Fig. 1: Longitudinal ECG reveals differential circadian regulation of sinoatrial (SA) and atrioventricular (AV) node function and decoupling by mistimed sleep.

A. Schematic of 4-day laboratory session²⁰, with total sleep deprivation (TSD) and recovery nap on day 3 (n = 14 individuals). B–F HR (B), HRV (C), and z-scored ECG parameter profiles under baseline (black) and TSD (orange) days (shading indicates + /−SEM), highlighting the profound impact of mistimed sleep on RR (D) and QT (E), but not PR_seg (F). HR has been derived from the RR interval and is shown for clarity. At baseline, all parameters were rhythmic based on cosinor analysis (P < 0.001). Individual traces were excluded from waveform analysis where data coverage fell <70% of the 5-min time bins; n (baseline/TSD) = 13/14 (B), 12/14 (C), 13/14 (D), 11/12 (E), 12/14 (F). Mean ECG parameters were quantified across a 4 h mid-night and mid-day (equivalent to the nap window on day 3) analysis windows on the baseline and TSD days (two-way RM ANOVA/Mixed model; n = 14 (B, C, D, F), 12 (E)). G, H Under baseline conditions, LOWESS fit of ECG profiles (G) and cross-correlation (H; yellow: RR vs RR, blue: QT vs RR, orange: PR_seg vs RR) revealed a significant phase delay in PR_seg rhythm relative to that of RR (Gaussian fit with one-sample T test; n = 13, 11, 12, respectively). I Acute changes in RR were mirrored by a concordant change in QT, but not PR_seg duration (ΔRR reflects z-scored difference in RR between sequential 5-min analysis bins; Δparam reflects the concurrent change in QT or PR). All data presented as group mean ± SEM; ns P > 0.05, **P < 0.01, ***P < 0.001. bpm = beats per minute; std = standard deviation. See Supplementary Fig. S2 for additional information; source data and statistical details are provided as a Source Data File.