Obstructive sleep apnea involves intermittent periods of airway occlusions that lead to repetitive oxygen desaturations. Exposure to chronic intermittent hypoxia (IH) in rats increases diurnal blood pressure and alters skeletal muscle physiology. The impact of IH on upper airway muscle function is unknown. We hypothesize that IH exposure increases upper airway collapsibility in rats due to alterations of the muscles surrounding the upper airway. Lean and obese rats were exposed to cyclic alterations in O₂ levels (20.6%-5%) every 90 seconds, 8 hours a day/6 days a week for 12 weeks. Following the exposure period, arterial pressure was recorded via the tail artery in conscious unrestrained rats. Mean arterial pressure was increased in lean IH but not in obese IH- exposed Zucker rats (p<0.05). The pharyngeal pressure associated with airway collapse (P_crit) was measured under anesthesia during baseline conditions and then during supramaximal stimulation of the hypoglossal nerve (cnXII). Baseline P_crit was more positive (more collapsible) in lean but not obese rats following 12-weeks of IH (p<0.05), while supra-maximal stimulation of cnXII increased airway stability (decreased P_crit) in both lean and obese Zucker rats following IH to levels that were similar to their respective room air controls. The in-vitro peak tension and the expression of the individual myosin heavy chain isoforms from the upper airway muscles were unaltered following IH. We conclude that IH leads to increases in baseline collapsibility in lean Zucker rats exposed to IH by non-myogenic mechanisms.