Aging and sympathetic transduction to blood pressure in humans: methodological and physiological considerations.

Recent reports suggest that quantification of signal-averaged sympathetic transduction is influenced by resting muscle sympathetic nerve activity (MSNA) and burst occurrence relative to the average mean arterial pressure (MAP). Herein, we asked how these findings may influence age-related reductions in sympathetic transduction. Beat-to-beat blood pressure and MSNA were recorded during 5 min of rest in 27 younger (13 females: age, 25 ± 5 yr; BMI, 25 ± 4 kg/m2) and 26 older (15 females: age, 59 ± 5 yr; BMI, 26 ± 4 kg/m2) healthy adults. All MSNA bursts were signal averaged together. Beat-to-beat MAP values were then split into low (T1), middle (T2), and high (T3) tertiles, and signal-averaged transduction was calculated within each tertile. Resting MSNA was higher in older adults and MAP was similar between groups. Older adults exhibited blunted overall MAP transduction (younger, Δ1.5 ± 0.6 vs. older, Δ0.9 ± 0.7 mmHg; P = 0.005), which was irrespective of relation to prevailing MAP. A greater proportion of bursts occurred above the average MAP in older adults (P < 0.001), and a larger proportion of these bursts were associated with depressor responses (P = 0.005). Nonetheless, assessment of bursts above the average MAP associated with pressor responses revealed similar age-associated reductions in transduction (younger, Δ2.6 ± 1.6 vs. older, Δ1.7 ± 0.8 mmHg; P = 0.016). These findings indicate an age-related increase in burst occurrence above the average resting MAP, which alone does not explain blunted transduction, thereby supporting the physiological underpinnings of age-related decrements in sympathetic transduction to blood pressure.NEW & NOTEWORTHY The current study demonstrated that aging is associated with a greater prevalence of sympathetic bursts occurring above the average blood pressure, which offers both methodologically and physiologically relevant information regarding aging and sympathetic control of blood pressure. These data support age-related reductions in sympathetic transduction via a reduced pressor response to sympathetic bursts irrespective of the prevailing absolute blood pressure value, along with increases in sympathetic outflow necessary to maintain blood pressure.

Actigraphy-Based Sleep and Muscle Sympathetic Nerve Activity in Humans.

Short and insufficient sleep are prevalent and associated with cardiovascular disease, with the sympathetic nervous system as a suspected mediator. The purpose of the present study was to investigate the association between objective, actigraphy-based total sleep time (TST), sleep efficiency (SE) and cardiovascular and sympathetic regulation in healthy adults. We hypothesized that short TST and low SE would be associated with elevated resting blood pressure, heart rate (HR), and muscle sympathetic nerve activity (MSNA). Participants included 94 individuals (46 males, 48 females, age: 30±15 years, body mass index (BMI): 26±4 kg/m2). All participants underwent at least 7 days of at-home, wristwatch actigraphy monitoring (avg: 10 ± 3 days). Seated blood pressures were assessed using brachial blood pressure measurements, followed by a 10-minute supine autonomic testing session consisting of continuous HR (electrocardiogram), beat-by-beat blood pressure (finger plethysmograph), and MSNA (microneurography) monitoring. Partial correlations were used to determine the relationship between sleep and cardiovascular parameters while accounting for the influence of age, sex, and BMI. TST was not associated with MAP (R=-0.105, p=0.321), HR (R=0.093, p=0.383), or MSNA burst frequency (BF; R=-0.168, p=0.112) and incidence (BI; R=-0.162, p=0.124). Similarly, SE was not associated with MAP (R=-0.088, p=0.408), HR (R=-0.118, p=0.263), MSNA BF (R=0.038, p=0.723), or MSNA BI (R=0.079, p=0.459). In contrast to recent preliminary findings, our results do not support a significant association between actigraphy-based sleep duration or efficiency and measures of resting blood pressure, heart rate, and MSNA.

Blood pressure and muscle sympathetic nerve activity are associated with trait anxiety in humans.

