Tobacco smoking is a risk factor for countless diseases, and smoking relapse remains a major public health concern. Subjective reports of stress by smokers are a common theme for relapse, however, the role of objective stress-related biomarkers in predicting tobacco relapse risk has been less studied. The aim of this manuscript was to review existing literature on the connection between biomarkers of stress and smoking relapse. Overall, trends indicate that blunted hypothalamic-pituitary-adrenal (HPA) responses to acute stress, larger reductions in HPA biomarkers during the initial days of abstinence during cessation (compared to pre-cessation levels), and exaggerated autonomic responses to stress predict increased risk of relapse. In addition, successful cessation is followed by changes in stress biomarkers (e.g., reductions in cortisol and heart rate, HR). This review also identifies potential modifiers, such as methodological differences, biological sex, and chronic stress, to account for heterogeneity of findings within and across studies. In addition, we identify gaps in the literature and suggest future research directions focusing on the roles of genetics and gene expression as well as the influence of neurobiological mechanisms on stress and relapse risk. Future clinical implications of this research include identifying reliable indicators of relapse risk and the potential of pharmacotherapeutic treatments to target stress response systems to correct dysregulation and potentially reduce stress-related risk of relapse.

The autonomic nervous system plays a key role in maintaining body hemostasis through both the sympathetic and parasympathetic nervous systems. Sympathetic overstimulation as a reflex to multiple pathologies, such as septic shock, brain injury, cardiogenic shock, and cardiac arrest, could be harmful and lead to autonomic and immunologic dysfunction. The continuous stimulation of the beta receptors on immune cells has an inhibitory effect on these cells and may lead to immunologic dysfunction through enhancing the production of anti-inflammatory cytokines, such as interleukin-10 (IL-10), and inhibiting the production of pro-inflammatory factors, such as interleukin-1B IL-1B and tissue necrotizing factor-alpha (TNF-alpha). Sympathetic overstimulation-induced autonomic dysfunction may also happen due to adrenergic receptor insensitivity or downregulation. Administering anti-adrenergic medication, such as beta-blockers, is a promising treatment to compensate against the undesired effects of adrenergic surge. Despite many misconceptions about beta-blockers, beta-blockers have shown a promising effect in decreasing mortality in patients with critical illness. In this review, we summarize the recently published articles that have discussed using beta-blockers as a promising treatment to decrease mortality in critically ill patients, such as patients with septic shock, traumatic brain injury, cardiogenic shock, acute decompensated heart failure, and electrical storm. We also discuss the potential pathophysiology of beta-blockers in various types of critical illness. More clinical trials are encouraged to evaluate the safety and effectiveness of beta-blockers in improving mortality among critically ill patients.

We aimed to assess the effect of exercise training on heart rate variability (HRV) in hypertensive patients and to provide practical recommendations. We systematically searched seven databases for randomized controlled trials (RCTs) comparing the efficacy of exercise interventions vs. non-exercise control for HRV in adults with hypertension. HRV parameters, blood pressure (BP), and heart rate (HR) from the experimental and control groups were extracted to carry out meta-analysis. To explore the heterogeneity, we performed sensitivity analysis, sub-analysis, and meta-regression. Twelve RCTs were included, and the main results demonstrated exercise produced improvement in root mean square of successive RR-intervals differences (RMSSD) and high frequency (HF), and reductions in LF/HF, resting systolic blood pressure (SBP), and HR. The sub-analysis and meta-regression showed that AE improved more HRV indices and was effective in reducing BP compared with RE. Follow-up duration was also an important factor. Data suggests exercise training has ameliorating effects on HRV parameters, resting SBP, and HR in hypertensive patients, showing enhanced autonomic nervous system function and vagal activity. This effect may be better realized with exercise interventions of 4 weeks or more. Considering our results and the hypertension practice guidelines, we tend to recommend patients choose supervised AE.

Autonomic symptoms may be local and general clinical manifestations of both epilepsy and migraine caused by the dysfunction of brain areas best known as the central autonomic network. Despite their prevalence, autonomic signs are often misdiagnosed and their treatment is undervalued. This review aims to describe the autonomic manifestations reported during seizures and migraineur attacks according to their presentation, focusing on the role of the central autonomic network (CAN) and on the parasympathetic outflow that often-induced cranial autonomic symptoms (CAS) during migraineur attacks. Further, our purpose is to analyze the pathophysiological meanings and whether their presence influences the prognosis and therapy of these disorders.

