Department of Physiology, Marmara University School of Medicine, Istanbul, Turkey.
Undergraduate Medical Students, Marmara University School of Medicine, Istanbul, Turkey.
Behav Brain Res. 2021 Jan 15;397:112923. doi: 10.1016/j.bbr.2020.112923. Epub 2020 Sep 22.
This study aimed to show the possible protective effects of high intensity interval training (HIIT) in PTSD-induced rats and probable underlying mechanisms. Female rats (n = 44) were separated as; Sedentary (SED), moderate intensity continuous training (MICT), HIIT groups. Then the groups were divided into subgroups according to PTSD induction (n = 6-8/group). Exercise groups performed HIIT or MICT for 6 weeks. On the fifth week, PTSD was induced by single prolonged stress protocol. Cognitive functions were evaluated by object recognition, anxiety levels by hole-board and elevated plus maze, and fear conditioning by passive avoidance tests. Following decapitation, malondialdehyde (MDA), glutathione (GSH), luminol and lucigenin chemiluminescence levels, and myeloperoxidase (MPO), superoxide dismutase (SOD) and catalase (CAT) activities were measured, and histopathological damage was evaluated. The data was analyzed by one-way ANOVA. Cognitive decline and aggravated anxiety levels in SED + PTSD group were improved in both PTSD-induced exercise groups (p < 0.05-0.001). The increased chemiluminescence levels, MPO activity and histological damage were depressed in both PTSD-induced exercise groups (p < 0.05-0.001). The risen MDA levels in SED + PTSD group were suppressed only in HIIT + PTSD group (p < 0.01-0.001). The decreased GSH levels were increased by MICT (p < 0.05-0.001), and CAT and SOD activities were improved via HIIT (p < 0.05). Compared to SED group, latency was decreased in SED + PTSD (p < 0.05-0.01) group. Neuronal damage scores were alleviated in both PTSD-induced exercise groups (p < 0.001). PTSD-induced memory decline was protected by both of the exercise models however more effectively by HIIT via decreasing oxidative stress, anxiety levels and by improving antioxidant capacity as a protective system for neuronal damage.
这项研究旨在展示高强度间歇训练(HIIT)对 PTSD 诱导大鼠的可能保护作用及其潜在机制。将 44 只雌性大鼠分为以下三组:安静组(SED)、中等强度持续训练组(MICT)和 HIIT 组。然后,根据 PTSD 诱导情况(每组 6-8 只)将这些组进一步分为亚组。运动组进行 HIIT 或 MICT 训练 6 周。第五周时,通过单次延长应激方案诱导 PTSD。通过物体识别评估认知功能,通过洞板和高架十字迷宫评估焦虑水平,通过被动回避测试评估恐惧条件反射。断头后,测量丙二醛(MDA)、谷胱甘肽(GSH)、鲁米诺和荧光素化学发光水平以及髓过氧化物酶(MPO)、超氧化物歧化酶(SOD)和过氧化氢酶(CAT)活性,并评估组织病理学损伤。数据采用单因素方差分析进行分析。SED + PTSD 组的认知能力下降和焦虑水平加重得到改善(p < 0.05-0.001)。两种 PTSD 诱导的运动组均降低了升高的化学发光水平、MPO 活性和组织病理学损伤(p < 0.05-0.001)。SED + PTSD 组 MDA 水平升高被 HIIT + PTSD 组抑制(p < 0.01-0.001)。MICT 增加了 GSH 水平(p < 0.05-0.001),HIIT 提高了 CAT 和 SOD 活性(p < 0.05)。与 SED 组相比,SED + PTSD 组潜伏期缩短(p < 0.05-0.01)。两种 PTSD 诱导的运动组均减轻了神经元损伤评分(p < 0.001)。两种运动模型均能保护 PTSD 诱导的记忆减退,但 HIIT 通过降低氧化应激、焦虑水平和改善抗氧化能力作为神经元损伤的保护系统,更有效地发挥作用。