Does cardiovascular autonomic modulation correspond to the increase in dim-light onset of melatonin? A preliminary analysis

Abstract

Introduction: The endogenous circadian system promotes the rise in melatonin approximately every 24 hours. In the laboratory, dim light melatonin onset (DLMO) is used as the gold standard method to assess circadian phase. Exogenous melatonin affects cardiac sympathovagal balance and vasomotor sympathetic modulation. Whether or not the endogenous increase in melatonin corresponds to changes in cardiovascular autonomic modulation is unclear. Objective: To evaluate if the timing of DLMO corresponds to the timing of changes in cardiovascular autonomic indices. Methods: Five healthy adults (3 females, age 23.8±SD1.8 y) completed a minimum of four nights of sleep regularization by maintaining a self-selected 8h in bed each night before the experiment. The day after regularization, they reported to the laboratory ~8 hours before bedtime. Measurements for melatonin and cardiovascular autonomic modulation started 6 hours before bedtime and continued 1 hour after. Saliva samples were collected every 30 minutes. At the end of every hour, 10 minutes of continuous R-R intervals (R-R) and systolic blood pressure (SBP) were recorded via electrocardiogram and beat-to-beat finger photoplethysmography, respectively. As currently established, DLMO was defined as the interpolated time for melatonin increase over 3pg/ml. Cardiovascular autonomic indexes were run through CardioSeries v.2 to create a temporal series for R-R interval and systolic blood pressure. Cardiac autonomic modulation was assessed by applying the spectral analysis using the fast Fourier transformation method and time domain analysis of heart rate variability (HRV) and spectral analysis of blood pressure variability (BPV). For each autonomic index, data were plotted and fitted with a segmental linear regression to reveal the intercept of the two segments to define the autonomic onset (AO). A paired t-test compared the difference between DLMO and AO times. Bland-Altman plots with a 95% limit of agreement (LOA) identified the distribution of differences between the methods. Additionally, a one-sample t-test compared the differences between methods to a fixed time clock range. Data are shown as mean ± SD and significance was set as p<0.05. Results: AO time calculated for all indexes from HRV and BPV were not statistically different compared to DLMO time (R-R: +16±86 mins, P=0.70; root mean square of successive differences (RMSSD): -20±91 mins, P=0.67; low frequency (LF) nu: +29±52 mins, P=0.74; high frequency (HF) nu: -43±91 mins, P=0.23; LFHF: -26±73 mins, P=0.47; SBP: -14±104 mins, P=0.78; LFSBP: -6±107 mins, P=0.90). The Bland Altman plots did not identify any systematic difference between AO and DLMO times. The smallest difference was LFnu with a LOA 95% from -73 to +131 minutes, while the largest difference was LFSBP with LOA 95% from -217 to +204 minutes. Additionally, the difference between DLMO and AO LFnu times (LFnu: +29±52) was statistically similar from -36 to +95 minutes. Conclusion: In young healthy adults, our preliminary data shows that AO times of cardiovascular autonomic indexes correspond to salivary DLMO. A larger dataset with more frequent simultaneous measurements of melatonin and cardiovascular autonomic modulation are essential to confirm our preliminary findings. Medical Research Foundation of Oregon, OHSU OFDIR, R01HL163232. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.