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Frequent extreme cold events in recent years have brought serious threats to outdoor workers and rescuers. Changes in ambient temperature are associated with altered cardiac autonomic function. The study aims to investigate heart rate variability (HRV) and its relationship to other physiological parameters under extreme cold exposures. Twelve males underwent a 30-min preconditioning phase in a neutral environment followed by a 30-min cold exposure (−5, −10, −15, and −20 °C). Time-domain indexes(meanRR, SDNN, RMSSD, and pNN50), frequency domain indexes [Log(HF), Log(LF), and low frequency/high frequency (LF/HF)], parasympathetic nervous system (PNS), and sympathetic nervous system (SNS) were analysed. Results showed all HRV indexes of four cold exposures were significant. The decrease in temperature was accompanied by progressive PNS activation with SNS retraction. SDNN was the most sensitive HRV index and had good linear relationships with blood pressure, pulse, and hand temperature. The results are significant for formulating safety protection strategies for workers in extremely cold environments. Practitioner Summary: This study investigated heart rate variability (HRV) in 12 males during a 30-min cold exposure (−5, −10, −15, and −20 °C). Results showed all HRV indexes of four cold exposures were significant. The decrease in temperature was accompanied by progressive PNS activation with SNS retraction. SDNN was the most sensitive HRV index and had good linear relationships with blood pressure, pulse, and hand temperature. [ABSTRACT FROM AUTHOR]

Background: Diabetic autonomic neuropathy is a common complication of type 2 diabetes mellitus (T2DM), especially in patients with long-term, poorly controlled diabetes. This study investigates the effects of exercise on autonomic nervous system activity in T2DM patients over time. Methods: A literature review using MEDLINE, Embase, Cochrane Library, Scopus, and PubMed identified studies assessed via heart rate variability. Papers were categorized into three groups: immediate effects (within 60 min), short-term effects (2–3 months), and long-term effects (over 4 months). Results: Nine articles with 161 T2DM patients were included in the meta-analysis. RMSSD changes after exercise were −4.3 (p = 0.227), 8.14 (p < 0.001), and 4.17 (p = 0.002) for the immediate, short-term, and long-term groups, respectively. LF/HF ratio changes were 0.21 (p = 0.264), −3.04 (p = 0.102), and −0.05 (p = 0.006) for the respective groups. Meta-regression indicated age, male gender, and exercise duration were associated with increased RMSSD, with coefficients of 2.36 (p = 0.001), 13.76 (p = 0.008), and 1.50 (p = 0.007), respectively. Age positively correlated with the LF/HF ratio, with a coefficient of 0.049 (p = 0.048). Conclusions: Regular exercise (≥3 times per week) for over 2 months increases parasympathetic activity in T2DM patients, while sympathetic activity decreases significantly after 4 months. Further study is needed to validate these findings. [ABSTRACT FROM AUTHOR]

Hypertension is recognised as a leading attributable risk factor for cardiovascular disease and premature mortality. Global initiatives towards the prevention and treatment of arterial hypertension are centred around non-pharmacological lifestyle modification. Exercise recommendations differ between professional and scientific organisations, but are generally unanimous on the primary role of traditional aerobic and dynamic resistance exercise. In recent years, isometric exercise training (IET) has emerged as an effective novel exercise intervention with consistent evidence of reductions in blood pressure (BP) superior to that reported from traditional guideline-recommended exercise modes. Despite a wealth of emerging new data and endorsement by select governing bodies, IET remains underutilised and is not widely prescribed in clinical practice. This expert-informed review critically examines the role of IET as a potential adjuvant tool in the future clinical management of BP. We explore the efficacy, prescription protocols, evidence quality and certainty, acute cardiovascular stimulus, and physiological mechanisms underpinning its anti-hypertensive effects. We end the review with take-home suggestions regarding the direction of future IET research. [ABSTRACT FROM AUTHOR]

