Blunted heart rate recovery to spontaneous nocturnal arousals in short-sleeping adults

Chronic insufficient sleep is a common occurrence around the world and results in numerous physiological detriments and consequences, including cardiovascular complications. The purpose of the present study was to assess the relationship between habitual total sleep time (TST) measured objectively via at-home actigraphy and heart rate (HR) reactivity to nocturnal cortical arousals. We hypothesized that short habitual TST would be associated with exaggerated cardiac reactivity to nocturnal cortical arousals. Participants included 35 healthy individuals [20 men, 15 women, age: 24 ± 1 yr, body mass index (BMI): 27 ± 1 kg/m], and were split using a median analysis into short-sleeping (SS; = 17) and normal-sleeping (NS; = 18) adults based on a minimum of 7 days of at-home actigraphy testing. All participants underwent a full overnight laboratory polysomnography (PSG) testing session, including continuous HR (electrocardiogram, ECG) sampling. HR reactivities to all spontaneous cortical arousals were assessed for 30 cardiac cycles following the onset of the arousal in all participants. Baseline HR was not significantly different between groups ( \u3e 0.05). Spontaneous nocturnal arousal elicited an augmented HR response in the SS group, specifically during the recovery period [(5.261,163.08) = 3.058, = 0.01, η = 0.09]. There were no significant differences in HR reactivity between sexes [(3.818,118.368) = 1.191, = 0.318]. These findings offer evidence of nocturnal cardiovascular dysregulation in habitual short sleepers, independent from any diagnosed sleep disorders. Short habitual sleep is associated with poor cardiovascular outcomes, but mechanisms remain equivocal. The present study used objectively measured habitual sleep via wrist actigraphy, and reports that habitual short sleepers have augmented heart rate recovery responses to spontaneous arousals as determined by gold-standard polysomnography. There were no reported sex differences. The augmented heart rate recovery to spontaneous cortical arousals may be an important mechanism contributing to the associations between insufficient sleep and cardiovascular risk

Morning Cardiovascular and Sympathetic Reactivity to Cold Pressor Test After Evening Binge Drinking: Sex Differences

Heavy alcohol consumption, including binge drinking, is associated with increased cardiovascular risk There is consistent evidence for increased muscle sympathetic nerve activity (MSNA) after acute alcohol consumption, and recent evidence for augmented sympathetic reactivity the morning after evening binge drinking. Given well documented differences in neural cardiovascular control between men and women, we hypothesized that women would exhibit augmented morning cardiovascular and sympathetic neural reactivity to cold stress following evening binge alcohol consumption. Thirty volunteers (15 women, 15 men; 25±1 years; 27±1 kg/m2 ) participated in the present study. Utilizing a randomized, cross-over design, participants visited the laboratory for fluid control and alcohol sessions separated by ~1 month. The alcohol dose was based upon biological sex and body weight (1 g/kg dose in men and 0.85 g/kg dose in women). Beverage consumption occurred at 8:00pm and 9:00pm to simulate binge alcohol consumption (i.e., 4-5 drink equivalent), with lights out at 11:00pm. An 8-hour sleep opportunity was allotted from 11:00pm to 7:00am for overnight polysomnography (NATUS, Middleton, WI). Following lights on, twenty-two (10 women, 12 men) participants were instrumented for a morning autonomic study with measurements of muscle sympathetic nerve activity (MSNA; microneurography), beat-to-beat blood pressure (finger plethysmography), and heart rate (electrocardiogram). MSNA, blood pressure, and heart rate were measured during a 3-minute baseline, 2-minute cold pressor test (CPT), and 3-minute recovery. MSNA was scored and confirmed by one trained investigator (JR Carter). Statistical analysis included repeated measures ANOVA with condition and time as within subject factors and sex as a between subject factor (α = 0.05). Total sleep time and sleep efficiency were reduced following binge alcohol consumption in both sexes (condition: p \u3c 0.05), but women had more frequent arousals following alcohol consumption (condition × sex: p = 0.008). During CPT, women exhibited an augmented pressor response via mean arterial pressure following evening binge alcohol consumption compared to fluid control, while men did not (condition × time × sex: p = 0.010). MSNA burst frequency was elevated during CPT following evening binge alcohol consumption compared to fluid control (condition × time: p = 0.033), but this was not different between sexes. Heart rate reactivity was not different across conditions (condition × time: p = 0.405) or between sexes (condition × time × sex: p = 0.818). In conclusion, our results indicate that evening binge drinking results in augmented cardiovascular reactivity in women compared to men, but these differences do not appear to be mediated via sympathetic neural reactivity