Department of Physiology, Zanjan University of Medical Sciences , Zanjan, Iran.
Department of Physiology.
J Sports Sci Med. 2006 Dec 15;5(4):682-91. eCollection 2006.
Despite the knowledge on the antiatherogenic effects of exercise, the mechanism by which exercise reduces atherogenic risk remains unknown. In this study, we investigated the hypothesis that chronic exercise-induced oxidative stress may increase plasma total antioxidant capacity and antioxidant defense in the red cells. For 8 weeks, 60 male Dutch rabbits were fed rabbit chow with or without the addition of 2% cholesterol. The animals were further divided into rest and exercise groups (n = 15 for each group). Animals in exercise groups ran on a rodent treadmill at 15 m/min for 10 to 60 minutes gradually for 5 days per week for a total of 8 weeks. At the end of experiments, blood samples were collected and glutathione peroxidase (GPX), superoxide dismutase (SOD), and catalase (CAT) activities were determined in red blood cells. Total antioxidant capacity (TAC), malondialdehyde (MDA) and total thiol (T-SH) levels were measured in plasma. Thoracic aorta and carotid arteries were isolated for histological examination to evaluate atherosclerosis. Eight weeks of chronic exercise reduced atherogenic diet-induced atherosclerotic lesions in all the arteries studied, along with positive changes in cholesterol profile, especially increase of serum HDL-C level. Plasma MDA, TAC and T-SH concentrations were enhanced by exercise in both control and hypercholesterolemic diet groups. Erythrocyte catalase activity was significantly increased by chronic exercise (p < 0.05), whereas total SOD activity rose with exercise only in the control group. Surprisingly, GPX activity was significantly reduced (P < 0.05) in response to exercise in the control group and also in the high cholesterol diet group. Exercise is a useful tool for the prevention and regression of atherosclerosis which is evident by our findings of the enhancement of plasma TAC and positive change in serum cholesterol profile. However, the effect of exercise on red cell antioxidant activities is limited in the hypercholesterolemic animals compared to control animals, possibly in part because of alterations in the ability to adapt to exercise-induced oxidative stress in high cholesterol diet. Key PointsPlasma MDA, TAC and T-SH concentrations were enhanced by exercise in both control and high cholesterol diet groups.GPX activity was significantly reduced in response to exercise in the control group and also in the high cholesterol diet group.Eight weeks of chronic exercise reduced atherogenic diet-induced atherosclerotic lesions in all the arteries studied.
尽管人们已经了解到运动具有抗动脉粥样硬化的作用,但运动降低动脉粥样硬化风险的机制仍不清楚。在这项研究中,我们假设慢性运动引起的氧化应激可能会增加血浆总抗氧化能力和红细胞中的抗氧化防御。
8 周内,60 只雄性荷兰兔用含有或不含有 2%胆固醇的兔饲料喂养。动物进一步分为休息和运动组(每组 15 只)。运动组的动物在啮齿动物跑步机上以 15m/min 的速度逐渐跑 10 到 60 分钟,每周 5 天,总共 8 周。实验结束时,采集血液样本,测定红细胞中的谷胱甘肽过氧化物酶(GPX)、超氧化物歧化酶(SOD)和过氧化氢酶(CAT)活性。测定血浆中的总抗氧化能力(TAC)、丙二醛(MDA)和总巯基(T-SH)水平。分离胸主动脉和颈动脉进行组织学检查,以评估动脉粥样硬化。
8 周的慢性运动减少了所有研究动脉的致动脉粥样硬化饮食引起的动脉粥样硬化病变,同时胆固醇谱也发生了积极变化,特别是血清高密度脂蛋白胆固醇(HDL-C)水平升高。在对照组和高胆固醇饮食组中,运动均增强了血浆 MDA、TAC 和 T-SH 浓度。慢性运动显著增加红细胞过氧化氢酶活性(p<0.05),而总 SOD 活性仅在对照组中随运动而升高。令人惊讶的是,对照组和高胆固醇饮食组中,GPX 活性在运动后显著降低(P<0.05)。
运动是预防和逆转动脉粥样硬化的有效工具,这一点从我们发现的血浆 TAC 增强和血清胆固醇谱的积极变化中可以明显看出。然而,与对照组动物相比,高胆固醇饮食动物的红细胞抗氧化活性的运动效应有限,这可能部分是由于高胆固醇饮食改变了对运动引起的氧化应激的适应能力。
在对照组和高胆固醇饮食组中,运动均增强了血浆 MDA、TAC 和 T-SH 浓度。
对照组和高胆固醇饮食组中,GPX 活性在运动后显著降低。
8 周的慢性运动减少了所有研究动脉的致动脉粥样硬化饮食引起的动脉粥样硬化病变。