高原缺氧负重训练动脉供血调控促进模型

Model of Artery Blood-supply Regulation and Promotion Under Plateau Hypoxia Weight Training

目的:研究磷酸化活对高原缺氧负重训练动脉供血调控促进模型,促进运动员的心肺功能,提高运动员的供血调控水平。方法:通过高原缺氧负重训练,产生大量的磷酸化活物,人体中的磷酸化活物重组质粒p ET-28a-Agr C在C43(DE3)中表达为末端苏氨酸物体,通过提取人体内的血液标本,进行样本测试,对采集的运动员血液样本进行蛋白脂质体先用膜不可渗透硫醇-非荧光试剂(4-acetamido-4'-maleidylstibene-2,2'-disulphonic acid,Amdi S)标记,得到采用磷酸化活测定分析高原缺氧负重训练下的动脉供血调控促进模型结构。结果:运动员心率HR和肺活量VC显著性差异P<0.01,缺氧负重训练中最大摄氧量VO2max的值都要大于台阶实验数值,达到最大摄氧量VO2max,心率HR的显著性差异P<0.01。得到的测试组TG的心肺功能由于对比组CG1和CG2的显著差异性,进而促进动脉供血调控。结论:采用磷酸化活测定方法对高原缺氧负重训练动脉供血调控促进模型进行分析建模,对促进运动员的心肺功能,提高运动员的供血调控水平具有帮助。

Objective： To study the phosphorylation of living on plateau hypoxia weight training artery regulation to promote the model, promote the athlete＇s heart and lung function, improve blood supply to control the level of athletes. Methods： The plateau hypoxia weight training, the phosphorylation of living large, the body of the phosphorylation of recombinant plasmid p ET-28a-Agr C in C43 was（DE3） expression in terminal threonine objects, through the blood samples from the human body, sample test, the acquisition of the athletes blood samples for protein liposome impermeable thiol non fluorescent reagent in the first film（4-acetamido-4＇-maleidylstibene-2, 2＇-disulphonic acid, Amdi S） marker, obtained by phosphorylation activity analysis of arterial blood supply regulation under hypoxia weight training to promote the model structure is obtained. Results： The heart rate and vital capacity of athletes HR VC significant difference in P0.01, the test group TG received cardiopulmonary function because of the significant differences between group CG1 and CG2., and then promote the arterial blood supply regulation. Conclusion： The method to measure living by phosphorylation analysis of plateau hypoxia weight training artery regulation to promote the model, to promote the athlete＇s heart and lung function, improve blood supply can help control the level of athletes.