Hypothesis

Combining morning bright‑light exposure with a brief period of mild ambient cooling before bedtime will increase the proportion of slow‑wave sleep (SWS) in healthy adults, independent of changes in total sleep time or sleep‑wake timing.

Mechanistic Rationale

Morning light activates melanopsin‑containing ipRGCs, which drive glutamate and peptide release in the SCN to entrain circadian clocks 1. The SCN, in turn, modulates the ventrolateral preoptic nucleus (VLPO) and the dorsomedial hypothalamus, regions that gate SWS and regulate core body temperature. Exposure to mild cold (≈16–18 °C) activates cutaneous cold receptors and stimulates brown adipose tissue thermogenesis, raising adenosine accumulation in the basal forebrain—a well‑known sleep‑promoting factor that specifically boosts SWS pressure. We propose that ipRGC‑SCN signaling primes the hypothalamic thermoregulatory set point to be more responsive to subsequent cooling, thereby amplifying the adenosine‑mediated drive for SWS. This creates a synergistic window where circadian alignment (light) and homeostatic sleep pressure (cold‑induced adenosine) converge to deepen sleep architecture without altering sleep onset latency.

Testable Predictions

• Participants receiving both morning light (≥10 000 lux for 30 min within 30 min of waking) and pre‑sleep mild cooling (16 °C ambient for 90 min ending 30 min before lights‑out) will show a ≥15 % increase in SWS percentage compared with baseline.
• The same light exposure alone will not significantly change SWS percentage, confirming that light’s effect on architecture requires the thermal cue.
• Mild cooling alone will produce a modest SWS increase (≥5 %), but the combined condition will exceed the sum of the individual effects, indicating a non‑additive interaction.
• No significant differences will be observed in REM sleep proportion, total sleep time, or sleep‑onset latency across conditions, isolating the effect to SWS.

Experimental Design

A within‑subject, randomized crossover trial with 30 healthy adults (aged 18–35). Each participant completes four 3‑night sessions separated by at least one week: (1) control (dim light <50 lux, neutral temperature 22 °C), (2) morning light only, (3) pre‑sleep cooling only, (4) combined light + cooling. Polysomnography records SWS, REM, total sleep time, and latency. Saliva melatonin and urinary 6‑sulfatoxymelatonin assess circadian phase; blood adenosine measured upon waking gauges homeostatic pressure. Statistical analysis uses repeated‑measures ANOVA with post‑hoc contrasts.

If the hypothesis holds, it would bridge the mechanistic gap between ipRGC‑driven circadian entrainment and tangible improvements in sleep architecture, offering a low‑cost, non‑pharmacological protocol to enhance restorative sleep.