目的通过建立大强度运动心肌肥大模型,探讨长期大强度运动下PI3K信号对运动性心肌肥大的影响。方法 7周龄雄性SD大鼠在适应性训练后随机分为安静组、中强度组和大强度组。中强度组和大强度组分别取4个观察点进行观察(末次运动后即刻、6 h、12 h和24 h),每个观测点6只。运动方案为递增负荷跑台训练,共进行7周。用Western blotting测定心肌PI3K p85、PI3K p110α和calcineurin蛋白表达。ELSIA检测血清cTnI。HE和HBFP染色观察心肌组织形态。结果 (1)心系数大强度组显著高于中强度组和安静组。(2)血清cTnI在运动后6 h达到峰值。大强度组显著高于中强度组,运动后24 h未恢复到安静组水平。(3)大强度组心肌形态学发生改变,缺血缺氧明显。(4)大强度组心肌PI3K p85、PI3K p110α蛋白表达运动后即刻达到峰值,然后回落。中强度组上述指标运动后6 h达到峰值,然后逐步回落。(5)大强度组心肌calcineurin在运动后12 h达到峰值,运动后24 h未恢复安静组水平。结论 (1)运动性心肌肥大程度随运动强度增大而增加,形态学和血清cTnI结果表明长期中等强度运动诱导的心肌肥大为生理性的,而长期大强度运动会造成严重的心肌损伤,使心肌肥大有向病理性发展的风险。(2)长期中等强度运动诱导的心肌肥大主要由PI3K信号调控;长期大强度运动下心肌PI3K信号未被激活,心肌肥大主要由calcineurin信号调控。 Objective To establish a model of myocardial hypertrophy induced by long-term high-intensity exercise to investigate the effect of PI3K signaling on exercise-induced cardiac hypertrophy. Methods Seven-week-old male Sprague-Dawley rats were randomly divided into two groups: sedentary group, moderate-intensity group and high-intensity group. Four observation points were observed in the middle-intensity group and the high-intensity group (immediately after the last exercise, 6 h, 12 h and 24 h) with 6 points per observation point. Exercise program for incremental load treadmill training, a total of 7 weeks. Western blotting was used to detect the protein expression of PI3K p85, PI3K p110α and calcineurin in myocardium. ELSIA serum cTnI. HE and HBFP staining myocardial morphology. Results (1) The cardiac coefficient of high intensity group was significantly higher than that of middle intensity group and quiet group. (2) Serum cTnI peaked at 6 h after exercise. High intensity group was significantly higher than the intensity group, 24 h after exercise did not return to the level of quiet group. (3) Myocardial morphological changes in high-intensity group, obvious ischemia and hypoxia. (4) The protein expression of PI3K p85 and PI3K p110α in high-intensity group peaked immediately after exercise, and then dropped back. The intensity of these indicators 6h after exercise peaked, and then gradually decline. (5) Calcineurin in high-intensity group peaked at 12 h after exercise, and did not recover to resting level at 24 h after exercise. Conclusions (1) The degree of exercise-induced myocardial hypertrophy increases with the increase of exercise intensity. The results of morphology and serum cTnI show that exercise induced by long-term moderate-intensity exercise is physiological, while long-term intensive exercise can cause severe myocardial injury, Hypertrophy and pathological development of the risk. (2) Long-term moderate-intensity exercise-induced cardiac hypertrophy is mainly regulated by PI3K signaling; PI3K signaling is not activated in long-term high-intensity exercise, and cardiac hypertrophy is mainly regulated by calcineurin signaling.