An imbalance in the amplitude of electrical activity of the upper airway and chest wall inspiratory muscles is associated with both collapse and reopening of the upper airway in obstructive sleep apnea (OSA). The purpose of this study was to examine whether timing of the phasic activity of these inspiratory muscles also was associated with changes in upper airway caliber in OSA. We hypothesized that activation of upper airway muscle phasic electrical activity before activation of the chest wall pump muscles would help preserve upper airway patency. In contrast, we anticipated that the reversal of this pattern with delayed activation of upper airway inspiratory muscles would be associated with upper airway narrowing or collapse. Therefore the timing and amplitude of midline transmandibular and costal margin moving time average (MTA) electromyogram (EMG) signals were analyzed from 58 apnea cycles in stage 2 sleep in six OSA patients. In 86% of the postapnea breaths analyzed the upper airway MTA peak activity preceded the chest wall peak activity. In 86% of the obstructed respiratory efforts the upper airway MTA peak activity followed the chest wall peak activity. The onset of phasic electrical activity followed this same pattern. During inspiratory efforts when phasic inspiratory EMG amplitude did not change from preapnea to apnea, the timing changes noted above occurred. Even within breaths the relative timing of the upper airway and chest wall electrical activities was closely associated with changes in the pressure-flow relationship. We conclude that the relative timing of inspiratory activity of the upper airway and chest wall inspiratory muscles fluctuates during sleep in OSA.(ABSTRACT TRUNCATED AT 250 WORDS)

We hypothesized that those obstructive sleep apnea (OSA) patients with upper airway collapse during sleep within the transpalatal airway would have a more favorable response to uvulopalatopharyngoplasty (UPP) than those patients with obstruction within the hypopharyngeal airway. We tested this hypothesis in seven OSA patients with transpalatal and seven with hypopharyngeal obstruction undergoing UPP. Preoperatively the apnea/hypopnea index (AHI) was different between palatal and hypopharyngeal obstructors, 37.8 +/- 6.0 (+/- SEM) and 63.9 +/- 6.3, respectively (p less than 0.05), but the apnea-associated arterial oxygen desaturation and the lowest sleep saturation level were not different between the two groups. Postoperatively the AHI was 17.6 +/- 7.2 in the palatal obstructors and 40.3 +/- 15.6 in the hypopharyngeal obstructors (both p less than 0.05 from preoperative AHI). The palatal obstructors had a significant decrease in the percentage of sleep time spent apneic and the hypopharyngeal obstructors had a significant decrease in the hypopnea, but not apnea, time following surgery. The palatal obstructors had a significantly higher postoperative arterial oxygen saturation than the hypopharyngeal obstructors. Two hypopharyngeal obstructors worsened postoperatively. In addition we found that regardless of the site of the obstruction preoperatively, all obstructions occurred at the level of the palate postoperatively. We conclude that patients with preoperative transpalatal obstruction had diminution in obstructive apneas and those with hypopharyngeal obstruction had diminution in hypopneas but not apneas. Oxygenation was better postoperatively in the palatal obstructors, and none worsened postoperatively. These results suggest that identification of the site of upper airway obstruction in OSA may be beneficial.(ABSTRACT TRUNCATED AT 250 WORDS)