Background: Autonomic nervous system (ANS) testing has aided in our ability to evaluate autonomic dysfunction in migraine patients. We reviewed the literature in multiple databases which investigate ANS function in migraine patients and healthy subjects. Methods: This systematic review and meta-analysis examined the respective deep breathing, Valsalva manoeuvre, orthostatic and isometric challenge results, using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) and Meta-analyses of Observational Studies in Epidemiology (MOOSE) statements. Results: Seven articles met all inclusion criteria. Fixed-effects meta-analysis showed migraine patients (n = 424), collectively, had lower interictal autonomic test results compared with healthy controls (n = 268). In detail, this was true for the standardized mean difference (g) of deep breathing (g= -0.32; 95% confidence interval (CI) -0.48, -0.16), orthostatic challenge (g= -0.28; 95% CI -0.44, -0.13) and isometric challenge (g= -0.55; 95% CI -0.71, -0.39) and for the difference of means (MD) of the Valsalva ratio (MD = -0.17; 95% CI -0.23, -0.10). Conclusions: Interictal ANS dysfunction can be identified in migraine patients when compared to healthy controls. These findings indicate the importance to evaluate ANS function in migraine patients - especially, as migraine-specific prophylactic therapies (such as anti-calcitonin gene-related peptide (CGRP) antibodies) may affect the function of the ANS. [ABSTRACT FROM AUTHOR]

Objectives: Chronic musculoskeletal pain is associated with decreased parasympathetic and increased sympathetic activity in the autonomic nervous system. The objective of this study was to determine the associations between objective measures of heart rate variability (a measure of autonomic nervous system function), actigraphy (a measure of activity and sleep quality), respiration rates, and subjective patient‐reported outcome measures (PROMs) of central sensitization, kinesiophobia, disability, the effect of pain on sleep, and life quality. Methods: Thirty‐eight study subjects were divided into two subgroups, including low symptoms of central sensitization (n = 18) and high symptoms of central sensitization (n = 20), based on patient‐reported scores on the Central Sensitization Inventory (CSI). Heart rate variability (HRV) and actigraphy measurements were carried out simultaneously in 24 h measurement during wakefulness and sleep. Results: A decrease in HRV during the first 2 h of sleep was stronger in the low CSI subgroup compared to the high CSI subgroup. Otherwise, all other HRV and actigraphy parameters and subjective measures of central sensitization, disability, kinesiophobia, the effect of pain on sleep, and quality of life showed only little associations. Discussion: The high CSI subgroup reported significantly more severe symptoms of disability, kinesiophobia, sleep, and quality of life compared to the low CSI subgroup. However, there were only small and nonsignificant trend in increased sympathetic nervous system activity and poorer sleep quality on the high central sensitization subgroup. Moreover, very little differences in respiratory rates were found between the groups. [ABSTRACT FROM AUTHOR]

Background: Myocardial ischemia–reperfusion can further exacerbate myocardial injury and increase the risk of death. Our previous research found that the paraventricular nucleus (PVN) of the hypothalamus plays a crucial role in the improvement of myocardial ischemia–reperfusion injury (MIRI) by electroacupuncture (EA) pretreatment, but its mechanism of action is still unclear. CRH neurons exhibit periodic concentrated expression in PVN, but further research is needed to determine whether they are involved in the improvement of MIRI by EA pretreatment. Meanwhile, numerous studies have shown that changes in sympathetic nervous system innervation and activity are associated with many heart diseases. This study aims to investigate whether EA pretreatment improves MIRI through sympathetic nervous system mediated by PVNCRH neurons. Methods: Integrated use of fiber-optic recording, chemical genetics and other methods to detect relevant indicators: ECG signals were acquired through Powerlab standard II leads, and LabChart 8 calculated heart rate, ST-segment offset, and heart rate variability (HRV); Left ventricular ejection fraction (LVEF), left ventricular short-axis shortening (LVFS), left ventricular end-systolic internal diameter (LVIDs) and interventricular septal thickness (IVSs) were measured by echocardiography; Myocardial infarct area (IA) and area at risk (AAR) were calculated by Evans-TTC staining. Pathological changes in cardiomyocytes were observed by HE staining; Changes in PVNCRH neuronal activity were recorded by fiber-optic photometry; Sympathetic nerve discharges were recorded for in vivo electrophysiology; NE and TH protein expression was assayed by Western blot. Results: Our data indicated that EA pretreatment can effectively alleviate MIRI. Meanwhile, we found that in the MIRI model, the number and activity of CRH neurons co labeled with c-Fos in the PVN area of the rat brain increased, and the frequency of sympathetic nerve discharge increased. EA pretreatment could reverse this change. In addition, the results of chemical genetics indicated that inhibiting PVNCRH neurons has a similar protective effect on MIRI as EA pretreatment, and the activation of PVNCRH neurons can counteract this protective effect. Conclusion: EA pretreatment can inhibit PVNCRH neurons and improve MIRI by inhibiting sympathetic nerve, which offers fresh perspectives on the application of acupuncture in the management of cardiovascular disease. [ABSTRACT FROM AUTHOR]

