Alzheimer’s disease (AD) is a progressive neurodegenerative disorder which predominantly affects the aging population and is strongly associated with cognitive decline and dementia. AD is the seventh leading cause of death in the United States, and deaths related to Alzheimer’s disease and other dementias have nearly quadrupled since 2000. Obstructive sleep apnea (OSA), characterized by repeated episodes of upper airway obstruction during sleep, leads to intermittent reductions in blood oxygen levels and disrupted rapid eye movement (REM) sleep. OSA-induced chronic intermittent hypoxia (CIH) disrupts neurophysiological processes and may exacerbate both respiratory and cognitive impairments in AD patients, suggesting that treating OSA could be a potential target to limit AD progression. We hypothesize that CIH exposure will change respiratory patterns in adult mice and that these effects will be more pronounced in older adult mice. As an initial test of our hypothesis, we tested the effects of CIH on respiratory pattern in three-month old and 18-month-old adult male and female mice. Each day of the protocol, mice were subjected to 8 hours of CIH with a nadir of 5% oxygen for 15 s and a recovery at 21% oxygen for 4 minutes and 45 seconds, resulting in ~60 hypoxic episodes/day. Respiratory parameters were collected using whole body plethysmography at day 0 (i.e. before CIH exposure) and then after 4, 7, and 10 days of CIH exposure. Respiratory parameters collected included: tidal volume (Vt), respiratory frequency, and minute ventilation (Ve). Our preliminary data indicate that in the three-month old male and female mice, respiratory patterns were relatively unaffected by CIH exposure. Specifically, respiratory frequency changes showed a similar pattern of response across the 10-day CIH (or sham) protocol. By contrast, respiratory frequency decreased in the old adult sham males whereas there was no change in old adult males exposed to CIH (Day 10 vs Day 0: 173 breaths/min vs 160 breaths/min, 165 breaths/min vs 168 breaths/min; sham vs CIH, respectively). Further research will be needed to evaluate the mechanisms through which CIH affects these respiratory control networks and whether there are further perturbations to the control of breathing. This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.
Carlblom et al. (Fri,) studied this question.