Sympathetic neural responses to sleep disorders and insufficiencies

Author(s):  
Ian M. Greenlund ◽  
Jason R. Carter

Short sleep duration and poor sleep quality are associated with cardiovascular risk, and sympathetic nervous system (SNS) dysfunction appears to be a key contributor. The present review will characterize sympathetic function across several sleep disorders and insufficiencies in humans, including sleep deprivation, insomnia, narcolepsy, and obstructive sleep apnea (OSA). We will focus on direct assessments of sympathetic activation (e.g., plasma norepinephrine and muscle sympathetic nerve activity), but include heart rate variability (HRV) when direct assessments are lacking. The review also emphasizes sex as a key biological variable. Experimental models of total sleep deprivation and sleep restriction are converging to support epidemiological studies reporting an association between short sleep duration and hypertension, especially in women. A systemic increase of SNS activity via plasma norepinephrine is present with insomnia, and has also been confirmed with direct, regionally-specific evidence from microneurographic studies. Narcolepsy is characterized by autonomic dysfunction via both HRV and microneurographic studies, but with opposing conclusions regarding SNS activation. Robust sympathoexcitation is well documented in OSA, and is related to baroreflex and chemoreflex dysfunction. Treatment of OSA with continuous positive airway pressure results in sympathoinhibition. In summary, sleep disorders and insufficiencies are often characterized by sympathoexcitation and/or sympathetic/baroreflex dysfunction, with several studies suggesting women may be at heightened risk.

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
G Seravalle ◽  
F Quarti Trevano ◽  
R Dell'oro ◽  
G Bertoli ◽  
G Mancia ◽  
...  

Abstract Background Short sleep duration and poor sleep quality has been reported to be associated with increased cardiovascular risk and increased incidence of cardiovascular events. Purpose Whether and what extent the pathophysiology of this association includes sympathetic abnormalities has never been examined via microneurography. Methods In 28 untreated mild-to moderate essential hypertensives aged 66.4±3.1 (mean±SEM) without other cardiovascular or non-cardiovascular disease (including obstructive sleep apnea) recruited from the outpatient clinic and referred for short sleep duration, we directly assessed at patients home via actigraphy (actiwatch spectrum activity monitor, Phillips) time sleep duration and efficiency. Measurements, performed during a day preceding or following the 7 day actigraphy evaluation, included microneurographic recording of efferent postganglionic sympathetic nerve traffic (MSNA), venous plasma norepinephrine (HPLC), clinic, 24 hour and beat to beat blood pressure and heart rate values. Sleep diary and a sleep questionnaire were also administered. Results Nine patients slept less than 6 hours per night (LSD), while the remaining ones between 6 to 7 (MSD, n=8) or more than 7 hours (GSD,N=11). The 3 groups showed similar age and gender distribution and a body mass index amounting to 28.1±0.8, 28.6±0.5 and 27.3±0.5 kg/m2 (P=NS). For similar mean blood pressure values LSD showed MSNA values significantly greater than GSD (53.4±4.9 vs 40.1±3.8bs/100hb, P<0.03), this being the case also for MSD (49.7±4.4, P<0.05 vs GSD but not SLD). HR was significantly elevated only in LSD group when compared to GSD, while no significant difference was found in plasma NE between the 3 groups. Conclusions The present study provides the first microneurographic direct evidence that short sleep duration is linked to a marked sympathetic activation, which may participate at the high cardiovascular risk of these subjects. The sympathetic overdrive affects both the cardiac and peripheral district but is not reflected by NE, which thus does not represent in this condition a valuable adrenergic marker.


2020 ◽  
pp. 1-8
Author(s):  
Dandan Zheng ◽  
Xiaodong Yuan ◽  
Chaoran Ma ◽  
Ying Liu ◽  
Hannah VanEvery ◽  
...  

Abstract Objective: To assess the association between total alcohol intake, specific alcoholic beverages and sleep quality in a community-based cohort. Design: A cross-sectional study. Setting: The Kailuan community, China. Participants: Included were 11 905 participants who were free of a history of CVD, cancer, Parkinson’s disease, dementia and head injury in or prior to 2012. Alcohol consumption (amount and frequency intake) and alcoholic beverage type were collected in 2006 (baseline) and 2012. Participants were grouped into non-, light- (women: 0–0·4 serving/d; men: 0–0·9 serving/d), moderate- (women: 0·5–1·0 serving/d; men: 1·0–2·0 servings/d) and heavy- (women: >1·0 servings/d; men: >2·0 servings/d) drinkers. Overall sleep quality was measured in 2012 and included four sleep parameters (insomnia, daytime sleepiness, sleep duration, snoring/obstructive sleep apnoea). Results: We observed a dose–response association between higher alcohol consumption in 2006 and worse sleep quality in 2012 (Ptrend < 0·001), after adjusting for age, sex, socio-economic status, smoking status, physical activity, obesity, plasma lipid profiles, diabetes and hypertension. A similar association was observed when alcohol consumption in 2012 was used as exposure. Alcohol was associated with higher odds of having short sleep duration (adjusted OR for heavy- v. non-drinkers = 1·31; 95 % CI: 1·09, 1·57) and snoring (adjusted OR for heavy- v. non-drinkers: 1·38; 95 % CI: 1·22, 1·57). Consumption of hard liquor, but not beer or wine, was significantly associated with poor sleep quality. Conclusions: Higher alcohol consumption was associated with poorer sleep quality and higher odds of having snoring and short sleep duration.


