Acute social jetlag augments morning blood pressure surge: a randomized crossover trial

The study investigates whether acute social jetlag (SJL)—a weekend-related shift in sleep-wake timing that induces circadian misalignment—acutely affects the cardiovascular system, specifically the morning blood pressure surge. Prior work links chronic SJL to adverse cardiovascular outcomes, and simulated jetlag in animals acutely affects cardiovascular physiology. Morning BP shows circadian variation and an exaggerated morning surge predicts cardiovascular events; this surge often peaks on Mondays, potentially influenced by weekend SJL. The research question: does a brief, weekend-like acute SJL augment the Monday morning BP surge in humans? The study also explores potential mechanisms involving central arterial stiffness and autonomic regulation.

Design: Open-label, randomized crossover trial with two conditions: Social Jetlag (SJL) trial and Control (CON) trial. Registration: University Hospital Medical Information Network-Clinical Trial Registry (UMIN-CTR), Unique ID UMIN000046639. Trial name: Effect of acute social jetlag on risk factors of lifestyle-related diseases. Registration date: 17/01/2022. URL: https://center6.umin.ac.jp/cgi-open-bin/ctr_e/ctr_view.cgi?recptno=R000053204 Ethics: Approved by the Human Research Committee of Waseda University (approval No. 2021-214); conducted in accordance with the Declaration of Helsinki. Written informed consent obtained. Participants: 20 healthy men; nonsmokers; no history of hypertension (SBP ≤ 140 mmHg and DBP ≤ 90 mmHg), overt cardiovascular disease, or diabetes. Randomization and schedule: Participants randomized to CON or SJL first, then crossed over after a washout. Four-week protocol:

• Week 1: Screening of habitual sleep (Wed–Tue) to determine stable weekday sleep timing; ensured intraindividual weekday midsleep variability ≤ 2 h.
• Week 2: Pre-intervention measurement 1 on Friday morning; weekend intervention (SJL or CON) Friday and Saturday nights.
• Week 3: Post-intervention measurement 1 on Monday morning; washout until Thursday; pre-intervention measurement 2 on Friday; crossover to the opposite trial with instruction to replicate prior weekend’s diet and physical activity.
• Week 4: Post-intervention measurement 2 on Monday morning; follow-up until Thursday. Interventions:
• SJL trial: Bedtime delayed by 3 h on Friday and Saturday nights.
• CON trial: Maintain weekday sleep-wake schedule on the weekend. SJL quantification: SJL (min) = average midsleep time on weekend of intervention − average midsleep time on weekdays during screening. Wearables and behavior monitoring: Fitbit Charge 5 used throughout for sleep staging (bedtime, wake time, duration, REM, light, deep) and energy expenditure (5-min epochs). Physical activity quantified as energy expenditure in the 2 h before and after wake time. Participants logged food intake; instructed to replicate diet and activity across crossover weekends to reduce confounding. Pre/post measurement timing: Friday (pre) and Monday (post) mornings between 09:00–11:00, same time per participant. Pre-test restrictions: no food for ≥12 h; no caffeine/alcohol for ≥24 h. Primary cardiovascular measures:
• Central arterial stiffness: Carotid-femoral pulse wave velocity (cfPWV) via form PWV/ABI (Omron Colin). Carotid and femoral applanation tonometry waveforms (30 s). cfPWV = (Lhf − Lhc) / Tcf; within-subject CV 4.9 ± 4.1%.
• Ambulatory BP and HR: ABPM (TM-2441, A&D Medical) oscillometric measurements every 30–60 min during sleep and until 2 h after wake. Validated per ISO 81060-2:2013. Nights monitored: pre (Thu night→Fri morning) and post (Sun night→Mon morning) around each intervention. Definitions for ABPM-derived metrics: • Sleep BP: average during sleep. • Lowest nocturnal BP: average of three readings over 1.5 h at the nocturnal nadir. • Preawakening BP: average of four readings in the 2 h pre-awakening. • Morning BP: average of four readings in the first 2 h post-awakening. Morning BP surge calculations: • Morning BP surge = morning SBP − lowest nocturnal SBP • Preawakening morning BP surge = preawakening SBP − lowest nocturnal SBP • Wakening morning BP surge = preawakening SBP − morning SBP Within-subject CVs: morning SBP 7.1 ± 6.6%; lowest nocturnal SBP 7.0 ± 7.3%. Autonomic and hemodynamic assessments:
• Cardiovagal baroreflex sensitivity (cvBRS): Beatscope analysis of spontaneous sequences (≥3 beats) relating SBP and R-R interval (RRI); criteria: ΔSBP ≥ 1 mmHg, ΔRRI ≥ 4 ms, r > 0.8; up-up and down-down slopes averaged over last 5 min of 10-min rest.
• HR variability (HRV): Time-domain RMSSD; frequency-domain LF (0.04–0.15 Hz) and HF (0.15–0.4 Hz); LF/HF ratio assessed (MLS 310, AD Instruments).
• BP variability: LF component of SBP power spectral density (LF-SBP) via frequency-domain analysis (MLS 370) as a marker of sympathetic vascular modulation.
• Resting hemodynamics: ECG (BSM-2401) and finger photoplethysmography (Finometer MIDI) to reconstruct brachial BP; stroke volume via model flow; cardiac output (CO = SV × HR), total peripheral resistance (TPR = MAP/CO). Carotid pressure waveforms sampled at 1000 Hz (PowerLab) and calibrated to brachial DBP and MAP. Variables recorded for 60 s after 10 min supine rest; carotid SBP CV 6.1 ± 4.1%. Body composition: Bioelectrical impedance (InBody 720) to measure percent body fat and lean body mass. Statistical analysis: A priori power analysis (G*Power v3.1.9.6) indicated n=12 for power >0.80 with effect size f=0.40, α=0.05, two-way repeated-measures ANOVA (trial × time). Recruited 20 anticipating attrition. Data expressed as mean ± SD. Two-way repeated-measures ANOVA (trial × time) for outcomes; Bonferroni post hoc when applicable. One-way repeated-measures ANOVA for sleep variables, SJL, and energy balance across conditions. Computed absolute changes from Friday to Monday within each trial for cfPWV (ΔcfPWV), morning BP surge (Δmorning BP surge), and LF-SBP (ΔLF-SBP). Pearson correlations examined relationships among these deltas. Significance set at P < 0.05. Data exclusion: Six participants excluded (four with SJL < 2 h during SJL trial; two due to ABPM device failure). Final analyses based on 14 participants; sensitivity analyses including all participants were also conducted for select outcomes (morning BP surge, cfPWV, ambulatory SBP time course).

