Exercise Physiology
Fatemeh Beiksay Afshar; Esmaeil Nasiri; Ali Samadi
Abstract
Aim: The purpose of this study was to investigate the effect of sprint interval training on hippocampal oxidative stress markers hippocampus of adult male Wistar rats.Method: This is an experimental study in which 16 male Wistar rats were obtained, and after environmental adaptation and reaching target ...
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Aim: The purpose of this study was to investigate the effect of sprint interval training on hippocampal oxidative stress markers hippocampus of adult male Wistar rats.Method: This is an experimental study in which 16 male Wistar rats were obtained, and after environmental adaptation and reaching target weight range randomly divided into two equal groups: control (CO) and sprint interval training (SIT). The SIT was performed for 8 weeks, 3 sessions per week, 4-9 repetitions of 10 seconds with 60 secs of active recovery between intervals. Forty-eight hours after the last exercise session the rats were anesthetized and the hippocampus was dissected and level of malondialdehyde (MDA) and superoxide dismutase (SOD), glutathione peroxidase (GPx), and total antioxidant capacity (TAC) were assessed in hippocampus homogenate. The independent samples T test was used for data analysis (P<0.05).Results: There were no significant difference between the SIT and CO groups in the hippocampal GPx, TAC and MDA levels (p < 0.05). However, the activity level of SOD in the SIT group was significantly higher than the CO group (p<0.05).Conclusion: The present research revealed that despite its strenuous nature, SIT did not induce oxidative stress in the hippocampus and trend of changes in GPx and TAC, as well as observed significant increase in SOD activity levels suggests that it may have favorable effects on hippocampus oxidative- antioxidative status.
A Fazeli Sani; hasan Matinhomaee; A Banaeifar
Abstract
Aim: The aim of the present study was to investigate the effect of 4 weeks of aerobic exercise on cognitive function and mitochondrial dynamics in the hippocampal tissue of male Wistar rats with Alzheimer's disease.Methods: For this purpose, 21 male Wistar rats at 20 months of age were randomly divided ...
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Aim: The aim of the present study was to investigate the effect of 4 weeks of aerobic exercise on cognitive function and mitochondrial dynamics in the hippocampal tissue of male Wistar rats with Alzheimer's disease.Methods: For this purpose, 21 male Wistar rats at 20 months of age were randomly divided into 3 groups: Alzheimer's disease (n = 7), Alzheimer's disease + aerobic exercise (n = 7) and control group (n = 7). Alzheimer's disease was induced by intrahippocampal injection of Aβ42 (1 microliter per side). Seven days after surgery, the exercise group performed 4 weeks of treadmill training (5 days per week at a speed of 10 to 15 m/min). Forty-eight hours after the last training session, the animals underwent behavioral tests. Twenty-four hours after the behavioral test, all rats were killed and hippocampal tissue was extracted. The mRNA expression of OPA1, Mfn2 and Drp1 genes was assayed using Real Time-PCR. One-way analysis of variance was used for statistical analysis.Ethical Considerations: All stages of the study were conducted according to the ethical guidelines and authorization of Research Deputy of Islamic Azad University, Central Tehran Branch No. IR.IAU.TMU.REC.1399.124.Results: The results showed that spatial learning (P ≤ 0.001) and memory performance (P ≤ 0.001) as well as the gene expression of OPA1 (P ≤ 0.001) and Mfn2 (P ≤ 0.001) in animals with Alzheimer's disease decreased compared to the control group, while the gene expression of Drp1 increased (P ≤ 0.001). Aerobic exercise in patient animals improved spatial learning (P ≤ 0.001) and memory performance (P ≤ 0.001), increased hippocampal OPA1 (P ≤ 0.001) and Mfn2 (P ≤ 0.001) genes expression, and decreased Drp1 gene expression compared with Alzheimer's disease group (P ≤ 0.001).Conclusion: In general, it seems that aerobic exercise can improve spatial learning and memory performance in Alzheimer's disease by modulating abnormal mitochondrial dynamics.
