This study evaluated the daily, temporal associations between sleep and daytime physical activity and sedentary behavior among adolescents from the Fragile Families & Child Wellbeing Study. A sub-sample of the cohort at age 15 (N = 417) wore actigraphy monitors for one week during the school year from which we derived daily minutes in sedentary and moderate-to-vigorous physical activity (MVPA) and nighttime sleep measures. Multilevel models tested temporal associations of nightly sleep onset, offset, duration, and sleep maintenance efficiency, with daily MVPA and sedentary behavior. More MVPA than an individual’s average was associated with earlier sleep onset (p < 0.0001), longer duration (p = 0.03), and higher sleep maintenance efficiency (p < 0.0001). On days with more sedentary behavior than an individual’s average, sleep onset and offset were delayed (p < 0.0001), duration was shorter (p < 0.0001), and sleep maintenance efficiency was higher (p = 0.0005). Conversely, nights with earlier sleep onset predicted more next-day sedentary behavior (p < 0.0001), and nights with later sleep offset and longer sleep duration were associated with less MVPA (p < 0.0001) and less sedentary time (p < 0.0001, p = 0.004) the next day. These bidirectional associations between sleep and physical activity suggest that promoting MVPA may help to elicit earlier bedtimes, lengthen sleep duration, and increase sleep efficiency, critical for healthy adolescent development.
Chronic inadequate sleep is associated with increased risk of cardiometabolic diseases. The mechanisms involved are poorly understood but involve changes in insulin sensitivity, including within adipose tissue. The aim of this study was to assess the effects of sleep restriction on nonesterified fatty acid (NEFA) suppression profiles in response to an intravenous glucose tolerance test (IVGTT) and to assess whether 2 nights of recovery sleep (a “weekend”) is sufficient to restore metabolic health. We hypothesized that sleep restriction impairs both glucose and lipid metabolism, specifically adipocyte insulin sensitivity, and the dynamic lipemic response of adipocyte NEFA release during an IVGTT. Fifteen healthy men completed an inpatient study of 3 baseline nights (10 h of time in bed/night), followed by 5 nights of 5 h of time in bed/night and 2 recovery nights (10 h of time in bed/night). IVGTTs were performed on the final day of each condition. Reductions in insulin sensitivity without a compensatory change in acute insulin response to glucose were consistent with prior studies (insulin sensitivity P = 0.002; acute insulin response to glucose P = 0.23). The disposition index was suppressed by sleep restriction and did not recover after recovery sleep ( P < 0.0001 and P = 0.01, respectively). Fasting NEFAs were not different from baseline in either the restriction or recovery conditions. NEFA rebound was significantly suppressed by sleep restriction ( P = 0.01) but returned to baseline values after recovery sleep. Our study indicates that sleep restriction impacts NEFA metabolism and demonstrates that 2 nights of recovery sleep may not be adequate to restore glycemic health.
OBJECTIVES High school start times are a key contributor to insufficient sleep. This study investigated associations of high school start times with bedtime, wake time, and time in bed among urban teenagers. DESIGN Daily-diary study nested within the prospective Fragile Families and Child Wellbeing Study. SETTING 20 US cities. PARTICIPANTS 413 teenagers who completed ≥1 daily diary report on a school day. MEASUREMENTS Participating teens were asked to complete daily diaries for 7 consecutive days. School-day daily diaries (3.8 ±1.6 entries per person) were used in analyses (N=1,555 school days). High school start time, the main predictor, was categorized as 7:00–7:29 AM (15%), 7:30–7:59 AM (22%), 8:00–8:29 AM (35%) and 8:30 AM or later (28%). Multilevel modeling examined the associations of school start times with bedtime, wake time, and time in bed. Models adjusted for age, sex, race/ethnicity, household income, caregiver’s education, and school type. RESULTS Teens with the earliest high school start times (7:00–7:29 AM) obtained 46 minutes less time in bed on average compared to teens with high school start times at 8:30 AM or later (p<0.001). Teens exhibited a dose-response relationship between earlier school start times and shorter time in bed, primarily due to earlier wake times (p<0.05). Start times after 8:30 AM were associated with increased time in bed, extending morning sleep by 27–57 minutes (p<0.05) when compared to teens with earlier school start times. CONCLUSION Later school start times are associated with later wake times in our large, diverse sample. Teens starting school at 8:30 AM or later are the only group with an average time in bed permitting 8 hours of sleep, the minimum recommended by expert consensus for health and wellbeing.
