Chronotype and Affective Response to Sleep Restriction and Subsequent Sleep Deprivation.

Prior research indicates that sleep restriction, sleep deprivation, and circadian misalignment diminish positive affect, whereas effects on negative affect are inconsistent. One potential factor that may influence an individual's affective response to sleep restriction, sleep deprivation, and circadian misalignment is chronotype. Later chronotypes generally report higher negative affect and lower positive affect under typical sleep conditions; however, there is mixed evidence for an influence of chronotype on affective responses to sleep restriction and sleep deprivation. The present study examined the effect of chronotype on positive and negative affect during sleep restriction and subsequent total sleep deprivation. Sixteen healthy adults (Mage = 28.2 years, SDage = 11.6 years) were classified as earlier or later chronotypes using multiple chronotype definitions: morningness-eveningness (MEQ), mid-sleep on free days corrected (MSFsc), habitual mid-sleep timing, dim light melatonin onset (DLMO), and phase relationship between DLMO and bedtime. Participants completed a 10-day protocol with one night of sleep restriction and subsequent 28 h total sleep deprivation. Affect was assessed hourly during scheduled wakefulness with the Positive and Negative Affect Schedule (PANAS). Data were analyzed with mixed-model analyses of variance (ANOVAs). During sleep restriction and subsequent sleep deprivation, positive affect decreased and negative affect increased. Across all chronotype measures, relatively later chronotypes demonstrated vulnerability to increased negative affect during sleep loss. The influence of chronotype on positive affect during sleep loss varied by chronotype measure. These findings suggest later chronotypes are more vulnerable to affective impairments during sleep loss and circadian misalignment, even when late chronotype is not extreme.

Distribution of dim light melatonin offset (DLMOff) and phase relationship to waketime in healthy adults and associations with chronotype.

OBJECTIVES: Dim light melatonin onset, or the rise in melatonin levels representing the beginning of the biological night, is the gold standard indicator of circadian phase. Considerably less is known about dim light melatonin offset, or the decrease in melatonin to low daytime levels representing the end of the biological night. In the context of insufficient sleep, morning circadian misalignment, or energy intake after waketime but before dim light melatonin offset, is linked to impaired insulin sensitivity, suggesting the need to characterize dim light melatonin offset and identify risk for morning circadian misalignment. METHODS: We examined the distributions of dim light melatonin offset clock hour and the phase relationship between dim light melatonin offset and waketime, and associations between dim light melatonin offset, phase relationship, and chronotype in healthy adults (N = 62) who completed baseline protocols measuring components of the circadian melatonin rhythm and chronotype. RESULTS: 74.4% demonstrated dim light melatonin offset after waketime, indicating most healthy adults wake up before the end of biological night. Later chronotype (morningness-eveningness, mid-sleep on free days corrected, and average mid-sleep) was associated with later dim light melatonin offset clock hour. Later chronotype was also associated with a larger, positive phase relationship between dim light melatonin offset and waketime, except for morningness-eveningness. CONCLUSIONS: These findings suggest morning circadian misalignment risk among healthy adults, which would not be detected if only dim light melatonin onset were assessed. Chronotype measured by sleep timing may better predict this risk in healthy adults keeping a consistent sleep schedule than morningness-eveningness preferences. Additional research is needed to develop circadian biomarkers to predict dim light melatonin offset and evaluate appropriate dim light melatonin offset timing to promote health.

Ad libitum Weekend Recovery Sleep Fails to Prevent Metabolic Dysregulation during a Repeating Pattern of Insufficient Sleep and Weekend Recovery Sleep.

People commonly increase sleep duration on the weekend to recover from sleep loss incurred during the workweek. Whether ad libitum weekend recovery sleep prevents metabolic dysregulation caused by recurrent insufficient sleep is unknown. Here, we assessed sleep, circadian timing, energy intake, weight gain, and insulin sensitivity during sustained insufficient sleep (9 nights) and during recurrent insufficient sleep following ad libitum weekend recovery sleep. Healthy, young adults were randomly assigned to one of three groups: (1) control (CON; 9-h sleep opportunities, n = 8), (2) sleep restriction without weekend recovery sleep (SR; 5-h sleep opportunities, n = 14), and (3) sleep restriction with weekend recovery sleep (WR; insufficient sleep for 5-day workweek, then 2 days of weekend recovery, then 2 nights of insufficient sleep, n = 14). For SR and WR groups, insufficient sleep increased after-dinner energy intake and body weight versus baseline. During ad libitum weekend recovery sleep, participants cumulatively slept ∼1.1 h more than baseline, and after-dinner energy intake decreased versus insufficient sleep. However, during recurrent insufficient sleep following the weekend, the circadian phase was delayed, and after-dinner energy intake and body weight increased versus baseline. In SR, whole-body insulin sensitivity decreased ∼13% during insufficient sleep versus baseline, and in WR, whole-body, hepatic, and muscle insulin sensitivity decreased ∼9%-27% during recurrent insufficient sleep versus baseline. Furthermore, during the weekend, total sleep duration was lower in women versus men, and energy intake decreased to baseline levels in women but not in men. Our findings suggest that weekend recovery sleep is not an effective strategy to prevent metabolic dysregulation associated with recurrent insufficient sleep.