Heart rate variability (HRV) is an early marker of risk for various health conditions, and its analysis serves as a valuable tool for assessing older adults. This study aimed to describe the reference values of HRV parameters in older adults through a systematic review of the literature. The review included searches in MEDLINE (via PubMed®), EMBASE, Latin American and Caribbean Health Literature, Scopus, and Web of Science (WOS). Studies presenting reference values for at least one HRV linear analysis measure in older adults were considered eligible. Out of 1618 studies identified, only 11 met the inclusion criteria. Sample sizes of older adults ranged from 21 to 6250 subjects. The HRV measures assessed (mean RR intervals, SDNN, RMSSD, PNN50, LF, HF, and LF/HF ratio) varied significantly between studies, with no standardized methods for HRV analysis. We concluded that reference values for HRV measures in older adults vary widely between studies. The scientific literature on HRV reference values in older adults is still limited, and future studies should standardize assessment methods for HRV measures in this population.

Autonomic nervous system (ANS) dysfunction is prevalent in end-stage kidney disease (ESKD) patients, carrying significant risks for morbidity and mortality. Heart rate variability (HRV) is a simple and non-invasive method to evaluate ANS functions and predict prognoses in specific patient populations. Since there is a lack of a clear understanding of the clinical significance of HRV in predicting prognoses in ESKD patients, an updated review on this topic is urgently warranted. The clinical significance of HRV in dialysis patients includes its associations with metabolic syndrome, nutritional status, intradialytic hypotension, vascular access failure, major adverse cardiovascular events, and mortality. These findings underscore the essential role of the autonomic reserve, which might denote the elevation of ANS activity as a response to external stimulus. Patients with a higher level of sympathetic activity at the resting stage, but who are unable to adequately elevate their sympathetic activity under stress might be susceptible to a worse outcome in critical circumstances. Further applications of HRV include HRV biofeedback, risk classification, and real-time HRV monitoring. Overall, HRV is an optimal tool for predicting prognoses in dialysis patients. Further study is encouraged in order to gain a clearer understanding of the clinical significance and application of HRV, and thereby enhance the care of ESKD patients.

OBJECTIVE: Polycystic ovary syndrome (PCOS) is a prevalent and complex endocrine disorder that affects women of reproductive age. It has significant implications for female endocrine function, reproductive health, and metabolic disturbances, including insulin resistance, impaired glucose tolerance, and dyslipidemia. Studies have shown that decreased heart rate variability (HRV), a marker of autonomic dysfunction, is associated with adverse cardiovascular events. Recent research has focused on investigating autonomic function in PCOS, and some studies have suggested altered autonomic drive in these patients. The aim of this systematic review and meta-analysis was to evaluate cardiac autonomic function by analyzing HRV in women with PCOS.
METHODS: This systematic review was prepared using PRISMA reporting guidelines. The databases searched were PubMed, Scopus, Web of Science, and Cochrane. Risk of Bias was assessed using ROBINS-I for non-RCTs. The GRADE approach was employed to evaluate the level of certainty in the evidence for each outcome. In order to identify the underlying cause of high heterogeneity, a subgroup analysis was conducted. Sensitivity analysis was checked. A random effect model was used and calculated a pooled standardized mean difference (SMD) with a 95% confidence interval (CI).
RESULTS: Seventeen articles were included in the final analysis, varied in quality, ranging from a \"low\" to a \"high risk of bias\". Combined analyses indicated a notable decrease in HRV among individuals with PCOS compared to the control group. Significant changes were observed in SDNN (SMD: -0.763, 95%CI [-1.289 to -0.237], p=0.004), PNN50 (SMD: -1.245, 95%CI [-2.07, -0.419], p=0.003), LF/HF ratio (SMD: 0.670, 95%CI [0.248, 1.091], p=0.002), HFnu (SMD: -0.873, 95%CI [-1.257, -0.489], p=0.000), LFnu (SMD: 0.840, 95%CI [0.428, 1.251], p=0.000) and TP (SMD: -1.997, 95%CI [-3.306, -0.687], p=0.003). The heterogeneity was partially explained by types of study design. Subgroup analysis revealed significant alterations of HRV in normal-weighted and overweight PCOS cases. Conversely, no significant changes in HRV were observed in obese PCOS cases.
CONCLUSIONS: The findings of this meta-analysis provide evidence suggesting diminished HRV in individuals with PCOS compared to non-PCOS control group.