Orthodontic forces are strongly associated with pain, the primary complaint among patients wearing orthodontic braces. Compared to other side effects of orthodontic treatment, orthodontic pain is often overlooked, with limited clinical management. Orthodontic forces lead to inflammatory responses in the periodontium, which triggers bone remodeling and eventually induces tooth movement. Mechanical forces and subsequent inflammation in the periodontium activate and sensitize periodontal nociceptors and produce orthodontic pain. Nociceptive afferents expressing transient receptor potential vanilloid subtype 1 (TRPV1) play central roles in transducing nociceptive signals, leading to transcriptional changes in the trigeminal ganglia. Nociceptive molecules, such as TRPV1, transient receptor potential ankyrin subtype 1, acid-sensing ion channel 3, and the P2X3 receptor, are believed to mediate orthodontic pain. Neuropeptides such as calcitonin gene-related peptides and substance P can also regulate orthodontic pain. While periodontal nociceptors transmit nociceptive signals to the brain, they are also known to modulate alveolar bone remodeling in periodontitis. Therefore, periodontal nociceptors and nociceptive molecules may contribute to the modulation of orthodontic tooth movement, which currently remains undetermined. Future studies are needed to better understand the fundamental mechanisms underlying neuroskeletal interactions in orthodontics to improve orthodontic treatment by developing novel methods to reduce pain and accelerate orthodontic tooth movement--thereby achieving "big gains with no pain" in clinical orthodontics. [ABSTRACT FROM AUTHOR]

Objective: This study aimed to examine the effects of binaural beat music (BBM) on sleep quality, heart rate variability, and depression in older people with poor sleep quality in a long‐term care institution. Methods: A single‐blind randomized controlled trial design was employed, and 64 older participants with poor sleep quality were recruited from a long‐term care institution in Taiwan. Participants were randomized into the BBM group or control group and received 14 days of intervention. During the intervention period, participants in the experimental group listened to 20 min of Taiwanese Hokkien oldies embedded with BBM once in the morning and afternoon three times a week. Participants in the control group only listened to Taiwanese Hokkien oldies. Questionnaires and heart rate variability analysis were used to assess participants' sleep quality, heart rate variability, and depressive symptoms. Results: Significant improvements were observed in sleep quality, along with an increase in heart rate variability means of heart rate and normal sinus beats, and a decrease in low‐frequency normalized units and depression severity in the BBM group after the intervention. In the control group, effects on sleep quality were inconsistent, heart rate variability showed significant improvements in some autonomic nervous function regulation, and depression severity was significantly decreased. Furthermore, the BBM group showed a significant improvement in sleep quality and a significant reduction in sympathetic nervous activity compared with the control group. Conclusion: This study demonstrates that 14 days of BBM intervention, a non‐invasive intervention, could improve sleep quality and depression in older people with poor sleep quality in long‐term care institutions. Geriatr Gerontol Int 2024; 24: 297–304. [ABSTRACT FROM AUTHOR]

