Nyberg Michael, Mortensen Stefan P, Cabo Helena, Gomez-Cabrera Mari-Carmen, Viña Jose, Hellsten Ylva
Department of Nutrition, Exercise, and Sports, University of Copenhagen, DK-2100 Copenhagen Ø, Denmark; Copenhagen Muscle Research Centre and University of Southern Denmark, Copenhagen, Denmark.
Copenhagen Muscle Research Centre and University of Southern Denmark, Copenhagen, Denmark; Department of Cardiovascular and Renal Research, University of Southern Denmark, Copenhagen, Denmark.
Free Radic Biol Med. 2014 Aug;73:166-73. doi: 10.1016/j.freeradbiomed.2014.05.008. Epub 2014 May 22.
Reactive oxygen species (ROS) are important signaling molecules with regulatory functions, and in young and adult organisms, the formation of ROS is increased during skeletal muscle contractions. However, ROS can be deleterious to cells when not sufficiently counterbalanced by the antioxidant system. Aging is associated with accumulation of oxidative damage to lipids, DNA, and proteins. Given the pro-oxidant effect of skeletal muscle contractions, this effect of age could be a result of excessive ROS formation. We evaluated the effect of acute exercise on changes in blood redox state across the leg of young (23 ± 1 years) and older (66 ± 2 years) sedentary humans by measuring the whole blood concentration of the reduced (GSH) and oxidized (GSSG) forms of the antioxidant glutathione. To assess the role of physical activity, lifelong physically active older subjects (62 ± 2 years) were included. Exercise increased the venous concentration of GSSG in an intensity-dependent manner in young sedentary subjects, suggesting an exercise-induced increase in ROS formation. In contrast, venous GSSG levels remained unaltered during exercise in the older sedentary and active groups despite a higher skeletal muscle expression of the superoxide-generating enzyme NADPH oxidase. Arterial concentration of GSH and expression of antioxidant enzymes in skeletal muscle of older active subjects were increased. The potential impairment in exercise-induced ROS formation may be an important mechanism underlying skeletal muscle and vascular dysfunction with sedentary aging. Lifelong physical activity upregulates antioxidant systems, which may be one of the mechanisms underlying the lack of exercise-induced increase in GSSG.
活性氧（ROS）是具有调节功能的重要信号分子，在幼年和成年生物体中，骨骼肌收缩期间ROS的生成会增加。然而，当抗氧化系统无法充分抵消ROS时，ROS会对细胞产生有害影响。衰老与脂质、DNA和蛋白质的氧化损伤积累有关。鉴于骨骼肌收缩的促氧化作用，年龄的这种影响可能是ROS生成过多的结果。我们通过测量抗氧化剂谷胱甘肽还原型（GSH）和氧化型（GSSG）的全血浓度，评估了急性运动对久坐不动的年轻人（23±1岁）和老年人（66±2岁）腿部血液氧化还原状态变化的影响。为了评估体育活动的作用，纳入了终身进行体育活动的老年受试者（62±2岁）。运动以强度依赖的方式增加了久坐不动的年轻受试者静脉血中GSSG的浓度，表明运动诱导ROS生成增加。相比之下，尽管超氧化物生成酶NADPH氧化酶在老年久坐和活跃组的骨骼肌中表达较高，但运动期间静脉血GSSG水平保持不变。老年活跃受试者动脉血中GSH的浓度和骨骼肌中抗氧化酶的表达增加。运动诱导ROS生成的潜在损害可能是久坐衰老导致骨骼肌和血管功能障碍的重要机制。终身体育活动上调抗氧化系统，这可能是缺乏运动诱导GSSG增加的机制之一。
