Marker Of Autonomic Nervous System Activity Research Articles

Direct and indirect effects of adiposity on markers of autonomic nervous system activity in older adults.

Several cardiovascular disease (CVD) risk factors (e.g., hypertension, poor glycemic control) can affect and be affected by autonomic nervous system (ANS) activity. Since excess adiposity can influence CVD development through its effect on hypertension and diabetes mellitus, it is important to determine how adiposity and altered ANS activity are related. The present study employed structural equation modeling to investigate the relation between adiposity and ANS activity both directly and indirectly through biological variables typically associated with glycemic impairment and cardiac stress in older adults. Utilizing the Atherosclerosis Risk in Communities (ARIC) dataset, 1,145 non-smoking adults (74±4.8 yrs, 62.8% female) free from known CVD, hypertension, and diabetes and not currently taking beta-blockers were evaluated for fasting blood glucose (FBG), insulin, and HbA1c concentrations, waist circumference (WC), blood pressure (BP), and markers of ANS activity. WC was recorded just above the iliac crest and was used to reflect central adiposity. Resting 2-minute electrocardiograph recordings, pulse wave velocity, and ankle-brachial index data were used to assess the root mean square of successive differences in RR intervals (RMSSD) and the pre-ejection period (PEP), markers of parasympathetic and sympathetic activity, respectively. FBG, insulin, and HbA1c inferred a latent variable termed glycemic impairment (GI), whereas heart rate and diastolic BP inferred a latent variable termed cardiac stress (CS). The structural equation model fit was acceptable [root mean square error of approximation = 0.050 (90% CI = .036, .066), comparative fit index = .970, Tucker Lewis Index = 0.929], with adiposity having both significant direct (β = 0.208, p = 0.018) and indirect (β = -.217, p = .041) effects on PEP through GI. Adiposity displayed no significant direct effect on RMSSD. CS displayed a significant pathway (β = -0.524, p = 0.035) on RMSSD, but the indirect effect of WC on RMSSD through CS did not reach statistical significance (β = -0.094, p = 0.137). These results suggest that adiposity's relation to ANS activity is multifaceted, as increased central adiposity had opposing direct and indirect effects on markers of sympathetic activity in this population of older adults.

Effects of Cigarette Smoking on Cardiac Autonomic Responses: A Cross-Sectional Study.

It has been suggested that some of the adverse, long-term cardiovascular outcomes of smoking are mediated by impaired autonomic nervous system (ANS) activity. Yet, this association is currently inconclusive. Heart rate variability (HRV) and the deep breathing test (DBT) represent common quantitative markers of ANS activity due to their simplicity and reliability. This large cross-sectional study was designed to assess the effect of active smoking on ANS function as manifested by HRV or DBT abnormalities. Electrocardiograms were recorded at rest for 5 min and during forced metronomic breathing. HRV and DBT were calculated according to accepted standards. Participants were divided into two groups based on current smoking status. The study included 242 healthy volunteers (196 nonsmokers and 46 smokers). There were no significant differences in age, sex, and BMI between groups. Cumulative smoking exposure burden (CSEB) for the study group was 5.3 ± 1.3 pack-years. Comparative analysis of HRV and DBT parameters according to smoking status revealed no significant differences between groups. Significant (p < 0.05), yet weak or moderate correlations (r < 0.7) were found between CSEB and abnormal change in HRV parameters consistent with sympathetic overactivity and decreased parasympathetic tone. In conclusion, smoking for a relatively short period in healthy adults does not seem to lead to significant impairment in ANS function. Yet, the consequences of smoking seem to be amplified when cumulative exposure burden increases.

Minimization of Heart Rate Bias in the Estimation of Heart Rate Variability

Background: Heart Rate (HR) is a time varying signal indicating the beating activity of the heart, whereas Heart Rate Variability (HRV) is a noninvasive tool to evaluate the cardiac autonomic regulations. The HRV is widely used to evaluate cardiac/autonomic health in normal healthy as well as chronic diseased population. The HR and HRV are significantly connected with each other. HRV is dependent on the average HR as well on the Autonomic Nervous System (ANS) activity. To make the HRV a potential marker of ANS activity, the influence of HR must be reduced. The present study is designed to minimize the effect of HR on HRV by normalization of the RR interval tachogram. Method: Forty six young adults participated in the non-invasive and benign study. 10 minutes of Electrocardiogram (ECG) lead II was recorded in each case in supine position. The electrocardiographic records of the subjects were divided into three groups based on their HR viz., slow, moderate and fast HR. The HRV indices were extracted at pre and post HR bias minimization. Results: The improved HRV was observed with HR bias minimization in all three categories of HR. The reduced HRV was found with increasing heart rate even after HR bias minimization. Conclusion: Significant impact of normalization was found on moderate and fast HR subjects. This suggests that the HRV studies would yield better results with HR bias reduced, thereby improving health monitoring systems based on HRV.

