Delchev Slavi D, Georgieva Katerina N, Koeva Yvetta A, Atanassova Pepa K
Department of Anatomy, Histology and Embryology, Medical University, Plovdiv, Bulgaria.
Folia Med (Plovdiv). 2006;48(2):50-6.
Mitochondria are an active and continuous source of reactive oxygen species (ROS) during respiration. The ROS increased production during endurance training is a result of an augmented electron transport through the respiratory chains, making in this way the mitochondria a potential target for oxidative damage. The Bcl-2 protein family plays a central role in the transition of apoptotic signals towards the mitochondria in stress-induced apoptosis.
The present work studied the effect of endurance training on the expression of the apoptotic proteins Bcl-2 and Bax in rat cardiomyocytes, as well as the concomitant changes in the ultrastructure of the mitochondria and activity of some enzymes residing there.
Two groups of male Wistar rats were used. One was the control and the other was trained on treadmill with submaximal loading for eight weeks. At the end of the trial, samples of the myocardium of all the experimental animals were obtained. Immunohistochemical reactions for Bcl-2 and Bax and enzymehistochemical reactions for succinate dehydrogenase and NADH2-cytochrome C-reductase were done. The results were analyzed using specialized software. Transmission electron microscopical study was carried out too.
In the myocardium of the trained animals the expression of Bcl-2 and Bcl-2/Bax ratio were significantly higher compared to the controls. The mitochondria had intact outer and inner membranes, with no signs of swelling. Mitochondria with denser packed cristae were found predominantly. No significant differences were found in the activity of the investigated enzymes in the cardiomyocytes of the animals from both groups.
In the myocardium of the experimental animals endurance training for eight weeks does not lead to activation of apoptotic processes via the mitochondrial pathway. This type of exercise training could be used for cardioprotection in order to elevate apoptotic threshold of cardiomyocytes.
线粒体是呼吸过程中活性氧（ROS）的活跃且持续的来源。耐力训练期间ROS产生增加是呼吸链中电子传递增强的结果，从而使线粒体成为氧化损伤的潜在靶点。Bcl-2蛋白家族在应激诱导的细胞凋亡中凋亡信号向线粒体的转变中起核心作用。
本研究探讨耐力训练对大鼠心肌细胞凋亡蛋白Bcl-2和Bax表达的影响，以及线粒体超微结构和线粒体中某些酶活性的相应变化。
使用两组雄性Wistar大鼠。一组为对照组，另一组在跑步机上进行次最大负荷训练八周。试验结束时，获取所有实验动物的心肌样本。进行Bcl-2和Bax的免疫组织化学反应以及琥珀酸脱氢酶和NADH2-细胞色素C还原酶的酶组织化学反应。使用专业软件分析结果。还进行了透射电子显微镜研究。
与对照组相比，训练动物心肌中Bcl-2的表达及Bcl-2/Bax比值显著更高。线粒体的外膜和内膜完整，无肿胀迹象。主要发现嵴排列更紧密的线粒体。两组动物心肌细胞中所研究酶的活性未发现显著差异。
在实验动物的心肌中，八周的耐力训练不会通过线粒体途径导致凋亡过程的激活。这种类型的运动训练可用于心脏保护，以提高心肌细胞的凋亡阈值。