This research aimed to explore the impact of plank exercise training (PET) on respiratory function, body composition, abdominis performance, and autonomic nervous system (ANS). Sixty‐one young adults participated and were divided into a control group (CG, n = 31) and an exercise group (EG, n = 30), wherein PET was administered 3 days per week for 12 weeks. After the experiment, the body composition of the CG deteriorated, whereas that of the EG improved (p < 0.001). The EG exhibited a reduction of ∼34% in the mean maximum displacement and a rise of ∼20% in the mean contraction time of the abdominis. The sit‐up in the EG demonstrated a significant increase of ∼55%. In the EG, there was a substantial increase in peak expiratory force by ∼24% and forced expiratory volume in 1 s by ∼14%, accompanied by a reduction in resting respiratory rate by ∼ −9%. When compared to the CG, these alterations were significant between the two groups (p = 0.001). In the EG, there was a significant decrease in resting heart rate by ∼2%, accompanied by a decrease in sympathetic nervous activity by ∼ −5% and by an increase in parasympathetic nervous activity by ∼5%. When compared to the CG, these alterations were significant between the two groups (p = 0.001). The findings of this study revealed that implementing PET in young adults, while controlling for dietary intake and physical activity, resulted in noteworthy changes in respiratory capacity. These changes were coupled with improvements in body composition, abdominal functions, and the ANS. Highlights: The plank exercise training (PET) resulted in a decrease in body weight, fat mass, body mass index, and waist‐to‐hip ratio, along with an increase in muscle mass over a 12‐week period.The PET led to a decrease in the maximum displacement and an increase in the contraction time, along with an improvement in abdominal muscle endurance.The peak expiratory flow and forced expiratory volume in 1 s exhibited increases as a result of the PET, accompanied by a notable decrease in resting respiratory rate.The PET led to a reduction in resting heart rate, influenced by a decrease in sympathetic nervous activity and an increase in parasympathetic nervous activity. [ABSTRACT FROM AUTHOR]

(1) Background: Snoring is a cardinal symptom of obstructive sleep apnea (OSA) and has been suggested to potentially increase sympathetic activity. On the other hand, sleep itself usually leads to a decrease in sympathetic activity. Heart rate variability (HRV) analysis is a non-invasive technique used to assess autonomic nervous system function. However, there is limited research on the combined impact of sleep and snoring on sympathetic activity in individuals with OSA, particularly during the first hour of sleep (non-rapid eye movement sleep). The current study aims to investigate the net effect of sleep and snoring on sympathetic activity and explore factors that might contribute to increased sympathetic activity in individuals with OSA during the first hour of sleep. (2) Methods: The participants were referred from the outpatient department for OSA diagnosis and underwent whole-night polysomnography (PSG). Electrocardiogram (EKG) data from the PSG were downloaded for HRV analysis. HRV measurements were conducted in both the time and frequency domain, including the root mean square of successive differences between normal heartbeats (RMSSD) and the ratio of the absolute power of the low-frequency (LF) band (0.04–0.15 Hz) to the absolute power of the high-frequency (HF) band (0.15–0.4 Hz) (LF/HF ratio), respectively. (3) Results: A total of 45 participants (38 men and 7 women) were included in the analysis. The RMSSD gradually increased from 0–5 min to 50–60 min (p = 0.024), while the LF/HF ratio decreased (p < 0.001) during the first hour of sleep (non-rapid eye movement sleep). The LF/HF ratios of the "S" (snoring) episodes were compared with those of the pre-S episodes. An elevated LF/HF ratio during the S episode was associated with the first snoring episode occurring more than 20 min after lying down to sleep (Odds ratio, OR = 10.9, p = 0.004) and with patients diagnosed with severe OSA (OR = 5.01, p = 0.045), as determined by logistic regression. (4) Conclusions: The study observed an increase in the value of RMSSD and a decrease in the value of the LF/HF ratio during the first hour of sleep for patients with OSA. Higher LF/HF ratios were associated with the first occurrence of snoring while lying down for more than 20 min and with patients with severe OSA. [ABSTRACT FROM AUTHOR]

