Acute anaerobic exercise promotes oxidative stress.However,previous studies indicate that high intensity sprint training can attenuate the effects of oxidative stress.It was hypothesized that an upregulation of reduced glutathione(GSH) is responsible for the protection against oxidative stress associated with sprint training.Thirty-three mice were randomly divided into three groups:control,acute and trained.Trained mice participated in a high intensity exercise program consisting of treadmill running two days a week for 12 weeks.At the end of the training period,trained and acute mice engaged in a single session of intense sprinting.Control mice did not exercise.Concentrations of GSH and oxidized glutathione(GSSG) were determined spectrophotometrically in the soleus and extensor digitorum longus(EDL) muscles,as well as the liver.Following acute exercise,GSH concentrations(mol/g tissue) in the soleus and EDL decreased significantly,relative to their respective controls.At the same time,GSSG concentrations(mol/g tissue) in both muscles increased significantly.After 12 weeks of sprint training,GSH concentrations in the soleus and EDL were not significantly different from their respective controls,even as GSSG concentrations in the muscles increased significantly.Data indicate that control levels of GSH can be recovered by skeletal muscle as a result of high intensity sprint training.However,the upregulated GSH does not appear to be imported from the liver.%急性无氧运动促进氧化应激。然而,之前的研究指出高强度短跑训练能减弱氧化应激效应。假设还原型谷胱甘肽（GSH）的上调在防护短跑训练中的氧化应激起重要作用。33只大鼠随机分为3组：对照组;急性运动组和训练组。训练组大鼠参与高强度训练,每周2天,共12周的跑台运动。在训练期结束,训练组和急性运动组大鼠进行一次高强度短跑。对照组大鼠不运动。用分光光度计测定比目鱼肌和趾长伸肌（EDL）以及肝脏的GSH和氧化型谷胱甘肽（GSSG）浓度。与对照组相比,急性运动后,比目鱼肌和EDL的GSH浓度显著下降,同时,两组肌肉中的GSSG浓度明显增加。12周短跑训练后,与对照组相比,两组肌肉中的GSH没有显著差异。同时肌肉中GSSG浓度显著增加。数据显示,由于高强度短跑导致骨骼肌恢复GSH水平。但是,不能说明GSH的上调是由肝脏输入的。
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