Respiratory and arousal responses to acoustic stimulation.

STUDY OBJECTIVES: Although sleep-related obstructive apnea is most often associated with transient arousal, the impact of this arousal on respiratory control remains unclear. We tested the hypotheses that acoustic arousing stimulation can generate a significant respiratory response during sleep in healthy subjects and that the magnitude or timing of this response is affected by the presence of electrocortical arousal or inhaled carbon dioxide. DESIGN: We employed binaural tone bursts (0.5-s duration, 4-KHz center frequency, 99-s interstimulus interval) to elicit repetitive transient arousals from sleep during nocturnal polysomnographic recordings beginning at 10 PM and ending at 6 AM. PARTICIPANTS: Recordings were conducted in five healthy adult volunteers aged 24 to 37 years. INTERVENTIONS: Inspired gas was alternated between room air and 3% to 7% CO2 (titrated to yield an approximate 50% increase in minute ventilation) at 1-h intervals. MEASUREMENTS AND RESULTS: Each 30-s epoch was scored for sleep/wake stage according to standard criteria. Only results obtained during nonrapid eye movement sleep are presented herein. Tone-evoked arousals were detected by computer analysis as increased EEG frequency occurring within 3 s of acoustic stimulation. For each tone, respiratory parameters for each of three prestimulus and four poststimulus breaths were normalized to the overall mean of prestimulus breaths measured during room air breathing for each subject. Tone bursts elicited repetitive transient arousals with a mean duration of approximately 10 s from all stages of sleep. With respect to the three prestimulus breaths, acoustic stimulation was associated with increased tidal volume and decreased inspiratory duration for at least four breaths. These respiratory responses to acoustic stimulation were not significantly influenced by either presence of transient arousal from sleep or inspired gas. CONCLUSIONS: We conclude that transient EEG arousal may be repeatedly evoked from nonrapid eye movement sleep by transient acoustic stimulation in normal sleepers. This sensory stimulation is associated with augmented ventilation, a response that is not significantly affected by inspired hypercapnia or the presence of generalized EEG arousal.

Respiratory and electrocortical responses to acoustic stimulation.

Although sleep-related obstructive apnea is most often associated with transient arousal, the impact of this arousal on respiratory control remains unclear. We employed binaural tone bursts (.5 second duration) to elicit repetitive transient arousals from sleep during polygraphic recordings in 5 adult volunteers. By this method, we elicited repetitive transient arousals with a mean duration of approximately 10 seconds from all stages of sleep. With respect to the 3 pre-stimulus breaths, acoustic stimulation was associated with increased tidal volume and decreased inspiratory duration for at least 4 breaths. These respiratory responses to acoustic stimulation were not significantly influenced by either presence of transient arousal from sleep or the sleep state from which arousal occurred. We conclude that transient electro-cortical state changes may be repeatedly evoked from all sleep stages by transient acoustic stimulation in normal sleepers. This sensory stimulation represents a significant respiratory stimulus even when generalized arousal from sleep does not occur.

Effect of induced transient arousal on obstructive apnea duration.

Six untreated male patients (age 19-55 yr) with obstructive sleep apnea underwent nocturnal polysomnography with acoustic stimulation to determine the effect of transient arousal on obstructive apneas during sleep. Binaural tone bursts (25-95 dB) were delivered in late expiration during the second obstructive apnea of a cycle consisting of four consecutive apneas. For the group, stimulated apneas were significantly shorter (P < 0.05, Fisher's protected least significant difference test) than were the unstimulated apneas when transient electrocortical arousal was elicited in both non-rapid-eye-movement (non-REM) sleep [mean 17 +/- 7 (SD) vs. 26 +/- 9, 23 +/- 10, and 26 +/- 12 s for 2nd vs. 1st, 3rd, and 4th apnea, respectively, of each cycle] and REM sleep (mean 19 +/- 10 vs. 35 +/- 15, 45 +/- 18, and 39 +/- 20 s). Without electrocortical arousal, the stimulated apnea was significantly shortened in non-REM (23 +/- 9 vs. 25 +/- 7, 24 +/- 8, and 26 +/- 8 s) but not in REM (32 +/- 16 vs. 37 +/- 12, 32 +/- 15, and 30 +/- 16 s). Tones delivered relatively early and late in the apnea were equally likely to be associated with resolution of the apnea. The nadir of arterial oxygen saturation of hemoglobin was inversely proportional to apnea length, with higher saturation nadirs associated with the stimulated apneas. These data indicate that transient arousal, induced by nonrespiratory stimulation, influences the resolution of obstructive apneas during sleep.

Acoustically induced cortical arousal increases phasic pharyngeal muscle and diaphragmatic EMG in NREM sleep.

Six healthy subjects (3 males, 3 females) were studied to assess phasic inspiratory responses of upper airway (UA) and diaphragm muscles to electrocortical arousal independent of other potential respiratory stimulation. Transient electroencephalographic (EEG) arousal (abrupt EEG frequency shift > or = 3 s without awakening) was induced during supine stage 2 non-rapid-eye-movement (NREM) sleep with binaural tone bursts (0.5 s, 4 kHz, 25-95 dB). Electromyograms (EMG) of levator veli palatini (EMGlvp) and genioglossus (EMGgg) were obtained with intramuscular electrodes, and EMG of diaphragm (EMGdi) was obtained with esophageal electrodes. EMG signals were processed as moving time-averaged inspiratory activity over 100-ms windows. For each arousal, each of five consecutive postarousal breaths (R1-R5) was scored for peak inspiratory phasic EMG and normalized as percent averaged EMG of the three prearousal breaths for all muscles. After arousal, EMGlvp was increased for R1-R5 and EMGgg and EMGdi were increased for R1-R4. The increase in EMGlvp was greater than those of EMGgg and EMGdi for all response breaths. There was a significant increase in EMGlvp in all subjects, and EMGgg and EMGdi were significantly increased in three and two subjects, respectively. These data indicate that isolated transient electrocortical arousal is generally associated with phasic inspiratory recruitment of UA and diaphragm muscles in normal humans during NREM sleep; velopharyngeal muscle recruitment appears to be more consistent and of greater magnitude and duration than that of oropharyngeal muscle or diaphragm. We speculate that transient arousal from sleep may contribute to UA patency independent of chemical and mechanical respiratory stimuli.