Sleep state instability is a potential mechanism of central apnea/hypo
pnea during non-rapid eye movement (NREM) sleep. To investigate this p
ostulate, we induced brief arousals by delivering transient (0.5 secon
d) auditory stimuli during stable NREM sleep in eight normal subjects.
Arousal was determined according to American Sleep Disorders Associat
ion (ASDA) criteria. A total of 96 trials were conducted; 59 resulted
in cortical arousal and 37 did not result in arousal. In trials associ
ated with arousal, minute ventilation ((V) over dot(E)) increased from
5.1 +/- 1.24 minutes to 7.5 +/- 2.24 minutes on the first posttone br
eath (p = 0.001). However, no subsequent hypopnea or apnea occurred as
(V) over dot(E) decreased gradually to 4.8 +/- 1.5 1/minute (p > 0.05
) on the fifth posttone breath. Trials without arousal did not result
in hyperpnea on the first breath nor subsequent hypopnea. We conclude
that 1) auditory stimulation resulted in transient hyperpnea only if a
ssociated with cortical arousal; 2) hypopnea or apnea did not occur fo
llowing arousal-induced hyperpnea in normal subjects; 3) interaction w
ith fluctuating chemical stimuli or upper airway resistance may be req
uired for arousals to cause sleep-disordered breathing.