Chronic anxiety is prevalent and associated with an increased risk of cardiovascular disease. Prior studies that have reported a relationship between muscle sympathetic nerve activity (MSNA) and anxiety have focused on participants with anxiety disorders and/or metabolic syndrome. The present study leverages a large cohort of healthy adults devoid of cardiometabolic disorders to examine the hypothesis that trait anxiety severity is positively associated with resting MSNA and blood pressure. Resting blood pressure (BP) (sphygmomanometer and finger plethysmography), MSNA (microneurography), and heart rate (HR; electrocardiogram) were collected in 88 healthy participants (52 males, 36 females, 25 ± 1 yr, 25 ± 1 kg/m2). Multiple linear regression was performed to assess the independent relationship between trait anxiety, MSNA, resting BP, and HR while controlling for age and sex. Trait anxiety was significantly correlated with systolic arterial pressure (SAP; r = 0.251, P = 0.018), diastolic arterial pressure (DAP; r = 0.291, P = 0.006), mean arterial pressure (MAP; r = 0.328, P = 0.002), MSNA burst frequency (BF; r = 0.237, P = 0.026), and MSNA burst incidence (BI; r = 0.225, P = 0.035). When controlling for the effects of age and sex, trait anxiety was independently associated with SAP (ß = 0.206, P = 0.028), DAP (ß = 0.317, P = 0.002), MAP (ß = 0.325, P = 0.001), MSNA BF (ß = 0.227, P = 0.030), and MSNA BI (ß = 0.214, P = 0.038). Trait anxiety is associated with increased blood pressure and MSNA, demonstrating an important relationship between anxiety and autonomic blood pressure regulation.NEW & NOTEWORTHY Anxiety is associated with development of cardiovascular disease. Although the sympathetic nervous system is a likely mediator of this relationship, populations with chronic anxiety have shown little, if any, alteration in resting levels of directly recorded muscle sympathetic nerve activity (MSNA). The present study is the first to reveal an independent relationship between trait anxiety, resting blood pressure, and MSNA in a large cohort of healthy males and females devoid of cardiometabolic comorbidities.

Sympathetic neural reactivity to the Trier social stress test.

Sympathetic responsiveness to laboratory mental stress is highly variable, making interpretations of its role in stress reactivity challenging. The present study assessed muscle sympathetic nerve activity (MSNA, microneurography) responsiveness to the Trier social stress test (TSST), which employs an anticipatory stress phase, followed by a public speaking and mental arithmetic task. We hypothesized that sympathetic reactivity to the anticipatory phase would offer a more uniform response between individuals due to elimination of confounds (i.e. respiratory changes, muscle movement, etc.) observed during more common stress tasks. Participants included 26 healthy adults (11 men, 15 women, age: 25 ± 6 years, body mass index: 24 ± 3 kg/m2 ). Continuous heart rate (electrocardiogram) and beat-to-beat blood pressure (finger plethysmography) were recorded from all participants, while MSNA recordings were obtained in 20 participants. MSNA burst frequency was significantly reduced during anticipatory stress. During the speech, although burst frequency was unchanged, total MSNA was significantly increased. Changes in diastolic arterial pressure were predictive of changes in MSNA during anticipatory (ß = -0.680, P = 0.001), but not the speech (P = 0.318) or mental maths (P = 0.051) phases. Lastly, sympathetic reactivity to anticipatory stress was predictive of subsequent reactivity to both speech (ß = 0.740, P = 0.0002) and maths (ß = 0.663, P = 0.001). In conclusion, anticipatory social stress may offer a more versatile means of assessing sympathetic reactivity to mental stress in the absence of confounds and appears to predict reactivity to subsequent mental stress paradigms. KEY POINTS: Cardiovascular reactivity to laboratory mental stress is predictive of future health outcomes. However, reactivity of the sympathetic nervous system to mental stress is highly variable. The current study assessed peripheral muscle sympathetic nerve activity in response to the Trier social stress test, a psychosocial stressor that includes anticipatory stress, public speaking and mental arithmetic. Our findings demonstrate that sympathetic neural activity is consistently reduced during anticipatory stress. Conversely, the classically observed inter-individual variability of sympathetic responsiveness was observed during speech and maths tasks. Additionally, sympathetic reactivity to the anticipatory period accurately predicted how an individual would respond to both speech and maths tasks, outlining the utility of anticipatory stress in future research surrounding stress reactivity. Utilization of the Trier social stress test in autonomic physiology may offer an alternative assessment of sympathetic responsiveness to stress with more consistent inter-individual responsiveness and may be a useful tool for further investigation of stress reactivity.

