TY - JOUR
T1 - The effect of dim light at night on cerebral hemodynamic oscillations during sleep
T2 - A near-infrared spectroscopy study
AU - Kim, Tae Joon
AU - Lee, Byeong Uk
AU - Sunwoo, Jun Sang
AU - Byun, Jung Ick
AU - Moon, Jangsup
AU - Lee, Soon Tae
AU - Jung, Keun Hwa
AU - Chu, Kon
AU - Kim, Manho
AU - Lim, Jong Min
AU - Lee, Eunil
AU - Lee, Sang Kun
AU - Jung, Ki Young
N1 - Funding Information:
This was not an industry-supported study. This study was supported by the Future Environmental R&D grant funded by the Korea Environmental Industry and Technology Institute (No. RE201206020) and was supported by a National Research Foundation of Korea (NRF) grant funded by the Korean government (MSIP) (No. 2014R1A2A2A04003858).
Publisher Copyright:
© 2017 Taylor & Francis Group, LLC.
PY - 2017/11/26
Y1 - 2017/11/26
N2 - Recent studies have reported that dim light at night (dLAN) is associated with risks of cardiovascular complications, such as hypertension and carotid atherosclerosis; however, little is known about the underlying mechanism. Here, we evaluated the effect of dLAN on the cerebrovascular system by analyzing cerebral hemodynamic oscillations using near-infrared spectroscopy (NIRS). Fourteen healthy male subjects underwent polysomnography coupled with cerebral NIRS. The data collected during sleep with dim light (10 lux) were compared with those collected during sleep under the control dark conditions for the sleep structure, cerebral hemodynamic oscillations, heart rate variability (HRV), and their electroencephalographic (EEG) power spectrum. Power spectral analysis was applied to oxy-hemoglobin concentrations calculated from the NIRS signal. Spectral densities over endothelial very-low-frequency oscillations (VLFOs) (0.003–0.02 Hz), neurogenic VLFOs (0.02–0.04 Hz), myogenic low-frequency oscillations (LFOs) (0.04–0.15 Hz), and total LFOs (0.003–0.15 Hz) were obtained for each sleep stage. The polysomnographic data revealed an increase in the N2 stage under the dLAN conditions. The spectral analysis of cerebral hemodynamics showed that the total LFOs increased significantly during slow-wave sleep (SWS) and decreased during rapid eye movement (REM) sleep. Specifically, endothelial (median of normalized value, 0.46 vs. 0.72, p = 0.019) and neurogenic (median, 0.58 vs. 0.84, p = 0.019) VLFOs were enhanced during SWS, whereas endothelial VLFOs (median, 1.93 vs. 1.47, p = 0.030) were attenuated during REM sleep. HRV analysis exhibited altered spectral densities during SWS induced by dLAN, including an increase in very-low-frequency and decreases in low-frequency and high-frequency ranges. In the EEG power spectral analysis, no significant difference was detected between the control and dLAN conditions. In conclusion, dLAN can disturb cerebral hemodynamics via the endothelial and autonomic systems without cortical involvement, predominantly during SWS, which might represent an underlying mechanism of the increased cerebrovascular risk associated with light exposure during sleep.
AB - Recent studies have reported that dim light at night (dLAN) is associated with risks of cardiovascular complications, such as hypertension and carotid atherosclerosis; however, little is known about the underlying mechanism. Here, we evaluated the effect of dLAN on the cerebrovascular system by analyzing cerebral hemodynamic oscillations using near-infrared spectroscopy (NIRS). Fourteen healthy male subjects underwent polysomnography coupled with cerebral NIRS. The data collected during sleep with dim light (10 lux) were compared with those collected during sleep under the control dark conditions for the sleep structure, cerebral hemodynamic oscillations, heart rate variability (HRV), and their electroencephalographic (EEG) power spectrum. Power spectral analysis was applied to oxy-hemoglobin concentrations calculated from the NIRS signal. Spectral densities over endothelial very-low-frequency oscillations (VLFOs) (0.003–0.02 Hz), neurogenic VLFOs (0.02–0.04 Hz), myogenic low-frequency oscillations (LFOs) (0.04–0.15 Hz), and total LFOs (0.003–0.15 Hz) were obtained for each sleep stage. The polysomnographic data revealed an increase in the N2 stage under the dLAN conditions. The spectral analysis of cerebral hemodynamics showed that the total LFOs increased significantly during slow-wave sleep (SWS) and decreased during rapid eye movement (REM) sleep. Specifically, endothelial (median of normalized value, 0.46 vs. 0.72, p = 0.019) and neurogenic (median, 0.58 vs. 0.84, p = 0.019) VLFOs were enhanced during SWS, whereas endothelial VLFOs (median, 1.93 vs. 1.47, p = 0.030) were attenuated during REM sleep. HRV analysis exhibited altered spectral densities during SWS induced by dLAN, including an increase in very-low-frequency and decreases in low-frequency and high-frequency ranges. In the EEG power spectral analysis, no significant difference was detected between the control and dLAN conditions. In conclusion, dLAN can disturb cerebral hemodynamics via the endothelial and autonomic systems without cortical involvement, predominantly during SWS, which might represent an underlying mechanism of the increased cerebrovascular risk associated with light exposure during sleep.
KW - Cerebral hemodynamics
KW - electroencephalographic spectral analysis
KW - heart rate variability
KW - light at night
KW - near-infrared spectroscopy
UR - http://www.scopus.com/inward/record.url?scp=85031994261&partnerID=8YFLogxK
U2 - 10.1080/07420528.2017.1363225
DO - 10.1080/07420528.2017.1363225
M3 - Article
C2 - 29064336
AN - SCOPUS:85031994261
SN - 0742-0528
VL - 34
SP - 1325
EP - 1338
JO - Chronobiology International
JF - Chronobiology International
IS - 10
ER -