Intermittent Hypoxia, Sleep Fragmentation and Glucose Tolerance

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Obstructive sleep apnea is a common sleep disorder affecting 17% of the total population and characterized by repeated bouts of intermittent hypoxia and sleep fragmentation. Both intermittent hypoxia and sleep fragmentation are hypothesized to have independent consequences on cardiometabolic health. In the clinical setting, the ability to tease apart the relative contributions of intermittent hypoxia from sleep fragmentation is limited. Here, we use mice exposed to intermittent hypoxia either during their rest or active phase to systematically determine the metabolic effects of intermittent hypoxia + sleep fragmentation or intermittent hypoxia alone. We find that 9 hours of mild, intermittent hypoxia, (a 30‐second, 12% 02 event occurring once per minute) is sufficient to impact glucose metabolism when applied during the resting phase, but not during the active phase (AUC 16733 ±1326 vs 21189 ±1395, respectively, p < 0.05). However, only a more severe intermittent hypoxia protocol (a 30‐second, 7% 02 event occurring once per minute) was found to affect the glucose tolerance of both resting and awake mice (AUC: 17063 ± 1328 vs 17167 ±696, respectively). These data demonstrate that the severity of intermittent hypoxia dictates the glucose response in awake mice, while sleep fragmentation may chiefly influence the glucose metabolism of a resting mouse. Taken together, these results demonstrate distinctive and interdependent roles for intermittent hypoxia and sleep fragmentation on glucose metabolism.Support or Funding InformationDr. Arble receives funding from the American Heart Association (PI Arble, 17SDG33660108) and Marquette Biological Sciences Department.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.