Study Objectives Insufficient sleep is believed to promote positive energy balance (EB) and weight-gain. Increasing weekend sleep duration to “recover” from weekday sleep loss is common, yet little is known regarding how weekend recovery sleep influences EB. We conducted a randomized controlled trial to assess how: 1) 2 days and 8 days of insufficient sleep and 2) ad libitum weekend recovery sleep impact EB (energy intake [EI] – energy expenditure [EE]). Methods Following ten baseline days with 9h per night sleep opportunities, participants completed one of three 10-day experimental protocols with ad libitum EI: control (9h sleep opportunities; n=8; 23±5y [mean±SD]); sleep restriction (SR; 5h sleep opportunities; n=14; 25±5y); sleep restriction with weekend recovery sleep (SR+WR; 5 days insufficient sleep, 2 days ad libitum weekend recovery sleep, 3 days recurrent insufficient sleep; n=14; 27±4y). Results 24h EB increased (P < 0.001; main effect) by an average of 797.7±96.7 (±SEM) kcal during the 10-day experimental protocol versus baseline with no significant differences between groups. Percent change from baseline in 24h-EE was higher (P < 0.05) on day 2 of insufficient sleep (SR and SR+WR groups; 10±1%) versus adequate sleep (control group; 4±3%). Conclusions In this between-group study, the effects of adequate sleep and insufficient sleep, with or without or weekend recovery sleep, on 24h-EB were similar. Examining EB and body weight changes using within-subject cross-over designs and “free-living” conditions outside the laboratory (e.g., sleep extension) are needed to advance our understanding of the links between insufficient sleep, weekend recovery sleep and weight-gain.

SummaryThis paper is an attempt to assess the relevance of the inhibitors of fibrinolysis for clot lysis in selected disease states and to discuss the mechanisms leading to acquired abnormal levels of such inhibitors. When compared to 20 control subjects the 30 hypertriglyceridemic patients (14 with type IIb and 16 with type IV) displayed significantly (p <0.001) increased plasma plasminogen activator inhibitor (PAI) activity (221 ± 88% and 290 ± 104% respectively; mean ± SD), moderately (p <0.01) increased α2 antiplasmin (α2AP) level (112 ± 11% and 115 ± 16%) and accordingly an obviously prolonged dilute blood clot lysis time (DBCLT). Neither PAI activity and α2AP level nor DBCLT were significantly different from controls in the 10 patients with hyperlipoproteinemia type IIa. The 18 patients with severe hepatic cirrhosis had low α2AP level (59 ± 19.7%) and accelerated clot lysis, while mean PAI activity (160 ± 87%) was slightly (p <0.05) increased. In the 17 nephrotic patients α2AP was increased (115 ±12%) while PAI activity was similar to controls and DBCLT rather shorter. Two liver secretion enzymes, namely serum Cholinesterase and plasma protein C, were found to be decreased in cirrhotic patients, similar to control values in hyperlipoproteinemia type Ha and obviously increased in nephrotic patients as well as in hypertriglyceridemic subjects. The relevance of PAI and α2AP for clot lysis was considered in relation to data in the literature concerning the behaviour of t-PA and factor XIII. Enhanced hepatic synthesis of protease inhibitors and factor XIII as a possible cause of delayed clot lysis in hypertriglyceridemia was envisaged.

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Introduction Late chronotypes have been shown to have decreased positive affect during the day and during sleep loss. Findings for negative affect are inconsistent. The present analysis examined the effect of chronotype on positive and negative affect during two sleep and circadian challenges. Methods In both studies, chronotype was determined by habitual mid-sleep time. In Study 1, 10 healthy adults (5 early, 5 late chronotypes) completed a 10-day protocol of sleep restriction followed by total sleep deprivation. Participants maintained habitual 8h sleep schedules at home for 1 week, then completed a 2-day in-laboratory protocol: 4h of sleep restriction, followed by a 4h sleep opportunity, followed by 28h of sleep deprivation. Affect was assessed with the Positive and Negative Affect Schedule (PANAS) every hour during scheduled wakefulness. In Study 2, 14 healthy adults (7 early, 7 late chronotypes) completed a 39-day protocol of combined sleep restriction and circadian misalignment. Participants maintained habitual 8h sleep schedules at home for 2 weeks, then completed a 4-day in-laboratory protocol with the following sleep opportunities: 8h on night 1, 3h on night 2, and 3h on mornings 3 and 4. After 3 days of at-home unscheduled recovery sleep opportunities, the protocol was repeated. Affect was assessed with the PANAS every 3h during scheduled wakefulness. Data from each study were analyzed separately with mixed-model ANOVA. Results Positive affect decreased during sleep restriction+sleep deprivation and sleep restriction+circadian misalignment (p&lt;.05), regardless of chronotype. However, late chronotypes reported lower positive affect than early chronotypes across both sleep/circadian challenges (p&lt;.05), and this effect was accounted for by baseline positive affect. Negative affect was not consistently impacted by sleep/circadian challenges or chronotype, with or without considering baseline negative affect. In both studies, chronotype did not interact with sleep/circadian challenges. Conclusion These findings are consistent with prior work showing later chronotypes have lower positive affect. Chronotype and sleep loss/circadian misalignment may impact affect through independent mechanisms. Future work is needed to replicate these findings in larger samples with more extreme chronotypes. Support (If Any) Office of Naval Research MURI N00014-15-1-2809; CurAegis Technologies Inc. (formerly Torvec, Inc), NIH HL109706, NIH TR001082; Undergraduate Research Opportunities Grant University of Colorado Boulder.

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