Masao Sakurai

Effect of repeated exercise on urinary 8-hydroxy-deoxyguanosine excretion in humans.

The purpose of this study was to investigate the effect of repeated exercise on oxidative damage to DNA in 10 well trained long distance runners who participated in an 8-day training camp. The average running distance during the camp was 30 +/- 3 km/day. The amount of urinary 8-hydroxy-deoxyguanosine (8-OHdG) excretion was used to estimate the oxidative DNA damage. Urine samples were collected for both a 3-day control period as well as throughout the camp. Blood samples were drawn after overnight fasting both before and after the camp. Urinary 8-OHdG excretion was significantly increased during the camp compared to the control period (265.7 +/- 75.5 vs. 335.6 +/- 107.4 pmol/kg/day, P < 0.05). The content of 8-OHdG in the lymphocyte DNA on the day after finishing the camp did not differ from that before the camp. Plasma TBARS, LDH, CK, CK-MB, and myoglobin significantly rose after the camp (P < 0.05). The plasma beta-carotene levels tended to rise after the camp, while the plasma alpha-tocopherol levels increased significantly after the camp (P < 0.05). These results indicate that repeated exercise augments oxidative stress and the DNA is also injured by exercise-induced reactive oxygen species. However, the oxidative damage to DNA is not accumulated by consecutive exercise, although it is sustained as long as the exercise is repeated.

EFFECT OF A SINGLE BOUT OF EXERCISE AND BETA -CAROTENE SUPPLEMENTATION ON THE URINARY EXCRETION OF 8-HYDROXY-DEOXYGUANOSINE IN HUMANS

We investigated the effects of acute exhaustive exercise and beta-carotene supplementation on urinary 8-hydroxy-deoxyguanosine (8-OHdG) excretion in healthy nonsmoking men. Fourteen untrained male (19-22 years old) volunteers participated in a double blind design. The subjects were randomly assigned to either the beta-carotene or placebo supplement group. Eight subjects were given 30 mg of beta-carotene per day for 1 month, while six subjects were given a placebo for the same period. All subjects performed incremental exercise to exhaustion on a bicycle ergometer both before and after the 1-month beta-carotene supplementation period. The blood lactate and pyruvate concentrations significantly increased immediately after exercise in both groups. The baseline plasma beta-carotene concentration was significantly 17-fold higher after beta-carotene supplementation. The plasma beta-carotene decreased immediately after both trials of exercise, suggesting that beta-carotene may contribute to the protection of the increasing oxidative stress during exercise. Both plasma hypoxanthine and xanthine increased immediately after exercise before and after supplementation. This thus suggests that both trials of exercise might enhance the oxidative stress. The 24-h urinary excretion of 8-OHdG was unchanged for 3 days after exercise before and after supplementation in both groups. However, the baseline urinary excretion of 8-OHdG before exercise tended to be lower after beta-carotene supplementation. These results thus suggest that a single bout of incremental exercise does not induce the oxidative DNA damage, while beta-carotene supplementation may attenuate it.

No influence of a single bout of exercise on urinary excretion of 8‐hydroxy‐deoxyguanosine in humans

We investigated the effect of a single bout of intensive exercise on the excretion of 8‐hydroxy‐deoxyguanosine in the 24 h urine from healthy non‐smokers. We studied three exercise tests in Experiment 1; which consisted of incremental exercise to exhaustion on a treadmill in eleven male long distance runners. Experiment 2; which comprised incremental exercise until reaching exhaustion on abicycle ergometer in six male untrained subjects. Experiment 3; which consisted of a 20 km run by eleven male long distance runners. No differences in the urinary 8‐hydroxy‐deoxyguanosine excretion were obselwed from days 1 or 3 after each respective exercise regimen. However, significant increases in the plasma creatine kinase activity were observed at 24 h or 48 h after exercise, except for Experiment 2. Our results thus suggest that the oxidative stress during a single bout of intensive exercise does not result in an accumulation of oxidative DNA damage.

Effect of endurance exercise on the tissue 8-hydroxy-deoxyguanosine content in dogs.

The purpose of this study was to investigate the effect of endurance exercise on both the tissue and lymphocyte 8-hydroxy-deoxyguanosine (8-OHdG) content. Six dogs ran on a treadmill for 7 hours. Another six dogs were assigned to a sedentary control group. The exercised dogs were sacrificed immediately after exercise and the counterpart of the sedentary group was also sacrificed at the same time. The brain, lung, liver, spleen, kidney, jejunum, colon, diaphragm, heart, splenius muscle, and the medial and lateral portion of gastrocnemius muscle samples were then collected. Lymphocytes were sampled before and after exercise in the exercised dogs. The 8-OHdG content of lymphocyte DNA was found to significantly decrease after exercise (0.57 +/- 0.19 vs 0.33 +/- 0.10/deoxyguanosine (dG) x 10(5), P < 0.05). The colon was the only tissue which showed a significant decrease in the content (0.83 +/- 0.24 vs 0.54 +/- 0.15/dG x 10(5), P < 0.05). No tissue except for the colon showed any significant changes after exercise. These results therefore indicate that, immediately after endurance exercise, an augmented repair mechanism might thus play a role in the decrease of 8-OHdG in the lymphocytes and the colon, while the 8-OHdG generation might be counterbalanced by its repair in other tissues.

Thermal Stress and Water Supplementation

Thermoregulatory responses induce dehydration, and dehydration itself raises body temperature, causing an increase in the threshold temperature for cutaneous vasodilation and sweating, especially during exercise in a hot environment. Heat-induced dehydration triggers regulatory responses maintaining blood volume and circulatory function, including a fluid shift between body fluid compartments and circulatory adjustment, but full recovery from thermal dehydration is only possible with sufficient water intake. During rehydration from heat-induced dehydration, a delay in rehydration by spontaneous drinking is observed that is defined as involuntary dehydration. Evidence showing the importance of the osmotic regulation of body fluid to prevent involuntary dehydration and also the effect of solute content on the time course of blood volume recovery are presented.