Supplementary key words triglycerides • nutrition • lipolysis and fatty acid metabolism • diet and dietary lipids • fatty acid • insulin resistance • inflammation • hormones • glucose According to the Centers for Disease Control and Prevention, one in three US adults sleeps fewer than 7 h per night, increasing their risk of obesity and for risk of developing CVD, type 2 diabetes, and earlier mortality, among other comorbidities (1-4). The mechanisms by which chronic insufficient sleep increases cardiometabolic disease risk are poorly understood, but results from carefully controlled laboratory studies demonstrate that sleep restriction simultaneously increases orexigenic hormonal signaling and impairs glucose metabolic functioning (5, 6). Furthermore, there is mounting evidence that adipocyte insulin sensitivity and function are impaired by sleep restriction resulting in aberrantly elevated overnight and early morning NEFAs (7-10). Adipocytes are a key integrator of systemic metabolism, absorbing and storing excess energy postprandially and releasing stored fatty acids as needed to meet the energy requirements of the body (11). Adipocytes respond to the postprandial increase in insulin by suppressing intracellular TG lipolysis and by increasing extracellular lipolysis by transporting LPL from intracellular vesicles to the surface Abstract Chronic sleep restriction, or inadequate sleep, is associated with increased risk of cardiometabolic disease. Laboratory studies demonstrate that sleep restriction causes impaired whole-body insulin sensitivity and glucose disposal. Evidence suggests that inadequate sleep also impairs adipose tissue insulin sensitivity and the NEFA rebound during intravenous glucose tolerance tests, yet no studies have examined the effects of sleep restriction on high-fat meal lipemia. We assessed the effect of 5 h time in bed (TIB) per night for four consecutive nights on postprandial lipemia following a standardized high-fat dinner (HFD). Furthermore, we assessed whether one night of recovery sleep (10 h TIB) was sufficient to restore postprandial metabolism to baseline. We found that postprandial triglyceride (TG) area under the curve was suppressed by sleep restriction (P = 0.01), but returned to baseline values following one night of recovery. Sleep restriction decreased NEFAs throughout the HFD (P = 0.02) and NEFAs remained suppressed in the recovery condition (P = 0.04). Sleep restriction also decreased participant-reported fullness or satiety (P = 0.03), and decreased postprandial interleukin-6 (P < 0.01). Our findings indicate that four nights of 5 h TIB per night impair postprandial lipemia and that one night of recovery sleep may be adequate for recovery of TG metabolism, but not for markers of adipocyte function.
Study Objectives: Having a regular, age-appropriate bedtime and sufficient sleep from early childhood may be important for healthy weight in adolescence. This study aimed to (1) identify heterogeneous groups of children by bedtime and sleep routines and (2) test longitudinal associations of childhood bedtime and sleep routine groups with adolescent body mass index (BMI). Methods: We analyzed longitudinal data from the Fragile Families and Child Wellbeing Study, a national birth cohort from 20 US cities (N = 2196). Childhood bedtime and sleep routines were assessed by mothers' reports of their children's presence and timing of bedtimes, adherence to bedtimes, and habitual sleep duration at ages 5 and 9. At age 15, these adolescents reported their height and weight, which were used to calculate BMI z-score. Results: Latent Class Analysis revealed four groups of childhood bedtime and sleep routines: No Bedtime Routine Age 5 (Group 1), No Bedtime Routine Age 9 (Group 2), Borderline Bedtimes Ages 5 and 9 (Group 3), and Age-Appropriate Bedtime and Sleep Routines Ages 5 and 9 (Group 4, reference). Compared with adolescents in the reference group, those in the No Bedtime Routine Age 9 (Group 2) had +0.38 SD greater BMI (95% CI = [0.13 to 0.63]), above the level for overweight (1.02 SD BMI/85th percentile). Associations persisted after adjusting for age 3 BMI and sociodemographic characteristics. Conclusions: Results demonstrate heterogeneity in childhood bedtime routine groups and their associations with adolescent BMI. Future studies should focus on whether childhood sleep behavior interventions promote healthier sleep and weight in later life course stages.
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