Ethanol depresses the respiratory response to hypercapnia and to hypoxia, even at blood alcohol levels (BALs) commonly seen in social drinkers. Sleep likewise depresses respiratory responses to hypoxia and hypercapnia. Deleterious, interactive effects on respiration of the unavoidable physiological state of sleep and the widely used substance of ethanol may underlie significant morbidity and mortality in the United States. This revised application expands a productive research program on ethanol and the control of breathing during sleep. Our previous work has shown that in younger men, inspiratory resistance is increased by ethanol, while some measures of respiratory drive are depressed. A major feature of our proposed research is the study of postmenopausal women. The rationale for evaluating this population is that female hormones seem to protect premenopausal women from sleep disordered breathing. However, postmenopausal women are not so protected, suggesting that some minimal level of female hormones is necessary for protection. Thus, the current phase of our work focuses on the influences of age and gender on respiration during sleep after bedtime ethanol. We will study three groups of subjects: 1) men between the ages of 55 and 75 years; 2) postmenopausal women (age 55-75) on hormone replacement therapy; 3) postmenopausal women (age 55-75) not on hormonal replacement. Measurements will include inspiratory occlusion pressure, total respiratory resistance and ventilatory response to hypercapnia and isocapnic hypoxia. In addition, we will observe phenomena associated with respiratory depression (periodic breathing, hypopneas or apneas and desaturations). We will test the following hypotheses: 1. Ethanol causes greater increases in upper airway resistance during sleep in older men and older women than in our previously studied younger men. 2. Ethanol causes more pronounced decreases in central chemoreceptor drive in older men and older women as manifested by a reduced response to hyperoxic hypercapnia than in our previously studied younger men. 3. In men, the age-related increase in inspiratory resistance will be greater than the ethanol-related depression of chemoreceptor drive and the net effect will be an augmentation in P0.1 and the hypercapnic response above its levels in younger men.
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