Intravascular hemolysis is one of the most emphasized mechanisms for destruction of erythrocytes during and after physical activity. Exercise-induced oxidative stress has been proposed among the different factors for explaining exercise-induced hemolysis. The validity of oxidative stress following exhaustive cycling exercise on erythrocyte damage was investigated in sedentary and trained subjects before and after antioxidant vitamin treatment (A, C, and E) for 2 mo. Exercise induced a significant increase in thiobarbituric acid-reactive substance and protein carbonyl content levels in sedentary subjects and resulted in an increase of osmotic fragility and decrease in deformability of erythrocytes, accompanied by signs for intravascular hemolysis (increase in plasma hemoglobin concentration and decrease in haptoglobulin levels). Administration of antioxidant vitamins for 2 mo prevented exercise-induced oxidative stress (thiobarbituric acid-reactive substance, protein carbonyl content) and deleterious effects of exhaustive exercise on erythrocytes in sedentary subjects. Trained subjects' erythrocyte responses to exercise were different from those of sedentary subjects before antioxidant vitamin treatment. Osmotic fragility and deformability of erythrocytes, plasma hemoglobin concentration, and haptoglobulin levels were not changed after exercise, although the increased oxidative stress was observed in trained subjects. After antioxidant vitamin treatment, functional and structural parameters of erythrocytes were not altered in the trained group, but exercise-induced oxidative stress was prevented. Increased percentage of young erythrocyte populations was determined in trained subjects by density separation of erythrocytes. These findings suggest that the exercise-induced oxidative stress may contribute to exercise-induced hemolysis in sedentary humans.

We concluded that although six months training results improvement in P3 latency, vitamin E supplementation does not affect cognitive function evaluated by event-related potentials in older subjects.

ABSTRACT.Purpose: The aim of the study was to investigate the effects of vitamin E on stress-induced changes in visual evoked potentials (VEPs) and lipid peroxidation. Methods: Eight experimental groups of 10 rats per group were formed. These consisted of the control group (C); the group treated with vitamin E (E); groups exposed to cold stress (CS), immobilization stress (IS) and both cold and immobilization stress (CIS), and groups exposed to equivalent stresses and treated with vitamin E (CSE, ISE, CISE). Vitamin E was injected intramuscularly in a dose of 30 mg/kg/day. Results: Following chronic stress (15 days), plasma corticosterone concentrations in all experimental groups were significantly increased over those in C group. Vitamin E significantly decreased corticosterone levels in all stress groups compared with their respective control groups. Brain nitrite levels were significantly more elevated in all stress groups than in the C group. Vitamin E reduced retina and brain nitrite levels in all stress and E groups compared with their respective control groups. Vitamin E decreased glutathione peroxidase (GSH-Px) activity in retina and brain tissues in the CSE group, but increased it in the ISE group compared with their respective control groups. Lipid peroxidation was increased in brain and retina tissues in all stress groups as indicated by the significant increase in thiobarbituric acid-reactive substance (TBARS) levels with respect to the C group. Vitamin E produced a significant decrease in brain and retina TBARS levels in all stress groups with respect to their corresponding control groups. The mean latencies of P 1 , N 1 , P 2 , N 2 and P 3 components were significantly prolonged in all stress groups compared with the C group. Conclusion: Vitamin E returned the VEP latencies in the stress groups to control values. Our findings clearly indicated that vitamin E has the potential to prevent VEP changes caused by stress.

Visual evoked potentials (VEP) can be used as an objective non-invasive method to study the electrical activity of the visual system. Latency and amplitude measurements of VEP demonstrated that diabetes mellitus has been associated with increases in the latencies whereas the amplitude measurements revealed contradictory results. Although physical exercise has been reported to reduce the complications of diabetes mellitus, the effect of exercise on the visual system remains unknown. We investigated the effects of long-term moderate physical exercise on VEP in streptozotocin (STZ)-diabetic rats. We also measured brain thiobarbituric acid-reactive substances (TBARS) to explore the possible contribution of lipid peroxidation on the visual system. Animals were divided into four groups: control (C), control exercise (CE), diabetic (D) and diabetic exercise (DE) groups. Diabetes was induced by a single intraperitoneal injection of STZ (60 mg/kg). Three days after the confi rmation of diabetes, DE and CE groups were trained by running on a motor-driven treadmill with a progressive eightweek programme. The animals began running at 10 m/min, 0° slope, 10 min/day and reached a level of 28 m/min, 6° slope, 60 min/day by week 8. TBARS were elevated and VEP latencies were delayed in diabetic rats, indicating diabetes-induced defects in the optic pathway. These prolonged latencies were restored by exercise training. VEP amplitudes of the DE group were found unaltered with the exception of a decrement in P 2 N 2 which represents an early component of VEP, suggesting that exercise improves visual system defects in diabetic animals at different levels of the optic pathway. diabetes mellitus; visual evoked potentials; exercise; lipid peroxidation; rat © 2007 Tohoku University Medical PressPhysical exercise is well known to have many benefi cial effects on human health. Recently, attention has largely focused on the increase of free radicals generated during exercise, especially during aerobic activities. This increase is related to the elevation of electron transport fl ux, mitochondrial oxygen consumption, energy demand, oxygen supply and body

Six months of vitamin E supplementation has no additive effect beyond that of aerobic training on indices of physical performance and body composition in older sedentary adults.