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首页> 外文期刊>Journal of exercise physiology online >Effects of Sprint Training on Glutathione Expression in Liver and Skeletal Muscle
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Effects of Sprint Training on Glutathione Expression in Liver and Skeletal Muscle

机译:短跑训练对肝脏和骨骼肌中谷胱甘肽表达的影响

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McCartney M, Keesee C, Fletcher L, Stover S. Effects of Sprint Training on Glutathione Expression in Liver and Skeletal Muscle. JEPonline 2011;14(5):66-74. 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 (mmol/g tissue) in the soleus and EDL decreased significantly, relative to their respective controls. At the same time, GSSG concentrations (mmol/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. Results of the study failed to demonstrate any change in liver glutathione after acute sprinting or sprint training. 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.
机译:McCartney M,Keesee C,Fletcher L,Stover S.短跑训练对肝脏和骨骼肌中谷胱甘肽表达的影响。 JEPonline 2011; 14(5):66-74。急性无氧运动可促进氧化应激。但是,以前的研究表明,高强度的短跑训练可以减弱氧化应激的影响。据推测,还原型谷胱甘肽(GSH)的上调负责保护与冲刺训练相关的氧化应激。 33只小鼠随机分为三组:对照组,急性和训练组。受过训练的小鼠参加了包括跑步机在内的高强度运动计划,跑步机每周运行两天,持续12周。在训练期结束时,训练有素的急性小鼠进行了一次强烈的冲刺。对照小鼠不运动。分光光度法测定比目鱼肌和趾长肌(EDL)肌肉以及肝脏中GSH和氧化型谷胱甘肽(GSSG)的浓度。急性运动后,比目鱼肌和EDL中的GSH浓度(mmol / g组织)相对于它们各自的对照明显降低。同时,两条肌肉中的GSSG浓度(mmol / g组织)显着增加。经过12周的短跑训练后,比目鱼肌和EDL中的GSH浓度与各自的对照组无显着差异,即使肌肉中的GSSG浓度显着增加。该研究结果未能证明急性冲刺或短跑训练后肝脏谷胱甘肽的任何变化。数据表明,由于进行了高强度的短跑训练,骨骼肌可以恢复GSH的控制水平。但是,上调的GSH似乎不是从肝脏输入的。

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