2021 ◽  
Vol 9 (7) ◽  
Author(s):  
Catherine McCall ◽  
Glen Duncan ◽  
Nathaniel Watson

Sleep and sleep disorders are complex phenotypes with genetic, epigenetic, and environmental influences. Twin studies allow researchers to parse out how these factors influence variability in sleep outcomes such as sleep duration and quality, chronotype, and disorders such as insomnia, hypersomnia, sleep apnea, sleep-related movement disorders, and parasomnias. Twin studies assess the overlap in genetic influences for sleep variance and other medical and psychiatric disorders and allow exploration of gene-environment interactions. Longitudinal twin studies demonstrate how these interactions change over the course of a lifetime. In general, twin studies demonstrate that the heritability of common sleep measures such as duration, quality, and chronotype is about 30-50%; however, this can vary widely between samples according to age, sex, comorbidities, and geographic location. Similarly, the heritability of sleep disorders including insomnia, obstructive sleep apnea, and parasomnias is also around 30-50%, with higher estimates for disorders known to run in families, such as sleepwalking. Heritability estimates for medical and psychiatric problems including obesity, depression, post-traumatic stress disorder, and mortality are higher with short sleep duration (typically < 7 h/n), suggesting that short sleep activates disease-related gene expression. Significant genetic overlap exists between insomnia and issues such as obesity, chronic pain, depression, and psychosis. In this review, we describe the major findings of twin studies related to sleep and how they impact our understanding of this critical component of health and disease.


Circulation ◽  
2018 ◽  
Vol 137 (suppl_1) ◽  
Author(s):  
Loretta Cain ◽  
LáShauntá Glover ◽  
Dayna Johnson ◽  
Mario Sims

Introduction: Research shows that compared to non-Hispanic whites, African Americans (AAs) have poorer sleep quality, lower mean sleep duration, and a higher prevalence of sleep-disordered breathing. AAs also report more frequent exposures to certain stressors over the life course, which may impact physiological processes that may impair sleep. Goal-striving-stress (GSS), the discrepancy between aspiration and achievement, weighted by the subjective probability of success, and the level of disappointment experienced if goals are not reached, may be an important stressor among AA’s that may influence sleep; however this has yet to be explored. The objective of this study was to assess the relationship between GSS and sleep duration and sleep quality in AAs. Hypothesis: We assessed the hypothesis that high (versus low) GSS would be associated with short or long sleep duration and poor sleep quality. Methods: We utilized data from the baseline exam of the Jackson Heart Study (JHS; n=5306), an AA sample of women and men, 35-84 years old. There were a total of 5082 participants in the sample; 63.34% female with a mean age of 55.30 (± 12.75) and mean sleep duration of 6.43 hours (±1.51). The sample was categorized into GSS tertiles: low (n=2121), moderate (n=1716), high (n=1296). Participants self-reported sleep duration (hours) and rated their sleep quality. Sleep duration was categorized as short ( < 6 hours), normal (7 or 8 hours) and long ( > 9 hours). Sleep quality was categorized as high (good/very good/excellent) and low (fair/poor). Logistic regression models were used to obtain odds ratios (OR, 95% confidence interval-CI) to assess the associations of GSS levels with sleep duration and sleep quality categories. Models were adjusted for sex, age, socioeconomic status, health behaviors, discrimination, and health outcomes. Results: Significant results showed that participants who reported high (versus low) GSS had a 29% increased odds [1.29 (1.10, 1.52)] of short (versus normal) sleep after full adjustment. Participants who reported high (versus low) GSS had a 42% increased odds [1.42 (1.20, 1.67)] of low (versus high) sleep quality after full adjustment. Conclusion In conclusion, the deficit between goal aspiration and achievement is associated with short sleep duration and poor sleep quality. Potential interventions should consider the extent to which GSS may contribute to the development of short sleep duration and poor sleep quality.


SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A315-A315
Author(s):  
C M Baldwin ◽  
D G Link ◽  
D W Coon ◽  
S F Quan

