Reliability of heart rate variability during stable and disrupted polysomnographic sleep.

Heart rate variability (HRV) is commonly used within sleep and cardiovascular research, yet HRV reliability across various sleep stages remains equivocal. The present study examined the reliability of frequency- and time-domain HRV within stage-2 (N2), slow-wave (SWS), and rapid-eye-movement (REM) sleep during both stable and disrupted sleep. We hypothesized that high-frequency (HF) HRV would be reliable in all three sleep stages, low-frequency (LF) HRV would be reliable during N2 and SWS, and that disrupted sleep via spontaneous cortical arousals would decrease HRV reliability. Twenty-seven participants (11 men, 16 women, 26 ± 1 yr) were equipped with laboratory polysomnography for 1 night. Both frequency- and time-domain HRV were analyzed in two 5- to 10-min blocks during multiple stable and disrupted sleep cycles across N2, SWS, and REM sleep. HF HRV was highly correlated across stable N2 (r = 0.839, P < 0.001), SWS (r = 0.765, P < 0.001), and REM (r = 0.881, P < 0.001). LF HRV was moderate-to-highly correlated during stable cycles of N2 sleep (r = 0.694, P < 0.001), SWS, (r = 0.765, P < 0.001), and REM (r = 0.699, P < 0.001) sleep. When stable sleep was compared with disrupted sleep, both time- and frequency-domain HRV were reliable (α > 0.90, P < 0.05) in N2, SWS, and REM, except for LF HRV during SWS (α = 0.62, P = 0.089). In conclusion, time- and frequency-domain HRV demonstrated reliability across stable N2, SWS, and REM sleep, and remained reliable during disrupted sleep. These findings support the use of HRV during sleep as a tool for assessing cardiovascular health and risk stratification.NEW & NOTEWORTHY Heart rate variability (HRV) is a commonly employed indirect estimate of cardiac autonomic activity during sleep with limited reliability studies. Nocturnal frequency-domain HRV was reliable across differing stable sleep cycles of stage-2 (N2), slow-wave (SWS), and rapid-eye-movement (REM) sleep. Moreover, frequency- and time-domain HRV were reliable during stable and disturbed sleep, except SWS low-frequency HRV. Our finding supports nocturnal HRV as a potential tool for cardiovascular risk stratification.

Morning sympathetic activity after evening binge alcohol consumption.

Binge alcohol consumption elicits acute and robust increases of muscle sympathetic nerve activity (MSNA), yet the impact of evening binge drinking on morning-after MSNA is unknown. The present study examined the effects of evening binge alcohol consumption on polysomnographic sleep and morning-after MSNA. We hypothesized that evening binge drinking (i.e. 4-5 drink equivalent in <2 h) would reduce sleep quality and increase morning-after blood pressure (BP) and MSNA. Following a familiarization night within the sleep laboratory, 22 participants (12 men, 10 women; 25 ± 1 yr) were examined after simulated binge drinking or fluid control (randomized, crossover design). Morning MSNA was successfully recorded across both conditions in 16 participants (8 men, 8 women) during a 10-min baseline and three Valsalva's maneuvers (VM). Binge drinking reduced rapid eye movement (REM) sleep (15 ± 1 vs. 20 ± 1%, P = 0.003), increased stage II sleep (54 ± 1 vs. 51 ± 1%, P = 0.002), and increased total urine output (2.9 ± 0.2 vs. 2.1 ± 0.1 liters, P < 0.001) but did not alter morning-after urine specific gravity. Binge drinking increased morning-after heart rate [65 (54-72) vs. 58 (51-67) beats/min, P = 0.013] but not resting BP or MSNA. Binge drinking elicited greater sympathoexcitation during VM (38 ± 3 vs. 43 ± 3 bursts/min, P = 0.036). Binge drinking augmented heart rate (P = 0.002), systolic BP (P = 0.022), and diastolic BP (P = 0.037) reactivity to VM phase IV and blunted cardiovagal baroreflex sensitivity during VM phases II (P = 0.028) and IV (P = 0.043). In conclusion, evening binge alcohol consumption disrupted REM sleep and morning-after autonomic function. These findings provide new mechanistic insight into the potential role of binge drinking on cardiovascular risk.NEW & NOTEWORTHY Chronic binge alcohol consumption is associated with future cardiovascular disease (CVD) risk in both men and women. In addition, binge alcohol consumption is known to disrupt normal sleep quality during the early morning hours, coinciding with the morning sympathetic surge. In the present study, an evening of binge alcohol consumption increased baseline morning heart rate and cardiovascular reactivity during the Valsalva maneuver (VM) strain. Specifically, muscle sympathetic nerve activity and phase IV hemodynamic responses increased during VM the morning after binge alcohol consumption. The autonomic dysfunction and increased cardiovascular reactivity during VM suggests a contributing mechanism to CVD risk present in individuals who binge drink.

