Cognitive control, bedtime patterns, and testing time in female adolescent students: behavioral and neuro-electrophysiological correlates.

Introduction: Shorter and/or disrupted sleep during adolescence is associated with cognitive and mental health risks, particularly in females. We explored the relationship between bedtime behavior patterns co-varying with Social Jet Lag (SJL) and School Start Times (SST) and neurocognitive performance in adolescent female students. Methods: To investigate whether time of day (morning vs. afternoon), early SSTs and days of the school week can be correlated with neurocognitive correlates of sleep insufficiency, we recruited 24 female students aged 16-18 to report sleep logs, and undergo event-related electroencephalographic recordings on Monday, Wednesday, mornings, and afternoons. Using a Stroop task paradigm, we analyzed correlations between reaction times (RTs), accuracy, time of day, day of week, electroencephalographic data, and sleep log data to understand what relationships may exist. Results: Participants reported a 2-h sleep phase delay and SJL. Stroop interference influenced accuracy on Monday and Wednesday similarly, with better performance in the afternoon. For RTs, the afternoon advantage was much larger on Monday than Wednesday. Midline Event-Related Potentials (ERPs) yielded higher amplitudes and shorter latencies on Wednesday morning and Monday afternoon, in time windows related to attention or response execution. A notable exception were delayed ERP latencies on Wednesday afternoon. The latter could be explained by the fact that delta EEG waves tended to be the most prominent, suggesting heightened error monitoring due to accumulating mental fatigue. Discussion: These findings provide insights into the interaction between SJL and SST and suggest evidence-based criteria for planning when female adolescents should engage in cognitive-heavy school activities such as tests or exams.

Circadian variation of heart rate variability across sleep stages.

STUDY OBJECTIVES: Nocturnal cardiovascular events are more frequent at the beginning and end of the night. It was proposed that this pattern reflects the nocturnal distribution of sleep and sleep stages. Using heart rate variability (HRV), we recently showed an interaction between the circadian system and vigilance states on the regulation of cardiac rhythmicity. Here, we further investigate this interaction in order to clarify the specific effects of sleep stages on the regulation of the heart. DESIGN: Participants underwent a 72-h ultradian sleep-wake cycle procedure in time isolation consisting of alternating 60-min wake episodes in dim light and 60-min nap opportunities in total darkness. SETTING: Time isolation suite. PATIENTS OR PARTICIPANTS: Fifteen healthy young participants; two were subsequently excluded. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: The current study revealed that sleep onset and progression to deeper sleep stages was associated with a shift toward greater parasympathetic modulation, whereas rapid eye movement (REM) sleep was associated with a shift toward greater sympathetic modulation. We found a circadian rhythm of heart rate (HR) and high-frequency power during wakefulness and all non-REM sleep stages. A significant circadian rhythm of HR and sympathovagal balance of the heart was also observed during REM sleep. During slow wave sleep, maximal parasympathetic modulation was observed at ∼02:00, whereas during REM sleep, maximal sympathetic modulation occurred in the early morning. CONCLUSION: The circadian and sleep stage-specific effects on heart rate variability are clinically relevant and contribute to the understanding of the degree of cardiovascular vulnerability during sleep.

A circadian rhythm in heart rate variability contributes to the increased cardiac sympathovagal response to awakening in the morning.

Morning hours are associated with a heightened risk of adverse cardiovascular events. Recent evidence suggests that the sleep-wake cycle and endogenous circadian system modulate cardiac function in humans and may contribute to these epidemiological findings. The aim of the present study was to investigate the interaction between circadian and sleep-wake-dependent processes on heart rate variability (HRV). Fifteen diurnally active healthy young adults underwent a 72-h ultradian sleep-wake cycle (USW) procedure (alternating 60-min wake episodes in dim light and 60-min nap opportunities in total darkness) in time isolation. The present study revealed a significant main effect of sleep-wake-dependent and circadian processes on cardiac rhythmicity, as well as a significant interaction between these processes. Turning the lights off was associated with a rapid increase in mean RR interval and cardiac parasympathetic modulation (high-frequency [HF] power), whereas low-frequency (LF) power and sympathovagal balance (LF:HF ratio) were reduced (p ≤ .001). A significant circadian rhythm in mean RR interval and HRV components was observed throughout the wake and nap episodes (p ≤ .001). Sleep-to-wake transitions occurring in the morning were associated with maximal shifts towards sympathetic autonomic activation as compared to those occurring during the rest of the day. Namely, peak LF:HF ratio was observed in the morning, coincidental with peak salivary cortisol levels. These results contribute to our understanding of the observed increase in cardiovascular vulnerability after awakening in the morning.