Ping Zheng, Qiu Weijia, Yang Mei, Zhang Xiaoli, Wang Dongying, Xu Peng, Wang Ziwen, Cao Xuebin
Department of Cardiology and Nephrology, Hospital of the 82nd Group Army of PLA, Baoding, 071000, China.
Sports Med Health Sci. 2021 Nov 1;3(4):218-227. doi: 10.1016/j.smhs.2021.10.006. eCollection 2021 Dec.
This study was to optimize the exercise preconditioning (EP) intensity in protecting from exhaustive exercise-induced cardiac injury (EECI). A total of 98 male Sprague-Dawley rats were divided into 7 groups ( = 14): the control group (C), the exhaustive exercise group (EE) and the EP + EE groups, which include the V10 (53.0%˙O), V15 (58.4%˙O), V20 (67.0%˙O), V26 (74.0%˙O) and V30 (80.0%˙O) groups. Except the C group, the other groups were subjected to treadmill running. The serum contents of N terminal pro B type natriuretic peptide (NT-proBNP) and cardiac troponin I (cTn-I) were detected by the enzyme-linked immunosorbent assay method, ECG was recorded, heart function was detected by pressure volume catheter and the activities of mitochondrial electron transfer pathway (ET pathway) complexes I, Ⅱ and IV were measured by high-resolution respiration instrument. Compared to the EE group, the EP groups have shown decrease of NT-proBNP and cTn-I, improvement of mitochondrial respiratory function and cardiac function. Compared to other EP groups, the V26 group has shown significant decrease of myocardial enzymes and improvement of mitochondrial function. The correlation analysis showed the EP effect was proportional to EP intensity in the range of 53.0%˙O-74.0%˙O. High intensity and long duration of exhaustive exercise caused cardiac injury and EP could decrease serum level of NT-proBNP and cTn-I, improve electrical derangement and the left ventricular function, and raise the activities of ET pathway complexes I, Ⅱ and IV. The protection of EP on EECI was improved as the EP intensity was increased from 53.0%˙O to 74.0%˙O and when EP intensity was 74.0%˙O, the effect was the most obvious among all the setting EP groups.
本研究旨在优化运动预处理(EP)强度,以预防力竭运动诱导的心脏损伤(EECI)。将98只雄性Sprague-Dawley大鼠分为7组(每组n = 14):对照组(C)、力竭运动组(EE)和EP + EE组,其中EP + EE组包括V10(53.0%VO₂)、V15(58.4%VO₂)、V20(67.0%VO₂)、V26(74.0%VO₂)和V30(80.0%VO₂)组。除C组外,其他组均进行跑步机跑步。采用酶联免疫吸附测定法检测血清N末端B型利钠肽原(NT-proBNP)和心肌肌钙蛋白I(cTn-I)含量,记录心电图,用压力容积导管检测心功能,并用高分辨率呼吸仪测量线粒体电子传递途径(ET途径)复合体I、Ⅱ和IV的活性。与EE组相比,EP组的NT-proBNP和cTn-I降低,线粒体呼吸功能和心功能得到改善。与其他EP组相比,V26组的心肌酶显著降低,线粒体功能得到改善。相关性分析表明,在53.0%VO₂-74. %VO₂范围内,EP效果与EP强度成正比。高强度和长时间的力竭运动导致心脏损伤,而EP可降低血清NT-proBNP和cTn-I水平,改善电紊乱和左心室功能,并提高ET途径复合体I、Ⅱ和IV的活性。随着EP强度从53.0%VO₂增加到74.0%VO₂,EP对EECI的保护作用增强,当EP强度为74.0%VO₂时,在所有设定的EP组中效果最明显。