• Manipulation check: SJL increased only in the SJL trial (SJL: 181 ± 24 min) versus minimal change in CON (8 ± 47 min).
• cfPWV increased on Monday after SJL relative to Friday within SJL (P = 0.001) and was higher than Monday in CON (P = 0.007), indicating increased central arterial stiffness after acute SJL.
• Morning BP surge on Monday was significantly greater after SJL versus Friday within SJL (P < 0.001) and versus Monday in CON (P < 0.001), demonstrating augmentation of morning BP surge by acute SJL.
• Correlation: The change in cfPWV correlated positively with the change in morning BP surge (R = 0.587, P = 0.004), suggesting a mechanistic link between increased central arterial stiffness and the augmented morning BP surge.
• Sample analyzed: 14 participants completed all measurements; results were robust in sensitivity analyses including all recruited participants for key outcomes (as noted by authors).

The study directly addresses whether a brief, weekend-like shift in sleep timing (acute SJL) alters Monday morning BP dynamics. The findings show that a two-night, 3-hour bedtime delay led to a marked augmentation of the Monday morning SBP surge relative to both pre-intervention Friday and to a control weekend with habitual sleep timing. This supports the hypothesis that even acute circadian misalignment can acutely elevate cardiovascular stress at a time associated with higher event risk. The concomitant increase in cfPWV and its positive correlation with the increase in morning BP surge suggest that transient increases in central arterial stiffness may underlie or contribute to the exaggerated surge. Together with observed autonomic measures (protocol included HRV and LF-SBP analyses), the data imply that both vascular mechanical properties and autonomic regulation could mediate the impact of acute SJL on morning BP. These results are relevant to public health because many individuals experience weekend shifts in sleep timing; mitigating acute SJL may reduce Monday morning BP surges and potentially lower cardiovascular risk.

A two-night, 3-hour delay of bedtime (acute social jetlag) significantly augments the Monday morning blood pressure surge and increases central arterial stiffness (cfPWV) in healthy men. The change in arterial stiffness correlates with the change in morning BP surge, suggesting a mechanistic link. These findings indicate that even short-term circadian misalignment can adversely affect cardiovascular dynamics. Future research should investigate broader populations (including women, older adults, and individuals with hypertension), explore longer-term consequences of repeated acute SJL, delineate autonomic and vascular mechanisms in more detail, and test behavioral or chronobiological interventions to prevent or attenuate SJL-induced BP surges.

• Sample size and composition: Small final sample (n = 14) after exclusions; all participants were healthy men, limiting generalizability to women, older adults, and clinical populations.
• Intervention adherence/device issues: Four participants exhibited insufficient SJL (< 2 h) in the SJL condition and two had ABPM failures, which reduced analyzable data.
• Open-label design: Participants were not blinded to condition, which could influence behavior despite instructions to replicate diet and physical activity.
• Short-term intervention: The study assessed only a two-night acute SJL; long-term or cumulative effects of repeated weekend SJL were not evaluated.
• ABPM sampling: Ambulatory BP was measured at intervals (every 30–60 min), which may limit temporal resolution of BP nadirs and surges, though standardized definitions and averaging were used.