Effect of bedtime alcohol on inspiratory resistance and respiratory drive in snoring and nonsnoring men.
We measured inspiratory resistance (R1), inspiratory occlusion pressure (P0.1), and the ventilatory responses to hypercapnia and isocapnic hypoxia during waking and during stage 2 non-rapid eye movement sleep in nine young men who were habitual snorers. They were studied on 2 nights during the 3 hours after receiving a bedtime drink containing either a placebo or 100-proof vodka (1.5 ml/kg) in orange juice. We compared the results with those we reported previously in 10 nonsnoring but otherwise similar men. Waking R1 was the same in nonsnorers and snorers, and it was not affected by ethanol. During sleep on the control night, R1 increased by 70% in nonsnorers and by 280% in snorers. On the ethanol night, the increase from waking to sleeping was more than doubled in both nonsnorers and snorers. P0.1 and the responses to hypercapnia and hypoxia showed no differences between nonsnorers and snorers, therefore the results from the two groups were pooled. Minute ventilation and the hypercapnic response decreased from waking to sleeping and P0.1 was more negative during sleep, but there was no significant effect of ethanol. There was a significant correlation between the changes from waking to sleeping in R1 and P0.1 on the ethanol night suggesting that inspiratory effort increased in response to the increased resistance. The response to isocapnic hypoxia showed no effect of either sleep state or drink. Inspiratory time did not change but mean inspiratory flow (VT/T1) was significantly reduced during sleep on both control and ethanol nights. The duty cycle ratio (T1/Ttot) was significantly increased during sleep on the ethanol night. Despite its great effect on inspiratory resistance, especially in snorers, ethanol, in the dose used in our study, does not augment the depression of minute ventilation or of the hypercapnic response that occur normally in stage 2 non-rapid eye movement sleep. After ethanol, our subjects showed the decreased VT/T1 and the increased T1/Ttot that occur normally during sleep in response to an inspiratory resistive load. However, they also showed increased inspiratory effort. The combination of increased inspiratory resistance and greater inspiratory effort would increase the tendency of an unstable upper airway to collapse and could account for the aggravation of obstructive sleep apnea by ethanol.
Dawson
A
A
Division of Sleep Disorders, Scripps Clinic and Research Foundation, La Jolla, California 92037, USA.
Bigby
B G
BG
Poceta
J S
JS
Mitler
M M
MM
D000328:Adult; D000403:Airway Resistance / Q000187:drug effects* / Q000502:physiology; D000428:Alcohol Drinking / Q000009:adverse effects* / Q000503:physiopathology; D002245:Carbon Dioxide / Q000097:blood; D006801:Humans; D008297:Male; D010100:Oxygen / Q000097:blood; D017286:Polysomnography; D012129:Respiratory Function Tests; D012891:Sleep Apnea Syndromes / Q000209:etiology* / Q000503:physiopathology; D012894:Sleep Stages / Q000187:drug effects* / Q000502:physiology; D012913:Snoring / Q000139:chemically induced* / Q000503:physiopathology; D014939:Work of Breathing / Q000187:drug effects / Q000502:physiology
D002245:Carbon Dioxide; D010100:Oxygen