Distinct temporal patterns of acute intermittent hypoxia differentially affect sleep, autonomic regulation, and...

Intermittent hypoxia (IH) is a defining physiological component of obstructive sleep apnea (OSA), yet clinical outcomes vary considerably among individuals with similar event frequencies. We investigated whether distinct temporal structures of IH-defined by hypoxic duration and cycling frequency-differentially affect sleep and autonomic regulation, and whether hypertensive status modifies vulnerability.

Male Wistar-Kyoto (WKY) (n = 13-20 across conditions) and spontaneously hypertensive rats (SHR) (n = 10-15 across conditions) aged 16 weeks were exposed to a single 8-h session of IH during the light phase. IH paradigms systematically varied hypoxic duration (5, 10, or 15 s) and cycle frequency (15, 30, or 60 cycles/h). Sleep architecture, EEG spectral activity, autonomic indices, arterial pressure, baroreflex sensitivity, and recognition memory were assessed, with analyses focused on the latter 4 h of exposure.

Distinct IH temporal patterns produced divergent physiological responses. High-frequency cycling (5s-60c) and intermediate-duration hypoxia (10s-30c) induced pronounced sleep fragmentation, suppression of quiet-sleep delta power, and enhanced sympathetic activation. Mean arterial pressure remained stable across paradigms, indicating preserved short-term cardiovascular compensation. Responses were strain-dependent: SHR exhibited exaggerated sympathetic activation, greater sleep instability, and selective recognition memory impairment under the 10s-30c condition, whereas WKY rats demonstrated relative resilience. Baroreflex sensitivity was preserved, with selective enhancement observed under prolonged hypoxic duration (15s-30c) in WKY rats.

Even within a single 8-h exposure, acute IH effects are determined by hypoxic temporal structure rather than cumulative burden alone. Hypertensive vulnerability amplifies susceptibility to specific IH patterns. These findings support the clinical relevance of hypoxic temporal characterization in understanding sleep-autonomic disturbances in OSA.