DIAGNOSTIC POTENTIAL OF SELECTED SALIVARY PROTEOMICS FOR AUTONOMIC NERVOUS SYSTEM ACTIVITY ASSESSMENT

The clinical assessment of autonomic nervous system (ANS) functioning, enabling the diagnosis of autonomic neuropathy present in the course of many diseases, is currently based on performing simple cardiovascular reflexes (Ewing tests), analyzing heart rate variability (HRV) or heart rate turbulence (HRT), examining skin sweating or recording neurophysiological tests (e.g. microneurography). Laboratory assessment of ANS function is very scarce and practically only includes the plasma assessment of noradrenaline as a surrogate for the biochemical indicator of sympathetic activity. Recently, the possibility of evaluation of selected compounds present in saliva as laboratory markers of not only oral diseases but also systemic diseases has been raised. This work focuses on a brief description of the anatomy and physiology of the salivary glands and describes the formation of saliva, its composition and the use of this bodily fluid in laboratory diagnostics. In addition, the paper specifically discusses the possibility of determining selected compounds that are considered to reflect autonomic activity. A review of the literature indicates primarily four proteomics: two neuropeptides (vasoactive intestinal peptide (VIP) and neuropeptide Y (NPY) that are co-transmitters in autonomic fibers, chromogranin A, a synaptic vesicle protein and α-amylase, a hydrolytic enzyme pre-digesting carbohydrates in the oral cavity. These are currently the most widely investigated agents for their usefulness as laboratory markers of ANS activity.

Salivary Alpha-Amylase as a Biomarker of Stress in Behavioral Medicine

In recent years, research in behavioral medicine has become increasingly focused on understanding how chronic and acute exposure to stress impacts health outcomes. During stress, the body’s physiological stress systems are activated. These systems closely interact with the immune system and are, thus, importantly implicated in the onset and maintenance of disease states. While much of the research in behavioral medicine that has investigated the effects of stress on disease has focused on the role of the hypothalamic-pituitary-adrenal axis and its downstream biomarker, cortisol, it is evident that the autonomic nervous system (ANS) also plays a crucial role in both the biological stress process and the manifestation and maintenance of stress-related symptoms. In recent years salivary alpha-amylase (sAA) has emerged as a valid and reliable marker of ANS activity in stress research and is therefore an important biomarker to consider in behavioral medicine. In this commentary, we will highlight research relevant for behavioral medicine that has utilized sAA measurements, both basally, and in response to stress, to examine ANS function in clinical populations. We will additionally summarize findings from studies that have examined the effects of various targeted interventions on changes in sAA levels. Through this, our aim is to present evidence that sAA can serve as a feasible biomarker of ANS (dys)function in health and disease. To this end, we will also highlight important methodological considerations for readers to keep in mind when including sAA assessments in their own studies. The overarching goal of this brief commentary is to highlight how a multidimensional approach toward physiological stress measurement can allow researchers to develop a better understanding of physical health and disease states.

Poor night’s sleep predicts following day’s salivary alpha-amylase under high but not low stress

Although sleep is linked to physiological stress systems like the autonomic nervous system (ANS), research is still limited regarding night-and-day interactions between nocturnal sleep characteristics, stress, and diurnal parameters of salivary alpha-amylase (sAA) as a surrogate marker of ANS activity. Fifty healthy university students rated their chronic stress burden and completed two five-day periods of ecological momentary assessment – under everyday conditions of both low stress (beginning of semester) and high stress (final examination preparation). Participants collected saliva six times daily and reported on the previous night’s sleep (quality, latency, duration, disturbances) immediately after awakening. Additionally, a sub-sample wore actigraphs recording ‘time in bed’. In contrast to previous assumptions, poor sleep predicted lower sAA awakening values, more decreased awakening responses, and steeper diurnal slopes the following day only under high stress, but not under low stress. Diurnal sAA parameters did not predict the following night’s sleep characteristics. The sAA profile does not seem to be sensitive to everyday occurring sleep variations, but rather seems to be an indicator of more prolonged stress induced ANS dysregulation.

Examining multiple sleep behaviors and diurnal salivary cortisol and alpha-amylase: Within- and between-person associations

Sleep has been linked to the daily patterns of stress-responsive physiological systems, specifically the hypothalamic–pituitary–adrenal (HPA) axis and autonomic nervous system (ANS). However, extant research examining sleep and diurnal patterns of cortisol, the primary end product of the HPA axis, has primarily focused on sleep duration with limited attention on other facets of sleep. For example, it is not clear how specific aspects of sleep (e.g., sleep quality, sleep duration variability) are related to specific components of diurnal cortisol rhythms. Salivary alpha-amylase (sAA) has been recognized as a surrogate marker of ANS activity, but limited research has explored relations between sleep and sAA diurnal rhythms. The current study utilized an ecological momentary assessment protocol to examine within- and between-person relations between several facets of sleep behavior using multiple methods (e.g., subjective report, actigraphy) and salivary cortisol and sAA. Older adolescents (N=76) provided saliva samples and diary entries five times per day over the course of three days. Sleep was assessed via questionnaire, through daily diaries, and monitored objectively using actigraphy over a four day period. Between-person results revealed that shorter average objective sleep duration and greater sleep duration variability were related to lower levels of waking cortisol and flatter diurnal slopes across the day. Within-person results revealed that on nights when individuals slept for shorter durations than usual they also had lower levels of waking cortisol the next day. Sleep was not related to the cortisol awakening response (CAR) or diurnal patterns of sAA, in either between-person or within-person analyses. However, typical sleep behaviors measured via questionnaire were related to waking levels of sAA. Overall, this study provides a greater understanding of how multiple components of sleep, measured in naturalistic environments, are related to cortisol and sAA diurnal rhythms, and how day-to-day, within-person changes in sleep duration contribute to daily variations in cortisol.