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/m2], and were split using a median analysis into short-sleeping (SS; n = 17) and normal-sleeping (NS; n = 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 (P > 0.05). Spontaneous nocturnal arousal elicited an augmented HR response in the SS group, specifically during the recovery period [F(5.261,163.08) = 3.058, P = 0.01, ηp2 = 0.09]. There were no significant differences in HR reactivity between sexes [F(3.818,118.368) = 1.191, P = 0.318]. These findings offer evidence of nocturnal cardiovascular dysregulation in habitual short sleepers, independent from any diagnosed sleep disorders.NEW & NOTEWORTHY 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.

Sympathetic neural responsiveness to sleep deprivation in older adults: sex differences.

Our laboratory has previously reported that total sleep deprivation (TSD) modifies muscle sympathetic neural activity (MSNA) differently in young men and women. Because postmenopausal women are among the highest risk for hypertension, this study compares MSNA responses with TSD in older men and women. We hypothesized that TSD would alter MSNA in older adults, with greater sympathoexcitation in postmenopausal women. Twenty-seven participants (14 men and 13 women) between the ages of 55 and 75 yr were tested twice, once after 24-h TSD and once after normal sleep (randomized, crossover design). Our primary outcome measure of MSNA (microneurography) was successful across both conditions in 20 participants (10 men and 10 women). Secondary outcome measures included seated blood pressure, heart rate, and fasting plasma testosterone, estradiol, and progesterone. Age (60 ± 1 vs. 61 ± 2 yr) and BMI (27 ± 1 vs. 26 ± 1 kg/m2) were not different between groups. TSD increased systolic blood pressure in both men (124 ± 5 to 130 ± 4 mmHg) and women (107 ± 5 to 116 ± 4 mmHg), but the increases were not different between groups (condition, P = 0.014; condition × sex, P > 0.05). In contrast, TSD elicited divergent MSNA responses in older men and women. Specifically, MSNA burst frequency increased in postmenopausal women (28 ± 3 to 34 ± 3 burst/min), but not older men (38 ± 3 to 35 ± 3 bursts/min; condition × sex, P = 0.032). In conclusion, TSD elicited sympathoexcitation in postmenopausal women but not age-matched men. These findings provide new mechanistic insight into reported links between sleep deprivation and hypertension.NEW & NOTEWORTHY Epidemiological studies report that sleep deprivation is more strongly associated with hypertension in women than in men. In the present study, 24-h total sleep deprivation (TSD) increased blood pressure in postmenopausal women and age-matched men. In contrast, only women demonstrated increases in muscle sympathetic nerve activity after TSD. The sympathoexcitation observed in postmenopausal women suggests a potential contributing mechanism for epidemiological observations and advances our understanding of the complex relations between sleep, sex, and hypertension.

Sex differences in blood pressure responsiveness to spontaneous K-complexes during stage II sleep.

