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.

本研究旨在展示高强度间歇训练 (HIIT) 对 PTSD 诱导的大鼠的可能保护作用和可能的潜在机制。雌性大鼠 (n = 44) 被分离为；久坐 (SED)、中等强度持续训练 (MICT)、HIIT 组。然后根据 PTSD 诱导情况将这些组划分为亚组（n = 6-8/组）。运动组进行 HIIT 或 MICT 6 周。在第五周，PTSD 是由单一的长期压力协议诱发的。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。斩首后，丙二醛 (MDA)、谷胱甘肽 (GSH)、鲁米诺和光泽精化学发光水平，以及髓过氧化物酶 (MPO)，测量超氧化物歧化酶 (SOD) 和过氧化氢酶 (CAT) 活性，并评估组织病理学损伤。数据通过单向方差分析进行分析。SED + PTSD 组的认知下降和加重的焦虑水平在两个 PTSD 诱导的运动组中都有所改善。p < 0.05-0.001)。在两个 PTSD 诱导的运动组中，增加的化学发光水平、MPO 活性和组织学损伤均受到抑制（p < 0.05-0.001）。SED + PTSD 组升高的 MDA 水平仅在 HIIT + PTSD 组中受到抑制（p < 0.01-0.001）。MICT 增加了降低的 GSH 水平（p < 0.05-0.001），并且通过 HIIT 提高了 CAT 和 SOD 活性（p < 0.05）。与 SED 组相比，SED + PTSD ( p < 0.05-0.01) 组的潜伏期减少。两个 PTSD 诱发的运动组的神经元损伤评分均有所减轻（p< 0.001)。PTSD 引起的记忆力下降受到两种运动模型的保护，但 HIIT 通过降低氧化应激、焦虑水平和通过提高抗氧化能力作为神经元损伤的保护系统来更有效。