Jan Bukartyk

Effects of Experimental Sleep Restriction on Caloric Intake and Activity Energy Expenditure

BACKGROUND Epidemiologic studies link short sleep duration to obesity and weight gain. Insufficient sleep appears to alter circulating levels of the hormones leptin and ghrelin, which may promote appetite, although the effects of sleep restriction on caloric intake and energy expenditure are unclear. We sought to determine the effect of 8 days/8 nights of sleep restriction on caloric intake, activity energy expenditure, and circulating levels of leptin and ghrelin. METHODS We conducted a randomized study of usual sleep vs a sleep restriction of two-thirds of normal sleep time for 8 days/8 nights in a hospital-based clinical research unit. The main outcomes were caloric intake, activity energy expenditure, and circulating levels of leptin and ghrelin. RESULTS Caloric intake in the sleep-restricted group increased by +559 kcal/d (SD, 706 kcal/d, P=.006) and decreased in the control group by -118 kcal/d (SD, 386 kcal/d, P=.51) for a net change of +677 kcal/d (95% CI, 148-1,206 kcal/d; P=.014). Sleep restriction was not associated with changes in activity energy expenditure (P=.62). No change was seen in levels of leptin (P=.27) or ghrelin (P=.21). CONCLUSIONS Sleep restriction was associated with an increase in caloric consumption with no change in activity energy expenditure or leptin and ghrelin concentrations. Increased caloric intake without any accompanying increase in energy expenditure may contribute to obesity in people who are exposed to long-term sleep restriction. TRIAL REGISTRATION ClinicalTrials.gov; No.: NCT01334788; URL: www.clinicaltrials.gov.

Experimental Sleep Restriction Causes Endothelial Dysfunction in Healthy Humans

Background Epidemiologic evidence suggests a link between short sleep duration and cardiovascular risk, although the nature of any relationship and mechanisms remain unclear. Short sleep duration has also been linked to an increase in cardiovascular events. Endothelial dysfunction has itself been implicated as a mediator of heightened cardiovascular risk. We sought to determine the effect of 8 days/8 nights of partial sleep restriction on endothelial function in healthy humans. Methods and Results Sixteen healthy volunteers underwent a randomized study of usual sleep versus sleep restriction of two‐thirds normal sleep time for 8 days/8 nights in a hospital‐based clinical research unit. The main outcome was endothelial function measured by flow‐mediated brachial artery vasodilatation (FMD). Those randomized to sleep restriction slept 5.1 hours/night during the experimental period compared with 6.9 hours/night in the control group. Sleep restriction was associated with significant impairment in FMD (8.6±4.6% during the initial pre‐randomization acclimation phase versus 5.2±3.4% during the randomized experimental phase, P=0.01) whereas no change was seen in the control group (5.0±3.0 during the acclimation phase versus 6.73±2.9% during the experimental phase, P=0.10) for a between‐groups difference of −4.40% (95% CI −7.00 to −1.81%, P=0.003). No change was seen in non‐flow mediated vasodilatation (NFMD) in either group. Conclusion In healthy individuals, moderate sleep restriction causes endothelial dysfunction. Clinical Trial Registration URL: ClinicalTrials.gov. Unique identifier: NCT01334788.

Sleep Disordered Breathing in Patients with the Brugada Syndrome

We investigated breathing patterns and the occurrence of arrhythmias and ST-segment changes during sleep in patients with Brugada syndrome. Patients with Brugada syndrome are more likely to die from ventricular arrhythmias during sleep. ST-segment changes have been correlated with risk of sudden cardiac death. Whether sleep disturbances may contribute to arrhythmogenesis is unknown. Patients with Brugada syndrome underwent overnight polysomnography with simultaneous 12-lead electrocardiographic recording. A control group matched by age, gender, and body mass index (BMI) also underwent polysomnography. Twenty patients were included (50 ± 15 years old, 75% men). Despite their normal BMI (24.7 ± 2.7 kg/m(2)), 45% had sleep-disordered breathing (SDB), with a mean apnea-hypopnea index of 17.2 ± 14 events/hour. In patients with a high risk of arrhythmias, 5 (63%) had SDB. In the control group, 27% had SDB. Atrial or ventricular arrhythmias were not observed. Spontaneous ST-segment changes occurred in 2 patients over 45 different time points. Most ST-segment changes were observed during rapid eye movement sleep (31%) or within 1 minute of arousals (44%). Regarding respiratory events, 25 (56%) of ST-segment changes were related to occurrence of apnea or hypopnea. In conclusion, patients with Brugada syndrome have a high prevalence of SDB even in the setting of normal BMI. The higher incidence of nocturnal death in patients with Brugada syndrome may be conceivably related to co-morbid SDB. Moreover, autonomic instability encountered in rapid eye movement sleep and arousals could potentiate the risk of arrhythmias.

A Randomized Trial of Cardiovascular Responses to Energy Drink Consumption in Healthy Adults

Author Affiliations: Center for Surgery and Public Health, Brigham and Women’s Hospital, Boston, Massachusetts (Sammon, Trinh); VUI Center for Outcomes Research, Analytics and Evaluation, Henry Ford Health System, Detroit, Michigan (Abdollah, Menon); Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts (Choueiri, Kantoff); Department of Radiation Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts (Nguyen).