K-complexes are a key marker of nonrapid eye movement sleep, specifically during stages II sleep. Recent evidence suggests the heart rate responses to a K-complexes may differ between men and women. The purpose of this study was to compare beat-to-beat blood pressure responses to K-complexes in men and women. We hypothesized that the pressor response following a spontaneous K-complex would be augmented in men compared with women. Ten men [age: 23 ± 2 yr, body mass index (BMI): 28 ± 4 kg/m2] and ten women (age: 23 ± 5 yr, BMI: 25 ± 4 kg/m2) were equipped with overnight finger plethysmography and standard 10-lead polysomnography. Hemodynamic responses to a spontaneous K-complex during stable stage II sleep were quantified for 10 consecutive cardiac cycles, and measurements included systolic arterial pressure (SAP), diastolic arterial pressure (DAP), and heart rate. K-complex elicited greater pressor responses in men when blood pressures were expressed as SAP (cardiac cycle × sex: P = 0.007) and DAP (cardiac cycle × sex: P = 0.004). Heart rate trended to be different between men and women (cardiac cycle × sex: P = 0.078). These findings suggest a divergent pressor response between men and women following a spontaneous K-complex during normal stage II sleep. These findings could contribute to sex-specific differences in cardiovascular risk that exist between men and women.NEW & NOTEWORTHY K-complexes during stage II sleep have been shown to elicit acute increases in blood pressure and heart rate, but the role of sex (i.e., male vs. female) in this response is unclear. In the present study, we demonstrate that the pressor response following spontaneous K-complexes were augmented in men compared to age-matched women. The augmented blood pressure reactivity to spontaneous K-complexes during stage II sleep in men advance the field of cardiovascular sex differences, with implications for nocturnal blood pressure control.

Evening binge alcohol disrupts cardiovagal tone and baroreflex function during polysomnographic sleep.

STUDY OBJECTIVES: Binge alcohol consumption is associated with increased cardiovascular risk. The effects of evening binge alcohol consumption (i.e. 4-5 beverages within 2 h) on the vagal components of HRV and cardiovagal baroreflex sensitivity (cvBRS) during sleep remain largely equivocal. The present study examined the effects of evening binge alcohol consumption on nocturnal cardiac vagal tone and baroreflex sensitivity during stage N2, slow wave (SWS), and rapid eye movement (REM) sleep. We hypothesized that evening binge drinking would reduce HRV and cvBRS in each sleep stage. METHODS: Following a familiarization night within the laboratory, twenty-three participants were examined following a night of binge alcohol consumption and a fluid control (randomized, crossover design). A quality nocturnal beat-to-beat blood pressure signal was obtained in both conditions in 16 participants (seven men, nine women; 25 ± 1 years). RESULTS: Binge drinking reduced both the high frequency (HF) and time-domain components (i.e. pNN50 and RMSSD) of HRV in stage N2 sleep, SWS, and REM. In addition, cvBRS up-up (vagal activation) was reduced following binge alcohol consumption in stage N2 (21 ± 3 vs. 15 ± 3 ms/mmHg, p = 0.035) and REM (15[11-28] vs. 11[9-18] ms/mmHg, p = 0.009). Binge alcohol consumption reduced cvBRS down-down (vagal withdrawal) in stage N2 (23 ± 2 vs. 14 ± 2 ms/mmHg, p < 0.001), SWS (20[14-30] vs. 14[9-17] ms/mmHg, p = 0.022), and REM (14[11-24] vs. 10[7-15] ms/mmHg, p = 0.006). CONCLUSIONS: Evening binge alcohol consumption disrupts cardiac vagal tone and baroreflex function during nearly all sleep stages. These findings provide mechanistic insight into the potential role of binge drinking and alcohol abuse on cardiovascular risk. CLINICAL TRIALS DETAILS: Alcohol and Neural Cardiovascular Control in Binge Drinkers, www.clinicaltrials.gov/ct2/show/NCT03567434, NCT03567434.