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作 者:王增喜[1] 李洁[1] 王悦 Wang Zengxi;Li Jie;Wang Yue(College of Physical Education, Northwest Normal University, Lanzhou 730070, China;Cansu Police Vocational College, Lanzhou, 730046, China)
机构地区:[1]西北师范大学体育学院,兰州730070 [2]甘肃警察职业学院,兰州730046
出 处:《中国运动医学杂志》2018年第4期315-322,共8页Chinese Journal of Sports Medicine
摘 要:目的:探讨长期高强度间歇训练(HIIT)诱导大鼠心肌肥大过程中心功能以及线粒体呼吸链活性的变化。方法:将90只健康Wistar大鼠随机分为HIIT组、持续中等强度训练(MICT)组和安静对照组(RC),每组按照观察时间点(2周、6周和10周)再分为3个亚组,共9组,每组10只。实验结束后利用超声心动图检测大鼠心功能,称量体重和心脏重量,心肌匀浆后用差速离心法提取心肌线粒体,分别测定心肌和线粒体柠檬酸合酶(CS)活性、呼吸链复合体Ⅰ~Ⅳ(CⅠ~Ⅳ)活性以及心肌过氧化物酶体增生物激活受体1α(PGC-1α)、α-肌球蛋白重链(α-MHC)、β-MHC、心钠素(ANF)和脑钠素(BNP)蛋白表达量。结果:HIIT组、MICT组大鼠分别于第2~10周和第10周出现心肌肥大。第2周和10周时,各组心功能、呼吸链复合体活性以及各蛋白表达量均无显著性差异(P>0.05)。第6周时,HIIT组左心室射血分数(LVEF)、左心室缩短分数(LVFS)、心肌α-MHC蛋白表达量以及呼吸链复合体CⅠ、CⅢ、CⅣ活性低于RC组和MICT组(P<0.05),心肌β-MHC和BNP表达量则高于RC组和MICT组(P<0.05)。结论:长期HIIT(而非MICT)能够诱导大鼠暂时性病理性心肌肥大以及心功能下降,其机制可能与心肌线粒体呼吸链复合体活性下调有关。Objective To explore the heart function and activity of the mitochondrial respiratorychain complex of rats with myocardial hypertrophy induced by the long-term high-intensity intervaltraining(HIIT). Methods Ninety Wistar rats were randomly divided into an HIIT group,a moderate in-tensity continuous training(MICT) group and a rest control(RC) group,with each group allocated threesubgroups according to the observation time(2,6 and 10 weeks),9 groups altogether(n=10 in eachgroup). Each group was given intervention as their names implied. Then,the heart function was mea-sured using the ultrasoundcardiogram,and the body weight as well as the weight of the heart wasweighted. The myocardium mitochondria were extracted using the differential centrifugation after homoge-nation to detect the activity of the myocardial and mitochondrial citrate synthase(CS),the activities ofthe respiratory chain complex CⅠ~CⅣ as well as myocardial protein expression of peroxisome prolifera-tor-activated receptor gamma coactivator 1α(PGC-1α),α-myosin heavy chain(α-MHC),β-MHC,atrialnatriuretic factor(ANF) and brain natriuretic peptide(BNP). Results The myocardial hypertrophy wasfound in HIIT and MICT groups after 1-week and 9-week intervention respectively. At the 2 nd and10 th week,no significant differences were found in the heart function,respiratory chain complex activityand protein expression of all three groups(P〉0.05). At the 6 th week,the left ventricular ejection frac-tion,left ventricular fractional shortening,myocardial α-MHC protein expression,and the activities of re-spiratory chain complex CⅠ,CⅢ and CⅣof HIIT group were significantly lower while the myocardialβ-MHC and BNP protein expression were significantly higher than those of RC and MICT groups(P〈0.05). Conclusion Long-term HIIT but not MICT can induce temporarily pathological myocardial hyper-trophy and reduced heart function in Wistar rats,and the mechanism might be related to the downregu-lation of the
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