Traustadóttir Tinna, Davies Sean S, Su Yali, Choi Leena, Brown-Borg Holly M, Roberts L Jackson, Harman S Mitchell
Kronos Longevity Research Institute, 2222 E. Highland Ave., Phoenix, AZ 85016, USA.
Age (Dordr). 2012 Aug;34(4):969-82. doi: 10.1007/s11357-011-9277-6. Epub 2011 Jun 14.
Acute exercise results in transient change in redox balance. High concentrations of reactive oxygen species (ROS) can lead to oxidative damage to macromolecules. However, moderate periodic increases in ROS, such as experienced with habitual exercise, may activate signal transduction pathways which stimulate increases in endogenous antioxidant systems. This study tested the hypothesis that physically fit older adults would have less oxidative stress than unfit age-matched controls, due to greater circulating concentrations of non-enzymatic antioxidants and greater capacity to upregulate antioxidant enzymes. We compared 37 fit (mean age 65.2 ± 5 years) and 35 unfit (mean age 67.7 ± 4 years) men and women. Fitness status was classified by VO(2 max) and maximal leg power. Basal levels of oxidative stress were assessed by measuring urinary markers of nucleic acid damage and lipid peroxidation. Antioxidant status was assessed by measuring total antioxidant power and ratios of reduced to oxidized glutathione in plasma, at rest. The capacity to counteract an oxidative insult was assessed by measuring changes in plasma F(2)-isoprostanes in response to forearm ischemia-reperfusion. The fit individuals had significantly lower levels of urinary markers of oxidative damage (all P <0.05) and lower F(2)-isoprostane response to the oxidative challenge (P < 0.05), but there were no group differences in antioxidant status. The lower levels of oxidative stress in the fit individuals were not mediated by known effects of exercise training such as adiposity, HDL concentrations, or small molecular weight antioxidants. These data suggest that reduced oxidative stress associated with physical fitness results from differences in activity of antioxidant enzymes.
急性运动导致氧化还原平衡的短暂变化。高浓度的活性氧（ROS）可导致大分子的氧化损伤。然而，适度的周期性ROS增加，如习惯性运动时所经历的，可能会激活信号转导通路，从而刺激内源性抗氧化系统的增加。本研究检验了这样一个假设：由于非酶抗氧化剂的循环浓度更高以及上调抗氧化酶的能力更强，身体健康的老年人比年龄匹配的身体不健康的对照组具有更低的氧化应激。我们比较了37名身体健康的（平均年龄65.2±5岁）和35名身体不健康的（平均年龄67.7±4岁）男性和女性。通过最大摄氧量（VO₂max）和最大腿部力量对健康状况进行分类。通过测量核酸损伤和脂质过氧化的尿液标志物来评估氧化应激的基础水平。通过测量静息时血浆中的总抗氧化能力以及还原型谷胱甘肽与氧化型谷胱甘肽的比率来评估抗氧化状态。通过测量前臂缺血再灌注后血浆F₂-异前列腺素的变化来评估抵抗氧化损伤的能力。身体健康的个体氧化损伤的尿液标志物水平显著更低（所有P<0.05），并且对氧化挑战的F₂-异前列腺素反应更低（P<0.05），但抗氧化状态在两组之间没有差异。身体健康个体较低的氧化应激水平并非由运动训练的已知效应如肥胖、高密度脂蛋白浓度或小分子抗氧化剂所介导。这些数据表明，与身体健康相关的氧化应激降低是由抗氧化酶活性的差异导致的。
