OBJECTIVESIn addition to having health-promoting effects, exercise is considered to induce oxidative stress. To clarify whether increased oxygen consumption during exercise induces oxidative stress, we investigated the effects of aerobic exercise and anaerobic exercise on a series of oxidative damage markers.

METHODSOne group of subjects performed aerobic exercise and another group performed anaerobic exercise with similar workloads, but with different levels of oxygen consumption. Blood and urine samples were collected before, immediately after, and 3, 9, and 24 h after exercise. Serum uric acid (UA) and creatine phosphokinase were evaluated. As markers of oxidative damage to lipids, proteins and DNA, we evaluated serum 4-hydroxy-2-nonenal, urinary F(2)-isoprostanes, serum protein carbonyls, and leukocyte 8-hydroxydeoxyguanosine.

RESULTSOxygen consumption was significantly greater during aerobic exercise. Although UA level increased immediately after aerobic exercise and decreased thereafter, UA level did not change after anaerobic exercise. The two types of exercise had significantly different effects on the change in UA level. After anaerobic exercise, the levels of 8-hydroxydeoxyguanosine and 4-hydroxy-2-nonenal significantly increased at 24 h and 3 h, respectively. The levels of creatine phosphokinase and F(2)-isoprostanes decreased after exercise. The two types of exercise caused no apparent significant differences in the levels of these biomarkers.

CONCLUSIONThe findings suggest that similar workloads of anaerobic exercise and aerobic exercise induce reactive oxygen species (ROS) differently: aerobic exercise seems to initially generate more ROS, whereas anaerobic exercise may induce prolonged ROS generation. Although more oxygen was consumed during aerobic exercise, the generated ROS did not induce significant oxidative damage. Oxygen consumption per se may not be the major cause of exercise-induced oxidative damage.

The aim of the present study was to evaluate the plaque components and the predictors of thin-cap fibroatheroma (TCFA) in anemic patients with acute coronary syndrome using virtual histology-intravascular ultrasound (VH-IVUS). Anemia was defined according to criteria of the World Health Organization, (i.e. , hemoglobin levels < 13 g/dL in men and < 12 g/dL in women) and we compared VH-IVUS findings between anemia group (171 patients, 260 lesions) and non-anemia group (569 patients, 881 lesions). Anemia group had greater % necrotic core (NC) volume (21% +/- 9% vs 19% +/- 9%, P = 0.001) compared with non-anemia group. Hemoglobin level correlated negatively with absolute NC volume (r = -0.235, P < 0.001) and %NC volume (r = -0.209, P < 0.001). Independent predictors of TCFA by multivariate analysis were diabetes mellitus (odds ratio [OR], 2.213; 95% confidence interval [CI], 1.403-3.612, P = 0.006), high-sensitivity C-reactive protein (OR, 1.143; 95% CI, 1.058-1.304, P = 0.012), microalbuminuria (albumin levels of 30 to 300 mg/g of creatinine) (OR, 2.124; 95% CI, 1.041-3.214, P = 0.018), and anemia (OR: 2.112; 95% CI 1.022-3.208, P = 0.028). VH-IVUS analysis demonstrates that anemia at the time of clinical presentation is associated with vulnerable plaque component in patients with acute coronary syndrome.
Acute Coronary Syndrome/complications/*pathology/ultrasonography ; Aged ; Albuminuria/urine ; Anemia/complications/*diagnosis ; C-Reactive Protein/analysis ; Coronary Angiography ; Creatinine/blood ; Diabetes Complications ; Female ; Hemoglobins/analysis ; Humans ; Male ; Middle Aged ; Necrosis/pathology ; Odds Ratio ; Plaque, Atherosclerotic/*ultrasonography ; Predictive Value of Tests ; *Ultrasonography, Interventional