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.

Core body temperature changes before sleep are associated with nocturnal heart rate variability.

Core body temperature (CBT) reductions occur before and during the sleep period, with the extent of presleep reductions corresponding to sleep onset and quality. Presleep reductions in CBT coincide with increased cardiac parasympathetic activity measured via heart rate variability (HRV), and while this appears to persist into the sleep period, individual differences in presleep CBT decline and nocturnal HRV remain unexplored. The purpose of the current study was to assess the relationship between individual differences in presleep CBT reductions and nocturnal heart rate (HR) and HRV in a population of 15 objectively poor sleeping adults [10 males, 5 females; age, 33 ± 4 yr; body mass index (BMI) 27 ± 1 kg/m2] with the hypothesis that blunted CBT rate of decline would be associated with elevated HR and reduced nocturnal HRV. Following an adaptation night, all participants underwent an overnight, in-laboratory sleep study with simultaneous recording of polysomnographic sleep including electrocardiography (ECG) and CBT recording. Correlations between CBT rate of change before sleep and nocturnal HRV were assessed. Blunted rate of CBT decline was significantly associated with increased heart rate (HR) in stage 2 (N2; R = 0.754, P = 0.001), stage 3 (N3; R = 0.748, P = 0.001), and rapid-eye movement (REM; R = 0.735, P = 0.002). Similarly, blunted rate of CBT decline before sleep was associated with reduced HRV across sleep stages. These findings indicate a relationship between individual differences in presleep thermoregulatory processes and nocturnal cardiac autonomic function in poor sleeping adults.NEW & NOTEWORTHY Core body temperature (CBT) reductions before sleep onset coincide with increases in heart rate variability (HRV) that persist throughout the sleep period. However, the relationship between individual differences in the efficiency of presleep core temperature regulation and nocturnal heart rate variability remains equivocal. The present study reports an association between the magnitude of presleep core body temperature changes and nocturnal parasympathetic activity, highlighting overlap between thermoregulatory processes before sleep and nocturnal cardiac autonomic function.

Orexin, Sleep, Sympathetic Neural Activity, and Cardiovascular Function.

Inadequate sleep duration and quality are associated with reduced cardiovascular health and increased mortality. Experimental evidence points to the sympathetic nervous system as a key mediator in the observed relationship between poor sleep and cardiovascular dysfunction. However, brain mechanisms underpinning the impaired sympathetic function associated with poor sleep remain unclear. Recent evidence suggests the central orexin system, particularly orexins A and B and their receptors, have a key regulatory role for sleep in animal and human models. While orexin system activity has been observed to significantly impact sympathetic regulation in animals, the extension of these findings to humans has been difficult due to an inability to directly assess orexin system activity in humans. However, direct measures of sympathetic activity in populations with narcolepsy and chronic insomnia, 2 sleep disorders associated with deficient and excessive orexin neural activity, have allowed indirect assessment of the relationships between orexin, sleep, and sympathetic regulation. Further, the recent pharmaceutical development of dual orexin receptor antagonists for use in clinical insomnia populations offers an unprecedented opportunity to examine the mechanistic role of orexin in sleep and cardiovascular health in humans. The current review assesses the role of orexin in both sleep and sympathetic regulation from a translational perspective, spanning animal and human studies. The review concludes with future research directions necessary to fully elucidate the mechanistic role for orexin in sleep and sympathetic regulation in humans.

