0117 Impact of Light Exposure during Sleep on Cardiometabolic Function

Abstract

Introduction
Artificial light exposure is increasingly widespread, particularly at night. Light exposure at night is known to impact circadian rhythms such as melatonin and sleep, and disturbances in these rhythms have been shown to affect cardiometabolic function. As such, the aim of this study was to test the hypothesis that light exposure at night during sleep negatively impacts cardiometabolic outcomes, possibly via disruptions to sleep architecture and melatonin profiles.

Methods
Twenty healthy adults 18–40 years of age were randomized into Dark-Dark (DD) or Dark-Light (DL) groups and run in parallel for a three day and two night stay. Participants had 8 hours of sleep opportunity each night starting at habitual bedtime determined from one week of actigraphy with sleep diary. The DL group (n=10, 2 males, ages 26.61 ± 4.64 years, BMI 23.25 ± 3.94 kg/m^2) slept in the dark < 3 lux on Night 1 and slept in overhead room light of 100 lux on Night 2, while the DD group (n=10, 4 males, ages 26.78 ± 5.15 years, BMI 24.25 ± 3.71 kg/m^2) slept in the dark <3 lux on both Nights 1 and 2. Overnight polysomnography and hourly blood sampling for melatonin were collected on both nights. Oral glucose tolerance tests were performed on both mornings following sleep in the dark or 100 lux of light. Repeated measures ANOVA were performed between groups (DL vs. DD) with Day (Day 1 vs Day 2) and Time of Day as within-subject factors.

Results
Homeostatic model assessment of insulin resistance values were significantly higher (p<0.05) in the morning following sleep in the light (DL group) compared to sleep in the dark (DD group). This effect was primarily due to increased insulin levels for DL compared to DD group, for which there was a trend for group by day effect (p<0.09).

Conclusion
A single night of light exposure during sleep acutely impacts insulin resistance, and chronic overnight exposure may have long-term effects on metabolic function.

Support (If Any)
This research was supported National Institutes of Health grants 5T32HL7909, P01AG11412, and 8UL1TR000150-05.

