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目的 :探讨运动性骨疲劳发生发展的机理。方法 :实验雄性成年兔 2 5只 ,运用高电压、低电流动物刺激仪 ,刺激实验兔进行主动跑跳训练 ,成功地模拟出运动性骨疲劳的动物模型。结果 :2周训练后 ,X线及核素骨显像均呈阴性 ,血甲状旁腺素 (PTH)和血骨钙素 (BGP)显著高于正常组 ,血睾酮 (T)显著低于正常组 ,胫骨皮质骨吸收腔显著增加 ,组织学表现为破骨细胞增加 ;电镜观察骨细胞呈吸收相。继续跑跳训练( 3 -4周 )可使疲劳向损伤转化 ,X线出现轻微骨膜反应 ,核素骨显像呈现阳性 ,血生化及组织学出现应力性损伤的变化。结论 :运动性骨疲劳的发生是一个由骨细胞直接参与的破骨细胞性重吸收大于成骨细胞性骨形成的生理过程 ;高血PTH、高血BGP和低血T是其发生发展过程中的血生化基础
Objective: To explore the mechanism of exercise-induced bone fatigue. METHODS: Twenty-five male adult rabbits were randomly divided into experimental group and control group. The experimental animals were stimulated by high-voltage and low-current animal stimulator, and the animal model of exercise-induced bone fatigue was successfully simulated. Results: After 2 weeks of training, X-ray and radionuclide bone imaging were all negative. PTH and BGP were significantly higher than those of the normal group. The serum testosterone (T) was significantly lower than that of the normal group Group, tibial cortical bone absorption chamber increased significantly, the histological examination of osteoclasts increased; electron microscope observation of bone cells was absorbed phase. Continuation of running training (3-4 weeks) led to the conversion of fatigue to injury, with a slight periosteal reaction on the X-ray, a positive appearance of radionuclide bone imaging, and a change of stress injury in blood biochemistry and histology. Conclusion: The occurrence of exercise-induced bone fatigue is a physiological process in which osteoclasts resorption, which is directly involved in osteoclasts, is greater than that of osteoblasts. High blood PTH, high blood BGP and low blood T are the pathogenesis and development Blood biochemical basis