Sympathetic Neural Control in Humans with Anxiety-Related Disorders.

Numerous conceptual models are used to describe the dynamic responsiveness of physiological systems to environmental pressures, originating with Claude Bernard's milieu intérieur and extending to more recent models such as allostasis. The impact of stress and anxiety upon these regulatory processes has both basic science and clinical relevance, extending from the pioneering work of Hans Selye who advanced the concept that stress can significantly impact physiological health and function. Of particular interest within the current article, anxiety is independently associated with cardiovascular risk, yet mechanisms underlying these associations remain equivocal. This link between anxiety and cardiovascular risk is relevant given the high prevalence of anxiety in the general population, as well as its early age of onset. Chronically anxious populations, such as those with anxiety disorders (i.e., generalized anxiety disorder, panic disorder, specific phobias, etc.) offer a human model that interrogates the deleterious effects that chronic stress and allostatic load can have on the nervous system and cardiovascular function. Further, while many of these disorders do not appear to exhibit baseline alterations in sympathetic neural activity, reactivity to mental stress offers insights into applicable, real-world scenarios in which heightened sympathetic reactivity may predispose those individuals to elevated cardiovascular risk. This article also assesses behavioral and lifestyle modifications that have been shown to concurrently improve anxiety symptoms, as well as sympathetic control. Lastly, future directions of research will be discussed, with a focus on better integration of psychological factors within physiological studies examining anxiety and neural cardiovascular health. © 2022 American Physiological Society. Compr Physiol 12:1-33, 2022.

Activation of Orexin 1 Receptors in the Paraventricular Nucleus Contributes to the Development of Deoxycorticosterone Acetate-Salt Hypertension Through Regulation of Vasopressin.

Salt-sensitivity is a major factor in the development of hypertension. The brain orexin system has been observed to play a role in numerous hypertensive animal models. However, orexin's role in the pathology of salt-sensitive hypertension (SSH) remains to be adequately explored. We assessed the impact of orexin hyperactivity in the pathogenesis of the deoxycorticosterone acetate (DOCA) - salt rat model, specifically through modulation of Arginine Vasopressin (AVP). Adult male rats were separated into three groups: vehicle control, DOCA-salt, and DOCA-salt+OX1R-shRNA. DOCA-salt rats received subcutaneous implantation of a 21-day release, 75 mg DOCA pellet in addition to saline drinking water (1% NaCl and 0.2% KCl). DOCA-salt+OX1R-shRNA rats received bilateral microinjection of AAV2-OX1R-shRNA into the paraventricular nucleus (PVN) to knockdown function of the Orexin 1-Receptor (OX1R) within that area. Following 2-week to allow full transgene expression, a DOCA pellet was administered in addition to saline drinking solution. Vehicle controls received sham DOCA implantation but were given normal water. During the 3-week DOCA-salt or sham treatment period, mean arterial pressure (MAP) and heart rate (HR) were monitored utilizing tail-cuff plethysmography. Following the 3-week period, rat brains were collected for either PCR mRNA analysis, as well as immunostaining. Plasma samples were collected and subjected to ELISA analysis. In line with our hypothesis, OX1R expression was elevated in the PVN of DOCA-salt treated rats when compared to controls. Furthermore, following chronic knockdown of OX1R, the hypertension development normally induced by DOCA-salt treatment was significantly diminished in the DOCA-salt+OX1R-shRNA group. A concurrent reduction in PVN OX1R and AVP mRNA was observed in concert with the reduced blood pressure following AAV2-OX1R-shRNA treatment. Similarly, plasma AVP concentrations appeared to be reduced in the DOCA-salt+OX1R-shRNA group when compared to DOCA-salt rats. These results indicate that orexin signaling, specifically through the OX1R in the PVN are critical for the onset and maintenance of hypertension in the DOCA-salt model. This relationship is mediated, at least in part, through orexin activation of AVP producing neurons, and the subsequent release of AVP into the periphery. Our results outline a promising mechanism underlying the development of SSH through interactions with the brain orexin system.

