Abstract
Objectives: Pre-sleep exposure to especially short-wavelength light (i.e., 460–480 nm) acutely suppresses melatonin, increases vigilance, and decrease sleepiness. Activating effects can also extend to sleep resulting in for instance decreased slow wave activity. The latter effects have mainly been attributed to melanopic effects of light on intrinsically photosensitive retinal ganglion cells (ipRGCs), but definite mechanistic answers are missing. Thus, we here investigated for the first time whether two metameric light conditions designed to exclusively differ in their melanopic effects (123 vs. 59 lux melanopic EDI) also differentially affect sleep besides neuroendocrine melatonin effects. Beyond this, we also studied whether the light conditions differentially modulate sensory processing during wakefulness and subsequent sleep.
Methods: In a preregistered study, twenty-nine healthy participants aged 18–30 years (15 women) were exposed to two metameric light conditions (high- vs. low-melanopic, differing by a factor of 2×, 7-day washout period) for one hour prior to their habitual bed time. Light exposure was followed by an 8-h sleep opportunity with full polysomnography. Objective sleep assessments were complemented by self-reported sleep evaluation after wake-up. Vespertine salivary melatonin levels, subjective sleepiness, and behavioural vigilance were assessed in regular intervals. Sensory processing was evaluated using an oddball paradigm participants completed during the light exposure in the evening and the following sleep period. Specifically, we were interested in neural responses (i.e., event-related potentials [ERPs]) to violations of expectations, that is, the mismatch response. For statistical analyses, we used standard non-parametric analyses except for ERPs, which were evaluated a using cluster-based permutation approach.
Results: Despite melatonin suppression by about 14% in the high- compared to the low-melanopic condition, light conditions did not differentially affect sleepiness, behavioural vigilance, objectively assessed sleep, or self-perceived sleep quality. A neural mismatch response was evident during wakefulness and all sleep stages and neither differentially modulated by light.
Conclusions: Light targeting the melanopsin system suppresses melatonin, but does not necessarily translate to altered levels of vigilance or sleepiness. Neither does it induce differential changes in sleep (quality), or basic sensory processing. This suggests that an interaction between melanopsin and cone-rod signals might be responsible for such effects to occur.