Adelaide Institute for Sleep Health, Repatriation General Hospital, Daw Park, South Australia 5041, Australia.
J Appl Physiol (1985). 2010 Oct;109(4):1027-36. doi: 10.1152/japplphysiol.01397.2009. Epub 2010 Aug 19.
Obese obstructive sleep apnea (OSA) patients potentially defend end-expiratory lung volume (EELV) during wakefulness via increased expiratory diaphragmatic activity (eEMG(dia)). A reduction in eEMG(dia) and EELV at sleep onset could, therefore, increase upper airway collapsibility via reduced tracheal traction. The aim of this study was to establish if eEMG(dia) is greater in obese OSA patients vs. healthy-weight controls during wakefulness, and to compare eEMG(dia) and EELV changes at sleep onset between groups as a function of stable breathing, hypopnea vs. apnea events developing within the first few breaths after sleep onset. Eight obese men with OSA and eight healthy-weight men without OSA were studied in the supine position while instrumented with an intraesophageal catheter to measure eEMG(dia) and magnetometer coils to assess changes in EELV. While eEMG(dia) expressed as %maximal activity was not significantly different between groups during wakefulness, OSA patients experienced a greater fall in eEMG(dia) following sleep onset (group × breath, P < 0.001) and a greater decrease when respiratory events accompanied sleep onsets (category × breath, P < 0.001). The decrease in EELV by the third postsleep onset breath was small (OSA, 61.4 ± 8.0 ml, P < 0.001; controls, 34.0 ± 4.2 ml, P < 0.001), with the decrease significantly greater in OSA patients over time (group × breath, P = 0.007). There was a greater decrease with more severe events (category × breath, P < 0.001), with EELV decreasing by 89.6 ± 14.2 ml (P < 0.001) at the onset of apneas in the OSA group. These data support that diaphragm tone and EELV frequently decrease following sleep onset, with greater falls at transitions accompanied by respiratory events. In addition to decrements in upper airway dilator muscle activity, decreasing lung volume potentially contributes to an increased propensity for upper airway collapse in OSA patients at sleep onset.
肥胖阻塞性睡眠呼吸暂停（OSA）患者在清醒时可能通过增加呼气膈肌活动（eEMG（dia））来保护呼气末肺容积（EELV）。因此，睡眠开始时 eEMG（dia）和 EELV 的减少可能会通过减少气管牵引力来增加上气道塌陷的可能性。本研究的目的是确定肥胖 OSA 患者与健康体重对照组在清醒时的 eEMG（dia）是否更大，并比较两组在睡眠开始时的 eEMG（dia）和 EELV 变化，作为稳定呼吸、呼吸暂停事件的函数与睡眠开始后的前几个呼吸中发展的低通气事件。八名肥胖 OSA 男性和八名健康体重无 OSA 男性在仰卧位时接受研究，使用食管内导管测量 eEMG（dia）和磁强计线圈评估 EELV 变化。虽然清醒时两组之间 eEMG（dia）的表达（%最大活动）没有显著差异，但 OSA 患者在睡眠开始后经历了更大的 eEMG（dia）下降（组×呼吸，P<0.001），并且在呼吸事件伴随睡眠开始时下降更大（类别×呼吸，P<0.001）。第三次睡眠后开始呼吸时 EELV 的下降幅度较小（OSA，61.4±8.0ml，P<0.001；对照组，34.0±4.2ml，P<0.001），随着时间的推移，OSA 患者的下降幅度明显更大（组×呼吸，P=0.007）。随着事件的严重程度增加，下降幅度更大（类别×呼吸，P<0.001），OSA 组呼吸暂停开始时 EELV 下降 89.6±14.2ml（P<0.001）。这些数据支持膈肌张力和 EELV 通常在睡眠开始后下降，并且在伴有呼吸事件的过渡时下降更大。除了上气道扩张肌活动的减少外，肺容积的减少可能导致 OSA 患者在睡眠开始时上气道塌陷的倾向增加。
