Insufficient sleep is associated with obesity, yet little is known about how repeated nights of insufficient sleep influence energy expenditure and balance. We studied 16 adults in a 14-to 15-d-long inpatient study and quantified effects of 5 d of insufficient sleep, equivalent to a work week, on energy expenditure and energy intake compared with adequate sleep. We found that insufficient sleep increased total daily energy expenditure by ∼5%; however, energy intake-especially at night after dinner-was in excess of energy needed to maintain energy balance. Insufficient sleep led to 0.82 ± 0.47 kg (±SD) weight gain despite changes in hunger and satiety hormones ghrelin and leptin, and peptide YY, which signaled excess energy stores. Insufficient sleep delayed circadian melatonin phase and also led to an earlier circadian phase of wake time. Sex differences showed women, not men, maintained weight during adequate sleep, whereas insufficient sleep reduced dietary restraint and led to weight gain in women. Our findings suggest that increased food intake during insufficient sleep is a physiological adaptation to provide energy needed to sustain additional wakefulness; yet when food is easily accessible, intake surpasses that needed. We also found that transitioning from an insufficient to adequate/recovery sleep schedule decreased energy intake, especially of fats and carbohydrates, and led to −0.03 ± 0.50 kg weight loss. These findings provide evidence that sleep plays a key role in energy metabolism. Importantly, they demonstrate physiological and behavioral mechanisms by which insufficient sleep may contribute to overweight and obesity.calorimetry | misalignment | dysregulated eating | deprivation | restriction M ore than 1.4 billion adults, 150 million school-aged children, and 43 million preschool children are estimated to be overweight or obese worldwide (1-3), substantially raising risk for cardiovascular diseases (4) hyperlipidemia (5), diabetes (5, 6), osteoarthritis (6), sleep apnea (7), depression (8), and cancer (9). Excessive food consumption and inadequate physical activity are primary factors contributing to the obesity epidemic. When daily energy intake is in excess of energy expenditure (EE) a state of positive energy balance occurs. Over weeks, months, or years, a small cumulative impact of sustained positive energy balance results in weight gain and obesity (10). Alongside the rise in obesity there has been a decline in the number of individuals who report obtaining the recommended 7-9 h of sleep, with many obtaining less than 6 h per night (11). Insufficient sleep is a risk factor of weight gain and obesity (11-13), yet how insufficient sleep contributes to this risk is unclear. Sleep influences energy metabolism (14, 15), and one function of sleep is to conserve energy (16). Proposed mechanisms that associate insufficient sleep and higher body mass index (BMI) include changes in satiety and hunger hormones altering food intake and changes in EE (17). Insufficient sleep is associated with decreases...

Study Objectives Consumer sleep-tracking devices are widely used and becoming more technologically advanced, creating strong interest from researchers and clinicians for their possible use as alternatives to standard actigraphy. We, therefore, tested the performance of many of the latest consumer sleep-tracking devices, alongside actigraphy, versus the gold-standard sleep assessment technique, polysomnography (PSG). Methods In total, 34 healthy young adults (22 women; 28.1 ± 3.9 years, mean ± SD) were tested on three consecutive nights (including a disrupted sleep condition) in a sleep laboratory with PSG, along with actigraphy (Philips Respironics Actiwatch 2) and a subset of consumer sleep-tracking devices. Altogether, four wearable (Fatigue Science Readiband, Fitbit Alta HR, Garmin Fenix 5S, Garmin Vivosmart 3) and three nonwearable (EarlySense Live, ResMed S+, SleepScore Max) devices were tested. Sleep/wake summary and epoch-by-epoch agreement measures were compared with PSG. Results Most devices (Fatigue Science Readiband, Fitbit Alta HR, EarlySense Live, ResMed S+, SleepScore Max) performed as well as or better than actigraphy on sleep/wake performance measures, while the Garmin devices performed worse. Overall, epoch-by-epoch sensitivity was high (all ≥0.93), specificity was low-to-medium (0.18–0.54), sleep stage comparisons were mixed, and devices tended to perform worse on nights with poorer/disrupted sleep. Conclusions Consumer sleep-tracking devices exhibited high performance in detecting sleep, and most performed equivalent to (or better than) actigraphy in detecting wake. Device sleep stage assessments were inconsistent. Findings indicate that many newer sleep-tracking devices demonstrate promising performance for tracking sleep and wake. Devices should be tested in different populations and settings to further examine their wider validity and utility.

