Abdominal Compression Increases Upper Airway Collapsibility During Sleep in Obese Male Obstructive Sleep Apnea Patients

OBSTRUCTIVE SLEEP APNEA (OSA) IS A COMMON SLEEP DISORDER CHARACTERIZED BY REPETITIVE PERIODS OF UPPER AIRWAY (UA) COLLAPSE DURING sleep. Male gender and obesity are 2 key predictors of OSA,1,2 but the mechanisms via which these factors contribute to OSA remain unclear. Central obesity, particularly common in obese male OSA patients, leads to increased intra-abdominal pressure (IAP). This pressure may have an important influence on diaphragm position, which may affect the degree of axial tension (caudal traction) exerted on the UA, and therefore the propensity for UA collapse. Such effects are likely to be most evident in the supine posture and during sleep, when other compensatory mechanisms are diminished and may at least partly explain gender and obesity influences in OSA. While airway patency is importantly modulated by respiratory drive and negative airway pressure reflex activation of UA dilator muscles during inspiration, caudal traction is also likely to influence UA patency throughout the respiratory cycle. Studies in anesthetized animals3,4 show that decreased UA tension via cranial tracheal movement promotes UA collapse, which emphasizes the potential importance of tracheal traction for maintaining airway patency. Investigating the influence of tracheal traction on UA function in humans is inevitably difficult. Changes in lung volume are well known to affect UA function and may reflect predominantly tracheal traction effects. Several studies have shown UA patency to decrease with compression of the abdominal and thoracic compartments via positive extrathoracic pressure.5–7 While data concerning the magnitude of lung volume changes during sleep with obesity are currently lacking, end-expiratory lung volume (EELV), which normally falls ~15% during sleep in healthy weight individuals,8,9 is profoundly reduced in obese patients during general anesthesia10 and likely during sleep. EELV reductions, at least in anesthesia, appear to be largely explained by cranial movement of the diaphragm.11 Consequently, changes in lung volume with obesity alone may substantially underpin the increased propensity for UA collapse in OSA. Extrathoracic pressure induced changes in lung volume may have different effects on transdiaphragmatic forces, lung volume and tracheal traction than the thoracoabdominal compressive effects of obesity. While closely related to lung volume changes, intra-abdominal and transdiaphragmatic pressure changes are potentially stronger determinants of UA function than lung volume change per se. IAP, a key determinant of transdiaphragmatic force is approximately doubled in obese compared to healthy-weight individuals.12 Consequently, abdominal mass loading effects of obesity appear likely to influence UA function during sleep via influences on tracheal traction. However, direct evidence that abdominal compression has any impact on UA function during sleep is currently lacking. The aim of this study was to examine the effect of experimental abdominal compression on UA function during sleep in obese male OSA patients, to test the hypothesis that acute abdominal compression would increase UA collapsibility and UA resistance (RUA) during sleep.