Objective: To investigate the pathogenesis of diaphragmatic fatigue by diaphragm fibers classification changes and diaphragmatic apoptosis in rats with chronic obstructive pulmonary disease(COPD),in order to find new treatment of diaphragmatic fatigue. Methods: Forty male Wistar rats were randomly averagely divided into healthy control group and COPD group. The rats in the COPD group were exposed to 5% smoke in a sealed box(twice for each day,30 minutes for each time,interval 8 hours,lasting for 28 days),and 200 -滋g lipopolysaccharide was injected intratracheally on the 1st and 14th day. On the 29th day,the rats were sacrificed for detection of apoptosis rate,Fas protein and Caspase-3 gene expression of diaphragmatic muscle cell,and observation of the morphologic changes by electron microscope and diaphragm myofibers classification dyeing. Results: On the 28th day,destruction of alveolar walls and enlargement of alveolar space were observed in the COPD group,the diaphragmatic muscle cell apoptosis rate,the Fas protein and Caspase-3 gene expression were higher than those of the control group(P < 0.01). Compared to the healthy controls,the type I fiber proportion in the COPD group was increased,while the Ⅱ type fiber proportion was reduced (both P < 0.01). Conclusion: Abnormal apoptosis of diaphragmatic muscle cell and fiber type of change were present in rats with COPD. Caspase-3 and Fas/FasL way could be involved in the apoptosis of diaphragmatic muscle cell,the regulation of fiber type of change in the late patients with COPD,which causes difficult to treat diaphragmatic muscle fatigue.