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Barati Z, Yaghoubi A, Jalilvand M R. Effect of Continuous and Interval Training on Amyloid β 42 (Aβ42) and Malondialdehyde (MDA) Levels in Hippocampus of Elderly Rats. JSSU 2021; 29 (9) :4083-4095
URL: http://jssu.ssu.ac.ir/article-1-5383-en.html

Introduction: Amyloid plaques in the brain increase with age. Thus, the present study aimed to evaluate the effect of continuous and interval training on Amyloid β 42 (Aβ42) and Malondialdehyde (MDA) levels in hippocampus of elderly rats.
Methods: The present study was experimental one with two experimental groups and one control group. Thirty old male Wistar rats (18 weeks-old) divided into 3 groups, including interval training, continuous training, and control. Continuous training was performed for 8 weeks with 65 to 70% VO2max and interval training was performed for 8 weeks with 5-8 repetitions of 2 minutes of working with 80-100% VO2max and 2 minutes active rest with 50% of VO2max for 8 weeks. Hippocampal samples were extracted 48 hours after the last training session to measure protein levels of Aβ42 and MDA. One-way ANOVA and Tukey post hoc test was used for data analysis.
Results: Hippocampus Aβ42 levels in continuous training groups were significantly lower than the control group (P=0.001). In addition, Aβ42 levels in hippocampus of interval training groups were significantly lower than the control group (P=0.001). However, no significant differences were found in Aβ42 levels between continuous and interval training groups (p=0.502). MDA levels in continuous training groups were significantly lower than the control group (P=0.016). In addition, MDA levels in interval training groups were significantly lower than the control group (P=0.046) But no significant differences were found in hippocampal MDA protein levels between continuous and interval training groups (p=866).
Conclusion: Continuous and interval training through decreasing oxidative stress, decrease Aβ42 levels in the hippocampus of the elderly rat, thus probably continuous and interval training can prevent neurodegenerative disease caused by aging through modulating oxidative stress and Aβ42.