Heart rate variability (HRV) analysis provides an assessment of cardiac vagal tone and consequently global cardiac health as well as systemic condition. In systemic diseases such as cancer and during treatments that affect the whole body, like chemotherapy, the vagus nerve activity is low and deregulated. Some studies focus on using HRV to predict mortality in oncology. However, in cancer patients, systemic alterations substantially increase artifacts during HRV measurement, especially atrial ectopic beats. Moreover, HRV may be altered by various factors (duration and time of measurement, breathing, drugs, and other confounding factors) that alter each metric in different ways. The Standard Deviation of all Normal to Normal intervals (SDNN) is the most commonly used metric to evaluate HRV in oncology, but it does not appear to be specific to the cardiac vagal tone. Thus, cardiac vagal activity diagnosis and vital prognosis of cancer patients can be biased. Our review presents the main HRV metrics that can be currently used in oncology studies and their links with vagus nerve and cancer. We present the influence of external factors and the required duration and time of measurement. Considering all these parameters, this review proposes seven key points for an assessment of HRV and cardiac vagal tone in patients with cancer.

This meta-analysis was conducted to investigate the effects of exercise training on heart rate variability (HRV) parameters associated with the autonomic nervous system (ANS) activity. Randomized controlled trials (RCTs) involving healthy adults (aged ≥ 18 years) were included. We searched PubMed, Scopus, Web of Science, and EBSCO databases to identify relevant studies. A random-effects meta-analysis was performed using the standardized mean difference (SMD) and 95% confidence interval (CI). Sixteen RCTs with a total of 623 participants were selected for the final analysis. The analysis showed that exercise training improved the standard deviation of normal-to-normal intervals (SDNN) (SMD: 0.58 (0.16, 1.00); p = 0.007), the root mean square of successive differences in heart period series (RMSSD) (SMD: 0.84 (0.36, 1.31); p = 0.0005), and the absolute power of high-frequency band (HF) (SMD: 0.89 (0.27, 1.51); p = 0.005) parameters compared to the control group. Analysis of the moderator variables showed that the effect of exercise on HRV indices may be influenced by sex, age, and type of exercise used, specifically in HF band, absolute power of low-frequency band (LF), and LF/HF ratio parameters. Despite the limited number of existing RCTs related to the subject, the results suggest that exercise training enhances HRV parameters associated with vagal-related activity (RMSSD and HF) and both sympathetic and parasympathetic activities (SDNN). This study overcomes the lack of meta-analyses on the effects of exercise training on autonomic modulation among healthy adults and may bridge the gap in understanding the potential physiological underpinnings of the acknowledged positive health benefits of exercise.

OBJECTIVE: To synthesise the literature examining the autonomic nervous system (ANS) and cortisol responses to an acute stressor following total sleep deprivation (TSD) in healthy adult subjects.
METHODS: We conducted a systematic review (CRD42022293857) following the latest PRISMA statement. We searched Medline (via Ovid), Embase (via Ovid), PsycINFO (via Ovid), CINAHL complete and Scopus databases, without year restriction, using search terms related to \"sleep deprivation\", \"stress\", \"autonomic nervous system\" and \"cortisol\". Two independent team members used pre-defined inclusion/exclusion criteria to assess eligibility and extract data. We used RoB 2 to assess the risk of bias in randomised controlled trials, and ROBINS-I for non-randomised studies.
RESULTS: Sixteen studies, with 581 participants (mean age = 29 ± 12 years), were eligible for inclusion in the descriptive syntheses. Half of the studies (n = 8) were conducted in the United States of America. The most commonly used study designs were randomised crossover studies (n = 7) and randomised controlled trials (n = 5). Most studies used a single night of TSD (n = 13) which was followed by a psychological (n = 6), physical (n = 5) or psychological and physical (n = 5) acute stressor event. Heart rate (n = 8), cortisol (n = 7) and blood pressure (n =6) were the most reported outcomes, while only a single study used forearm vascular conductance and forearm blood flow. Ten studies found that TSD changed, at least, one marker of ANS or cortisol response. TSD compared with a sleep control condition increased cortisol level (n=1), systolic blood pressure (n=3), diastolic blood pressure (n=2), mean arterial pressure (n=1), and electrodermal activity (n=1) after acute stress. Also, compared with a sleep control, TSD blunted cortisol (n=2), heart rate (n=1) and systolic blood pressure (n=2) responses after acute stress. However, TSD did not change ANS or cortisol responses to acute stressors in 73 % of the total reported outcomes. Furthermore, 10 RCT studies (62.5 %) were assigned as \"some concerns\" and two RCT studies (12.5 %) were attributed \"high\" risk of bias. Additionally, one non-randomised trial was classified as \"moderate\" and three non-randomised trials as \"serious\" risk of bias.
CONCLUSIONS: The markers of ANS and cortisol responses to acute stress after TSD in healthy individuals reveal a scarcity of consistent evidence. The included studies present enough evidence that TSD induces either blunted or exaggerated ANS or cortisol responses to laboratory stresses supporting the \"bidirectional multi-system reactivity hypothesis.\". It appears that a comprehensive understanding of this phenomenon still lacks robust evidence, and further research is needed to clarify these relationships.