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小鼠经锻炼和药物复合处理后进行低压舱模拟海拔５０００ｍ高度的低氧实验，同时设正常与５０００ｍ低氧对照，用图象分析法计量分析各组心肌线粒体长轴（Ｌ）、短轴（Ｓ）、截面积（Ａ）、比表面积（Ｓ／Ｖ）的变化。结果显示，５０００ｍ高度缺氧小鼠线粒体Ｌ、Ｓ、Ａ分别较正常组增高１２．９％、１８．９％（Ｐ＜０．０５）、２４．２％，Ｓ／Ｖ减少１２．０％（Ｐ＜０．０５）。经复合方案处理后再模拟５０００ｍ缺氧的小鼠，上述各项指标均可恢复至正常水平。结果表明，高原急性缺氧可致线粒体肿胀，脊减少，伴有空泡化，这是高原低氧下能量代谢障碍、劳动能力降低的病理学基础。复合处理对缺氧造成的心肌线粒体的结构改变有纠正作用，能良好地保护心肌，进而有助于提高高原劳动能力。
Mice were subjected to exercise and drug combination treatment to simulate hypoxia altitude 5000 m altitude hypoxia experiments, and set the normal and 5000 m hypoxia control, using image analysis method to measure myocardial mitochondrial long axis (L), short axis S), cross-sectional area (A), specific surface area (S / V). The results showed that the mitochondrial L, S and A levels in hypoxia mice at 5000m altitude were increased by 12.9%, 18.9% (P <0.05), 24.2% and S / V decreased by 12.0% (P <0.05). After treatment with compound regimen and simulate hypoxia 5000m mouse, the above indicators can be restored to normal levels. The results showed that acute hypoxia could cause swelling of mitochondria, decrease of ridges, and vacuolization, which is the pathological basis of energy metabolism disorder and reducing of working ability under plateau hypoxia. Compound treatment of myocardial mitochondria caused by hypoxia structural changes have a corrective effect, can well protect the myocardium, which in turn helps to improve the work ability of the plateau.