Applied Neuromechanics Group, Federal University of Pampa, Uruguaiana, 97501-970, Brazil; Memory Center, Brain Institute, Pontifical Catholic University of Rio Grande do Sul, Porto Alegre 90610-000, Brazil.
Physiology Research Group, Stress, Memory and Behavior Lab, Federal University of Pampa, Uruguaiana, 97501-970, Brazil.
Physiol Behav. 2019 Jul 1;206:206-212. doi: 10.1016/j.physbeh.2019.04.012. Epub 2019 Apr 14.
Aerobic exercise induces neuroprotection, but few studies investigated whether strength training has similar potential. Here we examine whether effects of strength training differ from those of running training concerning cognitive symptomatology, oxidative stress and cholinergic status in a model of AD-like cognitive impairment induced by intrahippocampal infusion of a mix of β-amyloid peptides (Aβ) in rats. Male Wistar rats were submitted to 8 weeks of running exercise (RunEx; 40 min sessions at 70% of indirect VO max, 3 times/week) or strength exercise (StrEx; 3 sessions/week, 12 repetitions in 8 sets, 2 sets with repetitions at 50%, 2 at 75%, 2 at 90% and 2 at 100% of the maximum load), followed by Aβ infusion in the dorsal hippocampus. Short-term (STM) and long-term (LTM) object recognition (OR) and social recognition (SR) memories were evaluated. Hippocampal oxidative status was determined by quantification of reactive oxygen species, lipid peroxidation by thiobarbituric acid reactive substance test, total antioxidant capacity by ferric reducing/antioxidant power, and acetylcholinesterase enzyme activity (AChE). Aβ infusion impaired STM and LTM and resulted in higher hippocampal oxidative damage and impaired AChE activity. StrEx results in better neuroprotection than RunEx by preventing deficits in OR and SR memories, prevents increases in lipid peroxidation, and decreases in AChE activity. RunEx elicits neuroprotection only for SR memory deficits, prevents increase in ROS and lipid peroxidation, and preserves the total antioxidant capacity. While RunEx effects are related to oxidative status, only StrEx shows potential to also influence the cholinergic system.
有氧运动可诱导神经保护，但很少有研究探讨力量训练是否具有类似的潜力。在这里，我们研究了在大鼠海马内注射混合β-淀粉样肽（Aβ）引起的 AD 样认知障碍模型中，力量训练的效果是否与跑步训练的效果不同，包括认知症状、氧化应激和胆碱能状态。雄性 Wistar 大鼠接受了 8 周的跑步运动（RunEx；70%间接 VO max，每周 3 次，每次 40 分钟）或力量运动（StrEx；每周 3 次，8 组每组 12 次重复，50%、75%、90%和 100%最大负荷的重复 2 次），然后在海马内注射 Aβ。评估短期（STM）和长期（LTM）物体识别（OR）和社会识别（SR）记忆。通过定量测定活性氧、硫代巴比妥酸反应物质试验测定脂质过氧化、铁还原/抗氧化能力测定总抗氧化能力和乙酰胆碱酯酶活性（AChE）来测定海马氧化状态。Aβ 注射损害了 STM 和 LTM，并导致海马氧化损伤增加和 AChE 活性受损。StrEx 比 RunEx 产生更好的神经保护作用，可防止 OR 和 SR 记忆缺陷，防止脂质过氧化增加，并降低 AChE 活性。RunEx 仅对 SR 记忆缺陷产生神经保护作用，可防止 ROS 和脂质过氧化增加，并保持总抗氧化能力。虽然 RunEx 的作用与氧化状态有关，但只有 StrEx 显示出对胆碱能系统也有影响的潜力。
