EFFECTS OF SLEEP-DEPRIVATION AND SLEEP FRAGMENTATION ON UPPER AIRWAY COLLAPSIBILITY IN NORMAL SUBJECTS

Sleep deprivation can induce or worsen nocturnal respiratory disturban ces. In patients with sleep apnea hypopnea, sleep abnormalities consis t of repetitive episodes of arousals and awakenings that lead to sleep fragmentation. Because the propensity for upper airway collapse is in creased in these patients, we wondered if sleep fragmentation could in crease upper airway collapsibility and contribute to the pathogenesis of this disease. In eight normal subjects, upper airway collapsibility was assessed during sleep by progressively decreasing the pressure in a nasal mask while recording airflow, mask, and esophageal pressures. The critical pressure was determined by the relationship between brea th-by-breath values of maximal inspiratory airflow of each flow-limite d inspiratory cycle and the corresponding mask pressure. Critical pres sure was measured twice in each subject: after one night of total slee p deprivation and after one night of sleep fragmentation using auditor y stimuli. The two measures were done in random order 1 wk apart. A po lysomnographic recording was obtained the night after each measurement of critical pressure. Sleep architecture was identical after sleep de privation and fragmentation. Sleep-related breathing abnormalities wer e more frequent after sleep fragmentation than after sleep deprivation . Critical pressure was -17.1 +/- 6.8 cm H2O (mean +/- SEM) after slee p deprivation, and -12.3 +/- 6.3 cm H2O after sleep fragmentation (p < 0.05), corresponding to an earlier closing of the upper airway We con clude that sleep fragmentation leads to a higher upper airway collapsi bility than does sleep deprivation.