EFFECTS OF ANTIOXIDANTS AND AGE ON OXUGEN STRESS BY VIGOROUS EXERCISE

我们研究了抗氧化功能的运动反应，通过使用动物和人类。在动物实验中。游泳运动后90 min，大鼠血浆和骨骼肌中脂质过氧化物水平升高，1 d后血浆维生素C水平降低。一次下坡跑可引起大鼠血浆CPK活性升高，血浆脂质过氧化物水平升高，48 h后CPK活性虽恢复至静息水平，但血浆抗氧化维生素水平仍低于运动前水平。我们评估了受过训练和未经训练的男性在一次或多次剧烈运动中引起的DNA损伤。淋巴细胞中自发的DNA损伤在训练和未训练的人中直到一轮剧烈跑步后30分钟才增加。训练组受试者静息状态下淋巴细胞自发性DNA损伤和血浆CPK活性明显高于对照组。自发性DNA损伤与血浆CPK活性呈显著正相关，提示大负荷运动可引起淋巴细胞DNA氧化损伤，并可能与肌肉损伤密切相关。此外，经过良好训练的吸烟者补充足够的抗氧化维生素（维生素C：200- 290 mg/d，维生素E：7- 12 mg/d），血浆维生素维持在正常范围内（维生素C：1.1mg/dl，维生素E：11- 12 ug/ml）。这些研究表明，可能需要足够的抗氧化维生素来保护运动引起的氧化损伤。

We studied antioxidative function in response to exercise by using animal and humans. In animal studies. we observed increased level of lipid peroxide in plasma and skeletal muscle after 90-min swimming exercise, and lower level of plasma vitamin C was observed rats one day after swimming. One bout of down-hill running in rats induced higher increase of plasma CPK activity with higher level of plasma lipid peroxide, and although plasma CPK activity returned to the resting level 48 hr after tunning, plasma antiocidant vitamines remained to the lower level compared with pre-exercise state. We evaluated DNA damage induced by one bout or repeated bouts of vigorous exercise in trained and untrained men. Spontaneous DNA damage in lymphocytes did not increase until 30 min after one bout of vigorous running in both trained and untrained men. The trained subjects had higher spontaneous DNA damage in lymphocytes and higher plasma CPK activity at the resting stale. The spontaneous DNA damage showed significant posotive correlation with plasma CPK activity, indicating that oxidative DNA damage in lymphocytes could be occured by extensive exercise, and might be closely associated with muscle damage. In addition, well-trained smimmers who had adequate antioxidative vitamins (vitamin C : 200-290mg/day, vitamin E : 7-12mg/day) maintained in the normal range of plasma vitamins (vitamin C : 1.1mg/dl, vitamin E : 11-12ug/ml). These studies suggest that adequate intke of antioxidative vitamins might be required for protecting oxidative damage induced by exercise.