Social isolation stress favors cardiometabolic comorbidities of sleep apnea

Sleep apnea (SA) is a multifactorial and sex-specific respiratory disorder characterized by repeated respiratory arrests during sleep. However, the origins of this disease are not clearly identified. Chronic stress increases risk for obesity, hypertension, and depression, which are common comorbidities of SA. With the increasing prevalence of obesity and about one-third of the world population reported feeling stressed, the study of the impact of stress on respiratory homeostasis has never been so relevant. Since chronic stress induces the main comorbidities of SA, we hypothesized that social isolation (SI) stress induces sex-specific cardiorespiratory and metabolic disorders in rats similar to patients with SA.80 Sprague Dawley male and female rats (8 weeks old) were kept in: 1) standard housing (2/cage; controls) or in 2) social isolation (1/cage). At the end of the three-week protocol, apneas were quantified by whole-body plethysmography during sleep; respiratory variability was assessed by Poincaré plot analysis. Cardiovascular measurements were obtained by tail cuff, body composition by preclinical magnetic resonance, and plasma leptin and corticosterone levels by multiplex immunoassay. The amount of food was weighed before and after the experiments to calculate the intake.By comparison with controls, SI elevated corticosterone levels in male but not females. SI increased the apnea index in intact rat by 21% and augmented respiratory instability. SI also increased blood pressure (+11mmHg) and food intake (+11g/day); however, females had lower increases than males. In males, SI increases weight gains, fat mass, and decreases plasma leptin levels; these effects were not observed in females.SI promotes the emergence of apnea and respiratory instability during sleep. Since the cardiorespiratory and metabolic disturbances are similar to clinical features of SA patient, we propose that stress plays an important role in the etiology of SA. SI offers a novel and unique opportunity to study the origins and pathophysiology of SA. This research is supported by operating grants from the Canadian Institutes of Health Research (CIRH, RK and VJ). N.J.M. was supported by a Sentinel North Partnered Research Chair in Sleep Pharmacometabolism and a Fonds de Recherche du Quebec Sante (FRQS) Research Scholar J1 award. MG is the recipient of a doctoral scholarship from the FRQS. This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.