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本文建立了运动心脏的实验动物模型，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的方法，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，以期了解运动心脏结构与功能重塑的细胞机制。结果显示：经过１２周耐力训练后，心肌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）。停止训练８周后，心肌收缩时胞内游离钙浓度峰值较训练时显著降低１４％（Ｐ＜０．０５），恢复到正常对照水平。研究结果提示，运动心脏可保持细胞内钙稳态，心肌收缩时收缩结构钙可获得量增多，是运动心脏心肌收缩性增强的重要机制之一，同时，心肌细胞内游离钙的增多对于运动心脏肥大的发生也起重要的介导作用，而且，运动心肌细胞内游离钙的改变是一种可逆性变化。
In this paper, an animal model of exercise heart was established. The dynamic changes of bioactive calcium in living heart cells were studied by laser scanning confocal microscopy and Fluo-3 / AM, a new generation of calcium fluorescence indicator. Understand the cellular mechanisms that remodel cardiac structure and function in exercise. The results showed that after 12 weeks of endurance training, there was no significant change in the resting value of intracellular free calcium concentration in myocardial cells. The peak value of free calcium concentration in myocardial contraction was significantly higher than that in control group by 11% (P <0.05). After 8 weeks of training, the peak of intracellular free calcium concentration in myocardial contractions was significantly reduced by 14% (P <0.05) compared with that in training, and returned to normal control level. The results suggest that exercise heart can maintain intracellular calcium homeostasis, myocardial contractile contraction of structurally available calcium is one of the important mechanisms of exercise-induced myocardial contractility increased at the same time, increased intracellular free calcium in cardiac muscle for exercise Hypertrophy also plays an important mediating role, and the change in intracellular free calcium in exercise-cardiomyocytes is a reversible change.