Abstract Introduction This work compares sleep knowledge of community-dwelling older adult men and women. Methods Data were derived from a community-based sleep training program that assessed pre- and post-test knowledge of obstructive sleep apnea (OSA), Insomnia, short sleep duration (SSD), restless leg syndrome (RLS), circadian rhythm disorders (CRD), and drowsy driving (DD) on a 1 (none) to 5 (great deal of knowledge) Likert-like scale. Data were analyzed with frequencies for age, sex, and sources of sleep information, and ANOVA to determine gender differences using SPSS (V24) with significance set at p&lt;.05. Results Participants (N=158; 68% women) were 56 years and older residing in a retirement community. Pre-test means±standard deviations showed women versus men had greater knowledge of Insomnia (3.5±1.3 vs. 2.9±1.0, p=.004) whereas men showed more knowledge of DD (3.2±1.1 vs. 2.6±1.3, p=.01). A trend was noted for women to have greater knowledge of SSD (3.6±1.2 vs. 3.2±1.0, p=.05). Post-test ANOVA showed a further increase in Insomnia knowledge for women versus men (4.4±0.8 vs. 4.1±0.7, p=.04); however, overall pre/post-test scores for each of the sleep disorders across men and women increased significantly at the p&lt;.001 level. Notably, more women to men reported accessing various resources for sleep information: newspapers/magazines (46:7), friends/family (29:9), the internet (25:11), TV (37:7), and physicians/nurses (45:20). Conclusion Findings indicate, prior to sleep training, women have greater knowledge of insomnia and short sleep duration, while men have more knowledge of drowsy driving. Women’s greater understanding of insomnia persists even after sleep training; however, pre- to post-test scores for both sexes across sleep disorders show significant learning outcomes. One possible reason for women’s greater knowledge of insomnia and short sleep could be their greater likelihood to access information on health and healthy lifestyle factors, including sleep, as well as their greater health care utilization. Support N/A


SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A352-A353
Author(s):  
S Griggs ◽  
N S Redeker ◽  
S Jeon ◽  
M Grey

Abstract Introduction The association between short sleep duration and poorer glycemic control in adolescents ages 10-16 with type 1 diabetes (T1D) is well established. Researchers have used cross-sectional, between-subjects’ methods, with limited focus on the potential intraindividual variation among these variables. The purpose of this analysis was to examine the within person associations between glucose variability indices (J index, low/high blood glucose index, time in range) and sleep characteristics (bedtime, waketime, total sleep time, sleep efficiency, wake after sleep onset [WASO], awakenings, and sleep fragmentation index) in adolescents with T1D. Methods Adolescents monitored their sleep and glucose patterns concurrently for 3-7 days with a wrist actigraph on their non-dominant wrist and either their own continuous glucose monitor (CGM) or a provided blinded CGM. General linear mixed models (GLMM) were used to determine within-person and day level associations. Results The sample included 38 adolescents (M age 13.4±1.8; 37.8% male; M A1C 8.2±1.2%). Average glucose levels were controlled in all GLMMs. Adolescents had earlier waketimes on days when more time was spent in hypoglycemia &lt;70mg/dL (β=-0.15, p&lt;0.001). At the person level, adolescents had greater WASO with more % time spent in severe hypoglycemia &lt;54mg/dL with more severe low blood glucose indices (β=0.35, p&lt;0.01 and β=0.34, p&lt;0.01 respectively). At the daily level, adolescents had greater WASO (β=0.20, p=0.01) and more awakenings (β=0.16, p=0.04) on the days they had more overall glucose variability (J index) and more severe high blood glucose indices (β=0.17, p=0.04), but were less likely to have more % time in hypoglycemia (β=-0.15, p=0.02). Conclusion Glucose variability was positively associated with poor sleep (e.g., WASO and awakenings) in adolescents with T1D both at the daily and intraindividual level. Monitoring over a longer period of time in subsequent studies would allow researchers to determine the within person associations between habitual short sleep duration and glucose variability. Support NINR T32NR0008346 & P20NR014126, Medtronic MiniMed provided CGMs at a discounted rate for the study.


2012 ◽  
Vol 302 (10) ◽  
pp. H1991-H1997 ◽  
Author(s):  
Jason R. Carter ◽  
John J. Durocher ◽  
Robert A. Larson ◽  
Joseph P. DellaValla ◽  
Huan Yang

Sleep deprivation has been linked to hypertension, and recent evidence suggests that associations between short sleep duration and hypertension are stronger in women. In the present study we hypothesized that 24 h of total sleep deprivation (TSD) would elicit an augmented pressor and sympathetic neural response in women compared with men. Resting heart rate (HR), blood pressure (BP), and muscle sympathetic nerve activity (MSNA) were measured in 30 healthy subjects (age, 22 ± 1; 15 men and 15 women). Relations between spontaneous fluctuations of diastolic arterial pressure and MSNA were used to assess sympathetic baroreflex function. Subjects were studied twice, once after normal sleep and once after TSD (randomized, crossover design). TSD elicited similar increases in systolic, diastolic, and mean BP in men and women (time, P < 0.05; time × sex, P > 0.05). TSD reduced MSNA in men (25 ± 2 to 16 ± 3 bursts/100 heart beats; P = 0.02), but not women. TSD did not alter spontaneous sympathetic or cardiovagal baroreflex sensitivities in either sex. However, TSD shifted the spontaneous sympathetic baroreflex operating point downward and rightward in men only. TSD reduced testosterone in men, and these changes were correlated to changes in resting MSNA ( r = 0.59; P = 0.04). Resting HR, respiratory rate, and estradiol were not altered by TSD in either sex. In conclusion, TSD-induced hypertension occurs in both sexes, but only men demonstrate altered resting MSNA. The sex differences in MSNA are associated with sex differences in sympathetic baroreflex function (i.e., operating point) and testosterone. These findings may help explain why associations between sleep deprivation and hypertension appear to be sex dependent.


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