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为了进一步探讨运动心脏结构与功能的可复性问题及其与病理心脏的本质差异，通过实验动物模拟运动心脏，观察了停止运动训练8周后心脏重量和某些超微结构的变化，并应用激光扫描共聚焦显微镜与新一代钙荧光指示剂fluo－3／AM负载方法对。心肌活细胞内具有生物活性的游离钙的动态变化进行了研究。结果显示，经过12周耐力训练后，心肌活细胞内游离钙浓度静息值无显著性改变，心肌收缩时其游离钙浓度峰值较对照组显著增高11％（P＜0．05）；心肌细胞内心房特殊颗粒的体密度、面密度及数密度分别显著增高41％、12％及5％；心肌细胞线粒体体密度及其与肌原纤维比值分别显著增高60％和61％，线粒体内膜和嵴体积密度显著增高18％；心肌毛细血管与肌纤维的比值显著增高78％；心肌毛细血管腔体密度和面密度分别显著增高28％和13％。停止训练8周后，心肌收缩时其胞内游离钙浓度峰值较训练时显著降低14％（＜0．05）；心肌细胞内心房特殊颗粒的体密度显著降低25％；心肌细胞线粒体体密度及其与肌原纤维比值分别显著降低25％和36％，线粒体内膜和嵴体积密度显著降低11％；心肌毛细血管与肌纤维的比值分别显著降低29％。心肌毛细血管腔体密度和面密度分别显著降低14％和12％，基本恢复到正常对照水平。研究结果表明?
In order to further investigate the refolding of cardiac structure and function of exercise heart and its essential difference from pathological heart, the change of heart weight and some ultrastructures after 8 weeks’ training was observed by simulating exercise heart in experimental animals. Confocal Laser Scanning Confocal Microscopy with a New Generation of Fluorescent Indicator Fluo-3 / AM Loading Methods. Dynamic changes of biologically active free calcium in living heart cells were studied. The results showed that after 12 weeks of endurance training, the intracellular free calcium concentration in resting myocardial cells had no significant change, and the peak value of free calcium concentration was significantly increased by 11% (P <0.05); the myocardial cells The body density, surface density and number density of special inner atria were significantly increased by 41%, 12% and 5%, respectively. The mitochondrial body density and the ratio of myofibrils to myofibrils were significantly increased by 60% and 61%, respectively. The crest volume density increased significantly by 18%, the ratio of myocardial capillary to muscle fiber increased significantly by 78%, and the myocardial capillary density and areal density increased by 28% and 13% respectively. After 8 weeks of training, the peak of intracellular free calcium concentration in myocardial contraction decreased significantly by 14% (P <0.05); the density of atrial specific particles in myocardial cells decreased significantly by 25%; the mitochondrial body density of myocardial cells and The ratios of myofibrils to myofibrils were significantly reduced by 25% and 36%, respectively, and the bulk density of mitochondrial inner membrane and crest was significantly reduced by 11%. The ratio of myocardial capillary to muscle fiber was significantly reduced by 29%. Myocardial capillary lumen density and areal density were significantly reduced by 14% and 12%, respectively, and returned to the normal control level. Research indicates?