Hemorrhage is a leading cause of preventable battlefield and civilian trauma deaths. Ketamine, fentanyl, and morphine are recommended analgesics for use in the prehospital (i.e., field) setting to reduce pain. However, it is unknown whether any of these analgesics reduce hemorrhagic tolerance in humans. We tested the hypothesis that fentanyl (75 µg) and morphine (5 mg), but not ketamine (20 mg), would reduce tolerance to simulated hemorrhage in conscious humans. Each of the three analgesics was evaluated independently among different cohorts of healthy adults in a randomized, crossover (within drug/placebo comparison), placebo-controlled fashion using doses derived from the Tactical Combat Casualty Care Guidelines for Medical Personnel. One minute after an intravenous infusion of the analgesic or placebo (saline), we employed a pre-syncopal limited progressive lower-body negative pressure (LBNP) protocol to determine hemorrhagic tolerance. Hemorrhagic tolerance was quantified as a cumulative stress index (CSI), which is the sum of products of the LBNP and the duration (e.g., [40 mmHg x 3 min] + [50 mmHg x 3 min] ...). Compared with ketamine (p = 0.002 post hoc result) and fentanyl (p = 0.02 post hoc result), morphine reduced the CSI (ketamine (n = 30): 99 [73–139], fentanyl (n = 28): 95 [68–130], morphine (n = 30): 62 [35–85]; values expressed as a % of the respective placebo trial's CSI; median [IQR]; Kruskal-Wallis test p = 0.002). Morphine-induced reductions in tolerance to central hypovolemia were not well explained by a prediction model including biological sex, body mass, and age (R2=0.05, p = 0.74). These experimental data demonstrate that morphine reduces tolerance to simulated hemorrhage while fentanyl and ketamine do not affect tolerance. Thus, these laboratory-based data, captured via simulated hemorrhage, suggest that morphine should not be used for a hemorrhaging individual in the prehospital setting. [ABSTRACT FROM AUTHOR]

Background: This study tested the hypothesis that training reduces resting sympathetic activity and improves baroreflex control in both hypertensive and normotensive men but reduces blood pressure only in hypertensive men. Methods: Middle‐aged/older un‐medicated stage‐1 hypertensive males (mean age 55 ± 3 years; n = 13) and normotensive controls (mean age 60 ± 5 years; n = 12) participated in 8 weeks of supervised high‐intensity interval spinning training. Before and after training, muscle sympathetic nerve activity (MSNA) and blood pressure were measured at rest and during a sympatho‐excitatory cold pressor test (CPT). Based on the measurements, baroreceptor sensitivity and baroreceptor threshold were calculated. Results: Resting MSNA and baroreceptor sensitivity were similar for the hypertensive and the normotensive groups. Training lowered MSNA (p < 0.05), expressed as burst frequency (burst/min), overall, and to a similar extent, in both groups (17% and 27%, respectively, in hypertensive and normotensive group), whereas blood pressure was only significantly (p < 0.05) lowered (by 4 mmHg in both systolic and diastolic pressure) in the hypertensive group. Training did not (p > 0.05) alter the MSNA or blood pressure response to CPT or increase baroreceptor sensitivity but reduced (p < 0.05) the baroreceptor threshold with a main effect for both groups. Training adherence and intensity were similar in both groups yet absolute maximal oxygen uptake increased by 15% in the normotensive group only. Conclusion: The dissociation between the training induced changes in resting MSNA, lack of change in baroreflex sensitivity and the change in blood pressure, suggests that MSNA is not a main cause of the blood pressure reduction with exercise training in un‐medicated middle‐aged/older men. [ABSTRACT FROM AUTHOR]

