MECHANISMS OF APNEA TERMINATION IN OBSTRUCTIVE SLEEP-APNEA - ROLE OF CHEMORECEPTOR AND MECHANORECEPTOR STIMULI

Previous work from our laboratory has indicated that mechanoreceptor f eedback from the respiratory muscles may play an important role in aro usal and apnea termination in obstructive sleep apnea (OSA). Other stu dies have pointed to a prominent role for chemoreceptor stimuli. We po stulated that mechanoreceptor stimuli from the respiratory system are the primary determinant of apnea termination, and that chemoreceptor s timuli exert their effect indirectly through stimulation of ventilatio n and thus proprioceptive feedback. To test this, we measured the diap hragmatic tension-time index (TTdi) during obstructive steep apneas in seven male subjects with severe untreated OSA. We compared the maxima l TTdi values at end-apnea during administration of air, O-2, and CO2. We reasoned that if mechanoreceptor stimuli mediate apnea termination , changing the degree of chemoreceptor stimulation during apneas shoul d not alter the level of respiratory effort at end-apnea. O-2 administ ration produced a significant increase in end-apneic arterial oxygen s aturation (Sa(O2)) and increased apnea duration. CO2 administration le d to an increase in pre- and postapneic end-tidal carbon dioxide press ure (PET(CO2)), and tended to shorten apneas. However, the mean value for maximal end-apneic TTdi was 0.12 +/- 0.01 (SEM) during room air br eathing and was unaltered by O-2 (0.12 +/- 0.01) or CO2 (0.11 +/- 0.01 ) administration. The consistency of end-apneic TTdi values despite th e varying chemical drive supports the hypothesis that apnea terminatio n in OSA is mediated by mechanoreceptor feedback from the respiratory system, most likely from the respiratory muscles. The influence of che moreceptor information may be mediated indirectly through an effect on ventilatory effort.