene expression in the hippocampus of diabetic rats. However, HIIT seems to be superior in more effective activation of downstream components of this pathway, especially mTOR and CREB, which could suggest it as a more efficient exercise strategy to target molecular abnormalities associated with diabetic neurological complications.
کلیدواژهها [English]
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