Full text

A46
SLEEP, Volume 41, Abstract Supplement, 2018
0116
AUTONOMIC AND SLEEP INTERACTION DURING
ACOUSTIC ENHANCEMENT OF SLEEP
Grimaldi D1, Papalambros NA1, Reid KJ1, Abbott SM1, Malkani RG1,
Santostasi G1, Sanchez DJ2, Paller KA3, Zee PC1
1Northwestern University, Chicago, IL, 2SRI International, Menlo
park, CA, 3Northwestern University, Evanston, IL, 4Northwestern
University, Chicago, IL
Introduction: Acoustic stimulation applied during sleep can enhance
slow wave activity (SWA). Given the relationship between sleep and
the autonomic nervous system (ANS), we aimed to explore how these
two systems interacted in healthy young adults receiving acoustic
stimulation.
Methods: Twenty subjects (25 ± 4 years, 75% female) participated
in a randomized cross-over study with two 2-night visits. After one
night of adaptation, participants were randomized to either receive
stimulation or sham stimulation on the following night. During NREM
sleep, a phase locked auditory stimulation procedure using single input
from the midline frontopolar channel, was used to deliver 50ms pulses
of pink noise in blocks of 5 (ON intervals) followed by a pause of
approximately 6 seconds (OFF intervals). Changes in EEG spectral
power across multiple frequency bands were calculated during ON and
OFF intervals for both conditions. ANS function was assessed using
heart rate variability (HRV) that was quantified before “lights off ” over
a 5-minute period in supine position and during 5-minute periods of
slow wave sleep (SWS) in the first three cycles of sleep. The follow-
ing HRV measures, representative of cardiac vagal regulation, were
calculated: RMSSD (square root of the mean squared differences of
successive NN-intervals) and HF% (high frequency, relative power).
Results: Acoustic stimulation increased SWA (0.5-4Hz) by 40% and
sigma activity (11-15Hz) by 14% during ON vs OFF intervals com-
pared to sham (p<0.01) without changing the overall spectral power
across the night. RMSSD before sleep was positively correlated with
both SWA (p=0.014, R=0.61) and sigma activity (p=0.006, R=0.60)
increase in ON vs OFF intervals during acoustic stimulation. During
SWS, HF% was higher in the 2nd and 3rd cycle of sleep during the
night of stimulation compared to sham (p=0.02).
Conclusion: Higher vagal cardiac modulation before sleep character-
ized participants who responded to acoustic stimulation with higher
SWA and sigma activity enhancement. Sound-induced EEG changes
were in turn associated with improved vagal modulation of the heart
during SWS. These results suggest the ANS plays a crucial role in the
in the brain’s response to acoustic stimulation.
Support (If Any): DARPA W911NF-16-2-0021.
0117
IMPACT OF LIGHT EXPOSURE DURING SLEEP ON
CARDIOMETABOLIC FUNCTION
Mason I, Grimaldi D, Malkani RG, Reid KJ, Zee PC
Northwestern University, Feinberg School of Medicine, Department
of Neurology, Chicago, IL
Introduction: Artificial light exposure is increasingly widespread,
particularly at night. Light exposure at night is known to impact cir-
cadian rhythms such as melatonin and sleep, and disturbances in these
rhythms have been shown to affect cardiometabolic function. As such,
the aim of this study was to test the hypothesis that light exposure at
night during sleep negatively impacts cardiometabolic outcomes, pos-
sibly via disruptions to sleep architecture and melatonin profiles.
Methods: Twenty healthy adults 18–40 years of age were randomized
into Dark-Dark (DD) or Dark-Light (DL) groups and run in parallel for
a three day and two night stay. Participants had 8 hours of sleep opportu-
nity each night starting at habitual bedtime determined from one week
of actigraphy with sleep diary. The DL group (n=10, 2 males, ages
26.61 ± 4.64 years, BMI 23.25 ± 3.94 kg/m^2) slept in the dark < 3 lux on
Night 1 and slept in overhead room light of 100 lux on Night 2, while the
DD group (n=10, 4 males, ages 26.78 ± 5.15 years, BMI 24.25 ± 3.71 kg/
m^2) slept in the dark <3 lux on both Nights 1 and 2. Overnight polysom-
nography and hourly blood sampling for melatonin were collected on both
nights. Oral glucose tolerance tests were performed on both mornings fol-
lowing sleep in the dark or 100 lux of light. Repeated measures ANOVA
were performed between groups (DL vs. DD) with Day (Day 1 vs Day
2) and Time of Day as within-subject factors.
Results: Homeostatic model assessment of insulin resistance values
were significantly higher (p<0.05) in the morning following sleep in
the light (DL group) compared to sleep in the dark (DD group). This
effect was primarily due to increased insulin levels for DL compared to
DD group, for which there was a trend for group by day effect (p<0.09).
Conclusion: A single night of light exposure during sleep acutely
impacts insulin resistance, and chronic overnight exposure may have
long-term effects on metabolic function.
Support (If Any): This research was supported National Institutes of
Health grants 5T32HL7909, P01AG11412, and 8UL1TR000150-05.
0118
ENDOGENOUS CIRCADIAN RHYTHM IN DIET-INDUCED
THERMOGENESIS IN HUMANS
Vujovic N, Barr D, Bowen JJ, Byrne S, Chaloka V, Chellappa S,
Heng S, Kelly LM, Kerlin K, Mistretta J, Nedeltcheva A, Qian J,
Rahman N, Van Zee C, Scheer FA
Harvard Medical School/Brigham and Women’s Hospital, Boston, MA
Introduction: Recent studies suggest that eating during the biological
night/habitual rest phase may increase obesity risk, even when caloric
intake and physical activity are controlled for. Preliminary data indicate
that the circadian timing system can influence energy expenditure (EE)
after a meal, i.e. diet-induced thermogenesis (DIT), with lower DIT in the
biological evening (during a night shift simulation protocol). Although
circadian unmasking protocols using constant routine (CR) have shown
rhythms in overall EE, they have not thus far revealed circadian rhythms
in DIT due to their high meal frequency (every 2 hours). To address this
question, we used a CR protocol with meals spaced 6 hours apart.
Methods: Eleven healthy, overweight adults (BMI 28.7 ± 0.7; age
36 ± 2.6; 2 female) maintained strict regular sleep and meal schedules
for 2-3weeks outpatient and 6 days inpatient before participating in a
metabolic CR assessment. During CR, participants remained awake
for 37 hours in dim (~4lux) light, in constant posture, consuming
identical test meals every 6 hours. Using the Vmax Encore indirect
calorimeter, EE was measured for 15–20 minutes immediately preced-
ing each meal, then again at 30, 90, 150 and 210 minutes after the
start of the meal. DIT for each meal was quantified as area under the
curve for that set of 5 recordings. Core body temperature (CBT) was
used to assess circadian phase during each individual DIT assessment.
A cosinor mixed model was applied to normalized DIT data.
Results: Our model indicates a significant circadian rhythm in DIT
(p=0.0076), with minimum occurring at 330 degrees (2 hours before
CBT minimum), elevated plateau at 90–220 degrees, and an amplitude
of 2.5% (of CR mean DIT). This protocol did not reveal significant cir-
cadian oscillations in 6-hour fasting EE or respiratory quotient.
Conclusion: This is the first characterization of an endogenous circa-
dian rhythm in DIT. Our results suggest that the timing of the circadian
nadir in DIT may contribute to positive energy balance in those eating
during the biological night.
A. Basic and Translational Sleep Science VI. Physiology
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