摘要
本文研究急性运动后糖皮质激素(GC)分泌增多对大鼠心、肾细胞糖皮质激素受体(GR)及Na^+-K^+-ATP 酶的影响,结果表明,无负荷游泳后造成 GR 的适度减少,伴有对 Na^+-K^+-ATP 酶的诱导加强,其发生可分别被 Trilostane 和 RU_(A86)抑制;6%体重负荷游泳1h 后,出现 GR 过度减少并伴有血浆 GC 对靶细胞 Na^+-K^+-ATP 酶诱导抑制,提示靶细胞对 GC 抵抗。本文提出运动时 GR 过度下降是限制机体运动能力的一个重要因素。
The purpose of this study was to determine the effects of exerccise-induced elevated glucecorticoid(GC)on the gluco-corticoid receptor(GR)on Na-K-ATPase of the kidneys and hearts in rats and to identify the correlation between the specif-ic binding of GR and the level of Na-K-ATPase activity,Male adult rats were randomly divided into three groups:1)controlgroup,2)moderate exercise group(Swimming without extra load for 60min),and 3)heavy exercise group(Swimming withan extra load equivalent to 6% of bodyweight for 60min).After exercise the rats were decapitated at intervals of 15min.3hr,12 hr and 24 hr and the plasma corticosterone(B),GR in cytosol and Na-K-ATPase activity of the heart and kidneyswere determined.The results showed that the Na-K-ATPase induced 15min,3hr and 12hr after exercise in the heavy exer-cise group was obviously lower than that in the control group,but it was much higher in the moderate exerccise group thanin the other two groups,though the plasma B of the heavy exerccise group was also very high.These results suggest a low-ered inducibility of Na-K-ATPase by the exercise-induced elevated glococorticoid hormone,or a decreased reactivity of thetarget cells to go in the heavy exercise group.The binding capacity of the GR was also much lower in the heavy exercisegroup 15min,3hr and 12hr after exercise.Nevertheless,the GC-induced stimmulation of Na-K-ATPasc in the moderate ex-ercise group could be eliminated by subcutaneous injection of trilostane(40mg/kg)before exercise,whereas injection oftrilostane(40mg/kg)and RU486(20mg/kg)effect.These results indicate that the decreased reactivity of target cells to GCwas caused by the decrease in GR;which may lead to fatigue.
出处
《体育科学》
CSSCI
北大核心
1993年第2期51-54,共4页
China Sport Science
关键词
运动生理
糖皮质激素
ATP酶
exercise,glucocorticoid,gluccocorticoid receptor,Na-K-ATPase.