The complexity of human DNA has been affected by aerobic metabolism, including endurance exercise and oxygen toxicity. Aerobic endurance exercise could play an important role in the evolution of Homo sapiens, and oxygen was not important just for survival, but it was crucial to redox-mediated adaptation. The metabolic challenge during physical exercise results in an elevated generation of reactive oxygen species (ROS) that are important modulators of muscle contraction, antioxidant protection, and oxidative damage repair, which at moderate levels generate physiological responses. Several factors of mitochondrial biogenesis, such as peroxisome proliferator-activated receptor-c coactivator 1a (PGC-1a), mitogen-activated protein kinase, and SIRT1, are modulated by exercise-associated changes in the redox milieu. PGC-1a activation could result in decreased oxidative challenge, either by upregulation of antioxidant enzymes and/or by an increased number of mitochondria that allows lower levels of respiratory activity for the same degree of ATP generation. Endogenous thiol antioxidants glutathione and thioredoxin are modulated with high oxygen consumption and ROS generation during physical exercise, controlling cellular function through redox-sensitive signaling and proteinprotein interactions. Endurance exercise-related angiogenesis, up to a significant degree, is regulated by ROSmediated activation of hypoxia-inducible factor 1a. Moreover, the exercise-associated ROS production could be important to DNA methylation and post-translation modifications of histone residues, which create heritable adaptive conditions based on epigenetic features of chromosomes. Accumulating data indicate that exercise with moderate intensity has systemic and complex health-promoting effects, which undoubtedly involve regulation of redox homeostasis and signaling. Antioxid. Redox Signal. 18, 1208Signal. 18, -1246

The aim of this study was to evaluate whether high-intensity endurance training would alleviate exercise-induced oxidative stress. Nine untrained male subjects (aged 19-21 years) participated in a 12-week training programme, and performed an acute period of exhausting exercise on a cycle ergometer before and after training. The training programme consisted of running at 80% maximal exercise heart rate for 60 min.day-1, 5 days.week-1 for 12 weeks. Blood samples were collected at rest and immediately after exhausting exercise for measurements of indices of oxidative stress, and antioxidant enzyme activities [superoxide dismutase (SOD), glutathione peroxidase (GPX), and catalase (CAT)] in the erythrocytes. Maximal oxygen uptake (VO2max) increased significantly (P < 0.001) after training, indicating an improvement in aerobic capacity. A period of exhausting exercise caused an increase (P < 0.01) in the ability to produce neutrophil superoxide anion (O2.-) both before and after endurance training, but the magnitude of the increase was smaller after training (P < 0.05). There was a significant increase in lipid peroxidation in the erythrocyte membrane, but not in oxidative protein, after exhausting exercise, however training attenuated this effect. At rest, SOD and GPX activities were increased after training. However, there was no evidence that exhausting exercise enhanced the levels of any antioxidant enzyme activity. The CAT activity was unchanged either by training or by exhausting exercise. These results indicate that high-intensity endurance training can elevate antioxidant enzyme activities in erythrocytes, and decrease neutrophil O2.- production in response to exhausting exercise. Furthermore, this up-regulation in antioxidant defences was accompanied by a reduction in exercise-induced lipid peroxidation in erythrocyte membrane.

No abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder affecting the elderly population. It is predicted that the incidence of AD will be increased in the future making this disease one of the greatest medical, social, and economic challenges for individuals, families, and the health care system worldwide. The etiology of AD is multifactorial. It features increased oxidative state and deposition of amyloid plaques and neurofibrillary tangles of protein tau in the central cortex and limbic system of the brain. Here we provide an overview of the positive impacts of exercise on this challenging disease. Regular physical activity increases the endurance of cells and tissues to oxidative stress, vascularization, energy metabolism, and neurotrophin synthesis, all important in neurogenesis, memory improvement, and brain plasticity. Although extensive studies are required to understand the mechanism, it is clear that physical exercise is beneficial in the prevention of AD and other age-associated neurodegenerative disorders.

The goal of this experiment was to examine contraction-mediated activation of superoxide dismutase (SOD) gene expression in rat superficial vastus lateralis (SVL, type IIb) and deep vastus lateralis (DVL, type IIa) muscles. Female Sprague-Dawley rats were randomly divided into exercise (E) and control (C) groups that were sacrificed at 0, 1, 2, 4, 10, 24, and 48 h (n=6) following an acute bout of treadmill exercise (25 m/min, 5% grade) to exhaustion (running time approximately equals 1 h). Nuclear factor-kappaB (NF-kappaB) in DVL and SVL showed maximal binding at 2 and 10 h respectively, and remained elevated. Activator protein-1 (AP-1) showed maximal binding at 1 h post-exercise, and returned to resting levels at 10 h in both muscles. Mn SOD mRNA abundance in the DVL was increased at 0 (P<0.01), 1, and 2 h (P<0.05) post-exercise, whereas Mn SOD protein was unchanged. In SVL, Mn SOD mRNA abundance was not altered by exercise, whereas Mn SOD protein content was increased at 10 (P<0.05) and 24 h (P<0.075) post-exercise. CuZn SOD mRNA was unchanged with exercise in DVL and SVL, but CuZn SOD protein was elevated 48 h after exercise in both DVL and SVL (P<0.01). Activities of Mn SOD, CuZn SOD and total SOD showed no change with exercise in either muscle examined. These findings indicate that an acute bout of exercise can increase binding of NF-kappaB and AP-1 in both SVL and DVL, which may stimulate Mn SOD mRNA transcription in the more oxidative type DVL muscle. The increased CuZn SOD protein contents seen post-exercise, without increases in mRNA abundance in both DVL and SVL, suggest a translational mechanism in this SOD isoform.