Effect of Weight Gain on Cardiac Autonomic Control During Wakefulness and Sleep

Obesity has been associated with increased cardiac sympathetic activation during wakefulness, but the effect on sleep-related sympathetic modulation is not known. The aim of this study was to investigate the effect of fat gain on cardiac autonomic control during wakefulness and sleep in humans. We performed a randomized, controlled study to assess the effects of fat gain on heart rate variability. We recruited 36 healthy volunteers, who were randomized to either a standardized diet to gain ≈4 kg over 8 weeks followed by an 8-week weight loss period (n=20) or to serve as a weight-maintainer control (n=16). An overnight polysomnogram with power spectral analysis of heart rate variability was performed at baseline, after weight gain, and after weight loss to determine the ratio of low-frequency to high-frequency power and to examine the relationship between changes in heart rate variability and changes in insulin, leptin, and adiponectin levels. Mean weight gain was 3.9 kg in the fat gain group versus 0.1 kg in the maintainer group. Low frequency/high frequency increased both during wakefulness and sleep after fat gain and returned to baseline after fat loss in the fat gain group and did not change in the control group. Insulin, leptin, and adiponectin also increased after fat gain and fell after fat loss, but no clear pattern of changes was seen that correlated consistently with changes in heart rate variability. Short-term fat gain in healthy subjects is associated with increased cardiac sympathetic activation during wakefulness and sleep, but the mechanisms remain unclear.

Interatrial pressure gradients during simulated obstructive sleep apnea: a catheter-based study.

We set to measure the interatrial pressure gradient during simulated obstructive sleep apnea (OSA).

Novel Bloodless Potassium Determination Using a Signal‐Processed Single‐Lead ECG

Background Hyper‐ and hypokalemia are clinically silent, common in patients with renal or cardiac disease, and are life threatening. A noninvasive, unobtrusive, blood‐free method for tracking potassium would be an important clinical advance. Methods and Results Two groups of hemodialysis patients (development group, n=26; validation group, n=19) underwent high‐resolution digital ECG recordings and had 2 to 3 blood tests during dialysis. Using advanced signal processing, we developed a personalized regression model for each patient to noninvasively calculate potassium values during the second and third dialysis sessions using only the processed single‐channel ECG. In addition, by analyzing the entire development groups first‐visit data, we created a global model for all patients that was validated against subsequent sessions in the development group and in a separate validation group. This global model sought to predict potassium, based on the T wave characteristics, with no blood tests required. For the personalized model, we successfully calculated potassium values with an absolute error of 0.36±0.34 mmol/L (or 10% of the measured blood potassium). For the global model, potassium prediction was also accurate, with an absolute error of 0.44±0.47 mmol/L for the training group (or 11% of the measured blood potassium) and 0.5±0.42 for the validation set (or 12% of the measured blood potassium). Conclusions The signal‐processed ECG derived from a single lead can be used to calculate potassium values with clinically meaningful resolution using a strategy that requires no blood tests. This enables a cost‐effective, noninvasive, unobtrusive strategy for potassium assessment that can be used during remote monitoring.

EXPERIMENTAL SLEEP RESTRICTION INCREASES NOCTURNAL BLOOD PRESSURE AND ATTENUATES BLOOD PRESSURE DIPPING IN HEALTHY INDIVIDUALS

Although growing evidence suggests that insufficient sleep is linked to enhanced risk of adverse events including hypertension, mechanistic investigations supporting causal relationships are lacking. In this study we sought to evaluate changes in ambulatory blood pressure in healthy individuals

POTENTIATED BLOOD PRESSURE RESPONSES TO ENERGY DRINK INTAKE IN CAFFEINE NAïVE HEALTHY ADULTS: A DOUBLE BLIND RANDOMIZED CONTROLLED STUDY

Energy drink consumption is widespread and rising among young adults. We and others have previously shown that energy drink consumption increases blood pressure, although the reported blood pressure increases among individuals are variable. Previous exposure to caffeine may be implicated in these

Cardiac autonomic control and complexity during sleep are preserved after chronic sleep restriction in healthy subjects

Acute sleep deprivation (SD) alters cardiovascular autonomic control (CAC) and is associated with an increased risk of cardiovascular disorders. However, the effects of partial SD on CAC are unclear. Thus, we aimed to investigate the effects of partial SD on CAC during sleep. We randomized seventeen healthy subjects to a restriction group (RES, n = 8, subjects slept two‐thirds of normal sleep time based on individual habitual sleep duration for 8 days and 8 nights) or a Control group (CON, n = 9, subjects were allowed to sleep their usual sleep time). Attended polysomnographic (PSG) studies were performed every night; a subset of them was selected for the analysis at baseline (day 3‐D3), the first night after sleep restriction (day 5‐D5), at the end of sleep restriction period (day 11‐D11), and at the end of recovery phase (day 14‐D14). We extracted electrocardiogram (ECG) and respiration from the PSG and divided into wakefulness (W), nonrapid eye movements (REM) sleep (N2 and N3) and REM sleep. CAC was evaluated by means of linear spectral analysis, nonlinear symbolic analysis and complexity indexes. In both RES and CON groups, sympathetic modulation decreased and parasympathetic modulation increased during N2 and N3 compared to W and REM at D3, D5, D11, D14. Complexity analysis revealed a reduction in complexity during REM compared to NREM sleep in both DEP and CON. After 8 days of moderate SD, cardiac autonomic dynamics, characterized by decreased sympathetic, and increased parasympathetic modulation, and higher cardiac complexity during NREM sleep, compared to W and REM, are preserved.