Evidence suggests that physical exercise has effects on neuronal plasticity as well as overall brain health. This effect has been linked to exercise capacity in modulating the antioxidant status, when the oxidative stress is usually linked to the neuronal damage. Although high-intensity interval training (HIIT) is the training-trend worldwide, its effect on brain function is still unclear. Thus, we aimed to assess the neuroplasticity, mitochondrial, and redox status after one-week HIIT training. Male (C57Bl/6) mice were assigned to non-trained or HIIT groups. The HIIT protocol consisted of three days with short bouts at 130% of maximum speed (Vmax), intercalated with moderate-intensity continuous exercise sessions of 30 min at 60% Vmax. The mass spectrometry analyses showed that one-week of HIIT increased minichromosome maintenance complex component 2 (MCM2), brain derived neutrophic factor (BDNF), doublecortin (DCX) and voltage-dependent anion-selective channel protein 2 (VDAC), and decreased mitochondrial superoxide dismutase 2 (SOD 2) in the hippocampus. In addition, one-week of HIIT promoted no changes in H₂O₂ production and carbonylated protein concentration in the hippocampus as well as in superoxide anion production in the dentate gyrus. In conclusion, our one-week HIIT protocol increased neuroplasticity and mitochondrial content regardless of changes in redox status, adding new insights into the neuronal modulation induced by new training models.

中文翻译：

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一周的高强度间歇训练可增加海马可塑性和线粒体含量，而氧化还原状态不变。

有证据表明，体育锻炼会影响神经元可塑性以及整个大脑健康。当氧化应激通常与神经元损伤有关时，这种作用与调节抗氧化剂状态的运动能力有关。尽管高强度间歇训练（HIIT）是全世界的训练趋势，但其对脑功能的影响仍不清楚。因此，我们的目的是评估为期一周的HIIT训练后的神经可塑性，线粒体和氧化还原状态。将雄性（C57Bl / 6）小鼠分为未训练组或HIIT组。HIIT方案包括三天，以最高速度（Vmax）的130％短暂发作，并以60％Vmax的中强度连续锻炼30分钟进行训练。质谱分析显示，HIIT的一周时间增加了微染色体维持复合物成分2（MCM2），脑源性神经营养因子（BDNF），双皮质素（DCX）和电压依赖性阴离子选择性通道蛋白2（VDAC）的表达，并降低了线粒体海马中的超氧化物歧化酶2（SOD 2）。此外，HIIT的一个星期没有促进H的变化海马中₂ O _2的产生和羰基化蛋白质的浓度以及齿状回中超氧阴离子的产生。总之，无论氧化还原状态如何变化，我们为期一周的HIIT协议均可增加神经可塑性和线粒体含量，从而为新训练模型诱导的神经元调节增添了新见解。