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on Inspiratory Resistance and Respiratory Drive
in Snoring and Nonsnoring Men
During normal sleep, air exchange decreases and the resistance to airflow in the upper airway increases. When resistance increases, compensating mechanisms act to restore the amount of air breathed. During waking, this is accomplished through a combination of increased inspiratory effort and longer inspiratory time. During sleep, increased inspiratory time is the first mechanism to come into play but then there is increased muscular effort in the diaphragm and abdomen.
During normal sleep, respiratory drive decreases and so does ventilation, which rises less than in waking in response to a rise in blood carbon dioxide or a fall in blood oxygen.
Alcohol is a respiratory depressant in awake humans but there is less information on its effects during sleep. It is known to increase upper airway resistance during sleep. Thus it would be expected to aggravate the disturbances of blood carbon dioxide and oxygen that normally accompany sleep.
A bedtime dose of alcohol has been shown to increase inspiratory resistance during stage 2 non-REM sleep in young nonsnoring men. The effect on their respiratory drive depends on how it is measured, but the response to increased blood carbon dioxide is decreased in most.
Snorers are expected to have higher inspiratory resistance during sleep than nonsnorers. The worsening of snoring by alcohol is well known. This study focused on young male snorers to compare with previous studies on nonsnoring young men.
Nine young men, nonobese habitual snorers with a history of light to moderate drinking, were studied for two nights during the three hours after a bedtime drink of orange juice which contained either placebo or alcohol (100-proof vodka). The amount of alcohol was adjusted according to body weight so that subjects received between 50 and 75 ml of pure alcohol in their drink, the equivalent of about a half bottle of wine. Measurements were then made during sleep of inspiratory resistance, inspiratory occlusion pressure, and breathing responses to elevated carbon dioxide and decreased oxygen in the blood. Esophageal pressure was measured with a balloon catheter.
Compared to the nonsnorers, the snorers showed more variation in air volume from breath to breath. One result was more variation in their blood carbon dioxide levels.
Most subjects had their best sleep in the hour after lights went out (one-half hour after finishing the drink). However, arousals were frequent, attributed to measurement procedures. Respiratory measurements were made once or twice during appropriate intervals of sleep. Blood was drawn for alcohol levels 25 minutes after, 60 minutes after, and 180 minutes after finishing the drink. Highest blood alcohol levels ranged from 15 mg/dl to 61, averaging 49 (SD=+/-15), comparable to the figures for nonsnorers (highest BAL average 54, SD=+/-20), and consistent with very mild intoxication.
Because of technical problems with the recordings, the final analyses compared only seven snorers with nine nonsnorers. Their waking inspiratory resistance did not differ. However, during sleep without alcohol, inspiratory resistance increased 70% in nonsnorers versus 280% in snorers. After alcohol, the increase in resistance from waking to sleeping was more than doubled for both nonsnorers and snorers. In quantitative terms, nonsnorers went from an inspiratory resistance of 9.5 waking to 16.3 sleeping without alcohol to 25.9 sleeping with alcohol, while snorers went from 10.5 waking to 30.2 sleeping without alcohol to 64.7 sleeping with alcohol, more than twice that of nonsnorers after alcohol.
The minute ventilation (amount of air exchanged per minute) was likewise lower during sleep than waking, lower with alcohol than without, and lower in snorers than nonsnorers. Blood carbon dioxide was greater during sleep than waking but there was no difference between snorers and nonsnorers or between alcohol and no alcohol. The breathing response to elevated carbon dioxide was lower during sleep than waking and lower with alcohol than without alcohol. The breathing response to low blood oxygen was variable, without any statistically significant effects of either sleep vs. waking, alcohol vs. no alcohol, or snorers vs. non-snorers.
In their discussion, the authors noted that inspiratory resistance increased during stage 2 NREM sleep, and increased about four times as much in snorers as in non-snorers. Bedtime alcohol doubled the resistance for both snorers and nonsnorers. Nevertheless, subjects maintained the volume of air breathed and the level of carbon dioxide in the blood did not rise above that on the night without alcohol, nor were the breathing responses to elevated blood carbon dioxide or lowered blood oxygen affected by alochol, indicating that compensatory mechanisms were able to deal adequately with the increased resistances.
The authors note that alcohol has been shown to suppress the arousal response to airway obstruction in normal men. The well-recognized tendency for alcohol to aggravate sleep apnea is understood in terms of alcohol’s depressant effect on upper airway musculature rendering the upper airway more collapsible. Furthermore, it impedes the ability of central nervous system to arouse the apneic sufficiently to resume breathing in the same time as would occur without alcohol.
Although the preservation of the breathing response to high carbon dioxide or low oxygen might seem reassuring with respect to the effect of alcohol on sleep, the authors point out that these were healthy young men (ages 21-32, average=26 years), that the dosage of alcohol was modest, and that the study focused on stage 2-NREM sleep whereas the greatest depression of respiratory drive occurs during REM sleep. Greater difficulties are likely during this stage of sleep, later in the night, with greater alcohol consumption and correspondingly higher and more persistent levels of blood alcohol, with preexistence of frank apnea, and in older subjects.
I had been waiting eagerly for a new article to come out on the relationship of alcohol to breathing during sleep. I regret that this particular study leaves a relatively benign impression of respiratory mechanisms compensating for the demonstrated increases in airway resistance with both alcohol and snoring during sleep. I regret this because alcohol appears to be one of the more toxic substances for people with sleep apnea to ingest, especially at bedtime, when they may often turn to it as a conveniently available “sleeping potion,” as well as a supposed “mood elevator” for those suffering from the depression that often accompanies sleep disorders.
Nevertheless, the article does serve to draw attention to the adverse effects of alcohol on upper airway muscular tone and resistance to airflow, especially in those with some subtle evidence of preexisting sleep-disordered breathing, in the form of simple snoring.
Perhaps the ordinary, non-alcoholic person can easily limit themselves to the equivalent of a few glasses of wine at bedtime. But the alcoholic, or the person driven to drink by insomnia or emotional distress, may find it much more difficult if not impossible to adhere to this limit.Such people can easily drink enough to maintain substantial blood alcohol levels throughout the night, including the critical periods of REM sleep most prone to be accompanied by apneas. Then the situation may be quite different, with resultant increased frequency and duration of apneas and hypoxic episodes, and difficulty arousing quickly to resume breathing, perhaps leading by way of hypoxic brain injury to some of the organic brain disease seen in about a third of alcoholics.
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