Resistance Exercise Modulates Oxidative Stress Parameters and TNF-α Content in the Heart of Mice with Diet-Induced Obesity

Abstract Background: Obesity can be characterized by low-grade chronic inflammation and is associated with an excesso production of reactive oxygen species, factors that contribute to coronary heart disease and other cardiomyopathies. Objective: To verify the effects of resistance exercise training on oxidative stress and inflammatory parameters on mice with obesity induced by a high-fat diet (HFD). Methods: 24 Swiss mice were divided into 4 groups: standard diet (SD), SD + resistance exercise (SD + RE), diet-induced obesity (DIO), DIO + RE. The animals were fed SD or HFD for 26 weeks and performed resistance exercises in the last 8 weeks of the study. The insulin tolerance test (ITT) and body weight monitoring were performed to assess the clinical parameters. Oxidative stress and inflammation parameters were evaluated in the cardiac tissue. Data were expressed by mean and standard deviation (p < 0.05). Results: The DIO group had a significant increase in reactive oxygen species levels and lipid peroxidation with reduction after exercise. Superoxide dismutase and the glutathione system showed no significant changes in DIO animals, with an increase in SD + RE. Only catalase activity decreased with both diet and exercise influence. There was an increase in tumor necrosis factor-alpha (TNF-α) in the DIO group, characterizing a possible inflammatory condition, with a decrease when exposed to resistance training (DIO+RE). Conclusion: The DIO resulted in a redox imbalance in cardiac tissue, but the RE was able to modulate these parameters, as well as to control the increase in TNF-α levels.

摘要 研究背景：肥胖可表现为低度慢性炎症状态，且伴随活性氧（reactive oxygen species, ROS）过度生成，上述因素均可诱发冠心病及其他心肌病变。研究目的：探究抗阻运动训练对高脂饮食（high-fat diet, HFD）诱导肥胖小鼠的氧化应激与炎症指标的调控效应。方法：将24只瑞士小鼠分为4组，分别为标准饮食组（standard diet, SD）、标准饮食+抗阻运动组（SD + RE）、饮食诱导肥胖组（diet-induced obesity, DIO）以及饮食诱导肥胖+抗阻运动组（DIO + RE）。所有小鼠分别饲喂标准饮食或高脂饮食，实验周期共计26周，并于实验最后8周开展抗阻运动训练。通过胰岛素耐量试验（insulin tolerance test, ITT）与体重监测评估临床相关指标，并对小鼠心脏组织中的氧化应激与炎症参数进行检测。实验数据以均值±标准差形式呈现，以p < 0.05作为统计学显著性检验阈值。结果：饮食诱导肥胖组小鼠的活性氧水平与脂质过氧化程度显著升高，经抗阻运动训练后上述指标均得到改善。超氧化物歧化酶与谷胱甘肽系统在饮食诱导肥胖小鼠中未出现显著变化，但在标准饮食+抗阻运动组中有所升高。仅过氧化氢酶活性因饮食与运动的共同影响出现下降。饮食诱导肥胖组小鼠的肿瘤坏死因子-α（tumor necrosis factor-alpha, TNF-α）水平显著升高，提示存在潜在炎症状态，经抗阻运动训练（DIO+RE组）后该指标显著降低。结论：高脂饮食诱导的肥胖会造成小鼠心脏组织氧化还原失衡，而抗阻运动训练可有效调节上述异常参数，并可抑制肿瘤坏死因子-α水平的异常升高。