BACKGROUND: Both hypoxia and carbon dioxide retention can damage phrenic nerve and muscle conduction, as well as diaphragm function. Diaphragm compound muscle action potential and phrenic nerve conduction time are reliable indicators for measuring phrenic nerve and diaphragm function. OBJECTIVES: To verify the hypothesis that changes of phrenic nerve conduction time (PNCT) and diaphragm compound muscle action potential (CMAP) in obstructive sleep apnea-hypopnea syndrome (OSAHS) patients might contribute to the decline of phrenic nerve and diaphragm function. PNCT and CMAP were measured with multipair esophageal electrodes combined with unilateral magnetic stimulation. DESIGN, TIME AND SETTING: Case controlled study. The experiment was carried out in Guangzhou Institute of Respiratory Disease, Guangzhou Medical College, from June 2005 to April 2006. PARTICIPANTS: Twenty seven OSAHS patients and eight primary snoring subjects from Guangzhou Institute of Respiratory Disease, Guangzhou Medical College were recruited and all subjects were diagnosed by polysomnography (PSG). Sixteen healthy, non-snoring subjects in the hospital for medical examination during the same time period were selected as the control group. METHODS: Esophageal electrodes, made by Guangzhou Institute of Respiratory Disease, combined with unilateral magnetic stimulation, were used to measure PNCT and CMAP of all subjects. PNCT was defined as the time from stimulation artifact to the onset of CMAP and diaphragm CMAP amplitude was measured from peak to peak. Oxygen desaturation index and apnea-hypopnea index were measured using PSG, and their relevance to PNCT and CMAP were analyzed. PNCT and CMAP in five OSAHS patients were repeatedly measured after effective nasal continuous positive airway pressure treatment for more than 2 months. MAIN OUTCOME MEASURES: (1) PNCT and diaphragm CMAP of subjects in each group. (2) Relevance of oxygen desaturation index and apnea-hypopnea index to PNCT and CMAP. (3) Changes of PNCT and CMAP of OSAHS patients before and after treatment. RESULTS: All subjects were included in the analyzed results. (1) PNCT of the OSAHS group was significantly longer compared to that of the control and primary snore groups, while CMAP of the OSAHS group was significantly lower (P < 0.05). (2) PNCT and CMAP recorded from both sides correlated significantly with oxygen desaturation index and with apnea-hypopnea index (P < 0.01). (3) PNCT shortened significantly after effective nasal continuous positive airway pressure treatment for more than 2 months ( P < 0.05). CONCLUSION: Prolongation of PNCT and decrease of CMAP might contribute to the decline of phrenic nerve and diaphragm function caused by repeated nocturnal hypoxia and carbon dioxide retention. The impairment of the phrenic nerve might also decrease diaphragm function. BACKGROUND: Both hypoxia and carbon dioxide retention can damage phrenic nerve and muscle conduction, as well as diaphragm function. Diaphragm compound muscle action potential and phrenic nerve conduction time are reliable indicators for measuring phrenic nerve and diaphragm function. OBJECTIVES: To verify the hypothesis that changes of phrenic nerve conduction time (PNCT) and diaphragm compound muscle action potential (CMAP) in obstructive sleep apnea-hypopnea syndrome (OSAHS) patients might contribute to the decline of phrenic nerve and diaphragm function. PNCT and CMAP were measured with multipair esophageal electrodes combined with unilateral magnetic stimulation. DESIGN, TIME AND SETTING: Case controlled study. The experiment was carried out in Guangzhou Institute of Respiratory Disease, Guangzhou Medical College, from June 2005 to April 2006. PARTICIPANTS: Twenty seven OSAHS patients and eight primary snoring subjects from Guangzhou Institute of Respiratory Disease, Guangzhou Med METHODS: Esophageal electrodes were made by the Guangzhou Institute of Technology Respiratory Disease, combined with unilateral magnetic stimulation, were used to measure PNCT and CMAP of all subjects. PNCT was defined as the time from the stimulation artifact to the onset of CMAP and diaphragm CMAP amplitude was measured from peak to peak. Oxygen desaturation index and apnea -hypopnea index were measured using PSG, and their relevance to PNCT and CMAP were five measured in five OSAHS patients were repeatedly measured after effective nasal continuous positive airway pressure treatment for more than 2 months. MAIN OUTCOME MEASURES: (1) PNCT and diaphragm CMAP of subjects in each group. (2) Relevance of oxygen desaturation index and apnea-hypopnea index to PNCT and CMAP. (3) Changes of PNCT and CMAP of OSAHS patients before and after treatment. RESULTS: All subjects were included in the analyzed results. (1) PNCT of the OSAHS group was significantly longer than that of the control and primary snore groups, while CMAP of the The OSAHS group was significantly lower (P <0.05). (2) PNCT and CMAP recorded from both sides correlated significantly with oxygen desaturation index and with apnea-hypopnea index Airway pressure treatment for more than 2 months (P <0.05). CONCLUSION: Prolongation of PNCT and decrease of CMAP might contribute to the decline of phrenic nerve and diaphragm function caused by repeated nocturnal hypoxia and carbon dioxide retention. The impairment of the phrenic nerve might also decrease diaphragm function.