0205 Sleep Restriction Suppresses Sleep Spindles but Preserves Slow-Wave Activity

Abstract Introduction Sleep restriction is known to alter sleep stages, but less is known about its effects on sleep microarchitecture. This is an important gap in knowledge because microevents, including sleep spindles and slow waves, are critical to sleep homeostasis, memory consolidation, and cognitive functioning. We experimentally investigated potential changes in sleep microevents during nights of normal sleep versus sleep restriction. Methods We monitored 75 healthy adults (mean age = 19.95; 55% female) using laboratory polysomnography across 7 nights. Following an adaptation night, participants alternated between three consecutive nights of normal sleep (9 hours time-in-bed) and three nights of restricted sleep (5.5 hours time-in-bed). Condition order was counterbalanced. Sleep stages were scored manually by a registered polysomnographic technician. YASA was employed to detect sleep microevents, including count, density, duration, amplitude, and frequency of N2 spindles, as well as count and density of N3 slow waves. Analyses were based on the C4-A1 channel. Results Experimental sleep restriction suppressed spindle count (Z=-12.02, p<.001), density (Z=-7, p<.001), and frequency (Z=-7.12, p<.001) whereas amplitude showed an increase (Z=-4.34, p<.001). Slow-wave count and density were unaffected (all p>.05). We next investigated whether these effects were static or dynamic across days. Across the normal sleep nights, there were no significant variations for spindles or slow waves. By contrast, across the sleep restriction nights, there was a decrease in spindle count (χ² = 17.6, p<.001) and density (χ² = 7.52, p<.001), whereas slow wave count showed a compensatory increase (χ² = 7.3, p<.001). Conclusion Sleep restriction significantly suppressed spindles, with the decline intensifying over consecutive nights, which has implications for cognitive functioning. There was a simultaneous increase in spindle amplitude and slow wave count, which may represent compensatory responses, reflecting a homeostatic drive to prioritize deep sleep during reduced sleep opportunities. Support (if any) Support provided by the National Science Foundation (1920730, 1943323).