Effect of evening blue light blocking glasses on subjective and objective sleep in healthy adults: A randomized control trial.

OBJECTIVES: Evening blue light has been shown to suppress melatonin, which can negatively impact sleep quality. The impact of evening blue light blocking (BLB) interventions on sleep remains ambiguous due to lack of randomized control trials. The present study tests the hypothesis that BLB glasses improve subjective and objective sleep in a population of healthy adults. DESIGN: Two-week, randomized, controlled, crossover design. SETTING: At-home testing of individuals in Michigan and Montana. PARTICIPANTS: Twenty healthy adults (11 men, 9 women, age: 32 ± 12, body mass index: 28 ± 4 kg/m2). INTERVENTION: Following a 1-week run-in baseline (ie, no glasses), participants were randomized to 1-week of BLB or control (ie, clear lens) glasses. Upon finishing the 1-week intervention, participants crossed over to the opposite condition. In both conditions, glasses were worn for 7 consecutive days from 6 PM until bedtime. MEASUREMENTS: Objective sleep parameters were obtained using wrist actigraphy. Subjective sleep measures were assessed using sleep diaries. Karolinska Sleep Diaries were used to assess perceived sleep quality. RESULTS: BLB reduced subjective sleep onset (21 ± 28 vs 24 ± 21 minute, P = .033) and awakenings (1.6 ± 1.0 vs 2.2 ± 1.0 awakenings, P = .019) compared to the control condition. In contrast, objective measures of sleep were not significantly impacted. In fact, our primary outcome variable of total sleep time (TST) tended to be paradoxically shorter in the BLB condition for both subjective (468 ± 45 vs 480 ± 48 minute, P = .066) and objective (433 ± 40 vs 449 ± 39 minute, P = .075) TST. CONCLUSIONS: Blue light blocking glasses did not improve objective measures of sleep time or quality in healthy adults.

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.

Sex differences in self-report anxiety and sleep quality during COVID-19 stay-at-home orders.

BACKGROUND: COVID-19 and home isolation has impacted quality of life, but the perceived impact on anxiety and sleep remains equivocal. The purpose of this study was to assess the impact of COVID-19 and stay-at-home orders on self-report anxiety and sleep quality, with a focus on sex differences. We hypothesized that the COVID-19 pandemic would be associated with increased anxiety and decreased sleep quality, with stronger associations in women. METHODS: One hundred three participants (61 female, 38 ± 1 years) reported perceived changes in anxiety and sleep quality due to stay-at-home orders during the COVID-19 pandemic and were administered the Spielberger State-Trait Anxiety Inventory (STAI), Pittsburgh Sleep Quality Index (PSQI), and Insomnia Severity Index (ISI). Chi-square and T test analyses were utilized to assess sex differences in reported anxiety and sleep. Analysis of covariance was used to compare the associations between reported impact of COVID-19 and anxiety/sleep parameters. RESULTS: Women (80.3%) reported higher prevalence of increased general anxiety due to COVID-19 when compared to men (50%; p = 0.001) and elevated STAI state anxiety compared to men (43 ± 1 vs. 38 ± 1 a.u., p = 0.007). Despite these differences in anxiety, the perceived impact of COVID-19 on PSQI was not different between sexes. However, when stratified by perceived changes in anxiety due to COVID-19, participants with higher anxiety responses to COVID-19 had higher ISI compared to those with no perceived changes in anxiety (9 ± 1 vs. 5 ± 1 a.u., p = 0.003). Additionally, participants who reported reduced sleep quality due to COVID-19 reported higher state anxiety (45 ± 1 a.u.) compared to those that perceived no change (36 ± 2 a.u., p = 0.002) or increased (36 ± 2 a.u., p < 0.001) sleep quality. CONCLUSION: COVID-19 and state-ordered home isolation was associated with higher anxiety and reduced sleep quality, with a stronger association in women with respect to anxiety.