We tested the hypothesis that mechanical deformation of forearm blood vessels via acute increases in extravascular pressure elicits rapid vasodilatation in humans. In healthy adults, we measured forearm blood flow (Doppler ultrasound) and calculated forearm vascular conductance (FVC) responses to whole forearm compressions and isometric muscle contractions with the arm above heart level. We used several experimental protocols to gain insight into how mechanical factors contribute to contraction-induced rapid vasodilatation. The findings from the present study clearly indicate that acute increases in extravascular pressure (200 mmHg for 2 s) elicit a significant rapid vasodilatation in the human forearm (peak ΔFVC∼155%). Brief, 6 s sustained compressions evoked the greatest vasodilatation (ΔFVC∼260%), whereas the responses to single (2 s) and repeated compressions (five repeated 2 s compressions) were not significantly different (ΔFVC∼155% versus ∼115%, respectively). This mechanically induced vasodilatation peaks within 1-2 cardiac cycles, and thus is dissociated from the temporal pattern normally observed in response to brief muscle contractions (∼4-7 cardiac cycles). A non-linear relation was found between graded increases in extravascular pressure and both the immediate and peak rapid vasodilatory response, such that the responses increased sharply from 25 to 100 mmHg, with no significant further dilatation until 300 mmHg (maximal ΔFVC∼185%). This was in contrast to the linear intensity-dependent relation observed with muscle contractions. Our collective findings indicate that mechanical influences contribute largely to the immediate vasodilatation (first cardiac cycle) observed in response to a brief, single contraction. However, it is clear that there are additional mechanisms related to muscle activation that continue to cause and sustain vasodilatation for several more cardiac cycles after contraction. Additionally, the potential contribution of mechanical influences to the total contraction-induced hyperaemia appears greatest for low to moderate intensity single muscle contractions, and this contribution becomes less significant for sustained and repeated contractions. Nevertheless, this mechanically induced vasodilatation could serve as a feedforward mechanism to increase muscle blood flow at the onset of exercise, as well as in response to changes in contraction intensity, prior to alterations in local vasodilating substances that influence vascular tone.

Caffeine’s wakefulness-promoting and sleep-disrupting effects are well established, yet whether caffeine affects human circadian timing is unknown. Here we show that evening caffeine consumption delays the human circadian melatonin rhythm in vivo, and chronic application of caffeine lengthens the circadian period of molecular oscillations in vitro primarily via an adenosine receptor/cyclic AMP-dependent mechanism. In a double-blind, placebo controlled, ~49-day long within-subject study, we found the equivalent amount of caffeine as that in a double espresso 3 hours before habitual bedtime induced a phase delay of the circadian melatonin rhythm in humans by ~40 minutes. This magnitude of delay was nearly half of the magnitude of the phase-delaying response induced by exposure to 3-hours of evening bright-light (~3000 lux; ~7 Watts/m2) that began at habitual bedtime. Furthermore, using human osteosarcoma U2OS cells expressing clock gene luciferase reporters, we found a dose-dependent lengthening of circadian period by caffeine. By pharmacological dissection and siRNA knockdown we established that perturbation of adenosine receptor signaling, but not ryanodine receptor or phosphodiesterase activity, is sufficient to account for caffeine’s effects on cellular timekeeping. We also used a cyclic AMP biosensor to show that caffeine increased cyclic AMP levels, indicating that caffeine can influence a core component of the cellular circadian clock. Taken together, our findings demonstrate that caffeine influences human circadian timing and gives new insight into how the world’s most widely consumed psychoactive drug impacts upon human physiology.