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Study Objectives The development of ambulatory technologies capable of monitoring brain activity during sleep longitudinally is critical for advancing sleep science. The aim of this study was to assess the signal acquisition and the performance of the automatic sleep staging algorithms of a reduced-montage dry-electroencephalographic (EEG) device (Dreem headband, DH) compared to the gold-standard polysomnography (PSG) scored by five sleep experts. Methods A total of 25 subjects who completed an overnight sleep study at a sleep center while wearing both a PSG and the DH simultaneously have been included in the analysis. We assessed (1) similarity of measured EEG brain waves between the DH and the PSG; (2) the heart rate, breathing frequency, and respiration rate variability (RRV) agreement between the DH and the PSG; and (3) the performance of the DH’s automatic sleep staging according to American Academy of Sleep Medicine guidelines versus PSG sleep experts manual scoring. Results The mean percentage error between the EEG signals acquired by the DH and those from the PSG for the monitoring of α was 15 ± 3.5%, 16 ± 4.3% for β, 16 ± 6.1% for λ, and 10 ± 1.4% for θ frequencies during sleep. The mean absolute error for heart rate, breathing frequency, and RRV was 1.2 ± 0.5 bpm, 0.3 ± 0.2 cpm, and 3.2 ± 0.6%, respectively. Automatic sleep staging reached an overall accuracy of 83.5 ± 6.4% (F1 score: 83.8 ± 6.3) for the DH to be compared with an average of 86.4 ± 8.0% (F1 score: 86.3 ± 7.4) for the 5 sleep experts. Conclusions These results demonstrate the capacity of the DH to both monitor sleep-related physiological signals and process them accurately into sleep stages. This device paves the way for, large-scale, longitudinal sleep studies. Clinical Trial Registration NCT03725943.

Sleep disorders are associated with inflammation and sympathetic activation, which are suspected to induce endothelial dysfunction, a key factor in the increased risk of cardiovascular disease. Less is known about the early effects of acute sleep deprivation on vascular function. We evaluated microvascular reactivity and biological markers of endothelial activation during continuous 40 h of total sleep deprivation (TSD) in 12 healthy men (29 +/- 3 yr). The days before [day 1 (D1)] and during TSD (D3), at 1200 and 1800, endothelium-dependent and -independent cutaneous vascular conductance was assessed by iontophoresis of acetylcholine and sodium nitroprusside, respectively, coupled to laser-Doppler flowmetry. At 0900, 1200, 1500, and 1800, heart rate (HR) and instantaneous blood pressure (BP) were recorded in the supine position. At D1, D3, and the day after one night of sleep recovery (D4), markers of vascular endothelial cell activation, including soluble intercellular adhesion molecule-1, vascular cell adhesion molecule-1, E-selectin, and interleukin-6 were measured from blood samples at 0800. Compared with D1, plasma levels of E-selectin were raised at D3, whereas intercellular adhesion molecule-1 and interleukin-6 were raised at D4 (P< 0.05). The endothelium-dependent and -independent CVC were significantly decreased after 29 h of TSD (P < 0.05). By contrast, HR, systolic BP, and the normalized low-frequency component of HR variability (0.04-0.15 Hz), a marker of the sympathetic activity, increased significantly within 32 h of TSD (P < 0.05). In conclusion, acute exposure to 40 h of TSD appears to cause vascular dysfunction before the increase in sympathetic activity and systolic BP.

Short sleep duration has been shown to be associated with elevated body mass index (BMI) in many epidemiological studies. Several pathways could link sleep deprivation to weight gain and obesity, including increased food intake, decreased energy expenditure, and changes in levels of appetite-regulating hormones, such as leptin and ghrelin. A relatively new factor that is contributing to sleep deprivation is the use of multimedia (e.g. television viewing, computer, and internet), which may aggravate sedentary behavior and increase caloric intake. In addition, shift-work, long working hours, and increased time commuting to and from work have also been hypothesized to favor weight gain and obesity-related metabolic disorders, because of their strong link to shorter sleep times. This article reviews the epidemiological, biological, and behavioral evidence linking sleep debt and obesity.

Here, we studied muscle-specific and muscle-related miRNAs in plasma of exercising humans. Our aim was to determine whether they are affected by eccentric and/or concentric exercise modes and could be biomarkers of muscle injuries or possible signaling molecules. On two separate days, nine healthy subjects randomly performed two 30-min walking exercises, one downhill (high eccentric component) and one uphill (high concentric component). Perceived exertion and heart rate were higher during the uphill exercise, while subjective pain and ankle plantar flexor strength losses within the first 48-h were higher following the downhill exercise. Both exercises increased serum creatine kinase and myoglobin with no significant differences between conditions. Plasma levels of circulating miRNAs assessed before, immediately after, and at 2-, 6-, 24-, 48-, and 72-h recovery showed that 1) hsa-mir-1, 133a, 133b, and 208b were not affected by concentric exercise but significantly increased during early recovery of eccentric exercise (2 to 6 h); 2) hsa-mir-181b and 214 significantly and transiently increased immediately after the uphill, but not downhill, exercise. The muscle-specific hsa-mir-206 was not reliably quantified and cardiac-specific hsa-mir-208a remained undetectable. In conclusion, changes in circulating miRNAs were dependent on the exercise mode. Circulating muscle-specific miRNAs primarily responded to a downhill exercise (high eccentric component) and could potentially be alternative biomarkers of muscle damage. Two muscle-related miRNAs primarily responded to an uphill exercise (high exercise intensity), suggesting they could be markers or mediators of physiological adaptations.

Six nights of extended sleep improve sustained attention and reduce sleep pressure. Sleep extension also protects against psychomotor vigilance task lapses and microsleep degradation during total sleep deprivation. These beneficial effects persist after one night of recovery sleep.

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