The link between childhood harsh parenting and later aggression is well established. However, harsh parenting may occur within the context of nonviolent discipline. Moreover, sympathetic nervous system activity may moderate the effects of harsh parenting on aggression. This study examined whether sympathetic nervous system activity, measured by skin conductance level (SCL), and childhood nonviolent discipline moderate the link between childhood harsh parenting and later aggression among emerging adults. Participants (N = 264, mean age = 19.37, 54% females) reported retrospectively on experiences of childhood harsh parenting and nonviolent discipline as well as current anger, hostility, verbal, and physical aggression. We also measured resting SCL. Regression analyses revealed a significant three-way interaction between childhood harsh parenting, nonviolent discipline, and resting SCL accounting for anger and a significant two-way interaction between childhood harsh parenting and resting SCL accounting for hostility. Results suggested that (1) at high levels of resting SCL and low levels of childhood nonviolent discipline and (2) at low levels of resting SCL and high levels of childhood nonviolent discipline, the link between childhood harsh parenting and anger was stronger. Moreover, the association between childhood harsh parenting and hostility was stronger among participants who exhibited high resting SCL. The findings are consistent with the biological sensitivity to context theory. Our study highlighted the importance to examine the influence of both environmental and biological variables underlying emerging adults' aggression. [ABSTRACT FROM AUTHOR]

Background: Various diagnostic tools are used to assess cutaneous psoriasis, but most of it were subjective. Sympathetic skin response (SSR), skin PH and temperature objectively measure the skin barrier functions that could aid clinicians to evaluate accurately and predict skin disease incidence even before the onset of clinical symptoms. Aim and Objectives: The study's objective was to assess the utility of cutaneous parameters (skin temperature and pH) and SSRs influencing psoriatic patients' diagnosis management and treatment compared to controls. Materials and Methods: A total of 40 healthy participants and 40 psoriasis patients aged 18 to 65 years were recruited for this study. SSR, skin temperature and pH were assessed. The psoriasis disability index (PDI) was recorded from all the patients. Data analysis was carried out using SPSS version 20.0. Results: The results shows significantly increased skin temperature, prolonged SSR latency (bilaterally) and decreased SSR amplitude (bilaterally) among patients affected with psoriasis compared to control subjects. There is a positive correlation between SSR latency with PDI and a negative correlation between SSR amplitude and PDI in psoriasis patients. Conclusion: SSR reveals sympathetic sudomotor dysfunction and increased skin temperature in psoriasis. Furthermore, there is a link between increased SSR latency and PDI, which shows that local nervous system impairment significantly contributes to the inflammatory process in psoriasis. Thus, SSR can be used as a complementary tool for the early identification and assessment of epidermal barrier integrity in psoriasis patients, along with the clinician's standard protocols. [ABSTRACT FROM AUTHOR]

We investigated whether parasympathetic and sympathetic nervous system (SNS) responses to social‐evaluative threat at age 14 were related to the number of substances used between ages 14 and 16 among Mexican‐origin adolescents (N = 243; 70.4% had never used substances by 14). Participants completed the Trier Social Stress Test, while cardiac measures of parasympathetic and SNS activity were measured continuously using respiratory sinus arrhythmia (RSA) and pre‐ejection period (PEP), respectively. Participants reported whether they had ever used alcohol, marijuana, and cigarettes, and had ever vaped nicotine in their lifetime at ages 14 and 16. Multilevel models were used to test associations between RSA and PEP responses at age 14 and substance use at 16. Among youth who had not used substances by 14, dampened RSA and PEP responses, and profiles of greater coinhibition and lower reciprocal SNS activation between RSA and PEP, at age 14 were associated with using substances by 16. Among youth who used by 14, exaggerated PEP responses were associated with using more substances by age 16. Taken together, dampened autonomic responses to social‐evaluative threat predicted initiation of substance use over two years, and difficulties with coordination of physiological responses may confer risk for substance use in adolescence. [ABSTRACT FROM AUTHOR]

Suicide is among the most devastating problems facing clinicians, who currently have limited tools to predict and prevent suicidal behavior. Here we report on real-time, continuous smartphone and sensor data collected before, during, and after a suicide attempt made by a patient during a psychiatric inpatient hospitalization. We observed elevated and persistent sympathetic nervous system arousal and suicidal thinking leading up to the suicide attempt. This case provides the highest resolution data to date on the psychological, psychophysiological, and behavioral markers of imminent suicidal behavior and highlights new directions for prediction and prevention efforts. [ABSTRACT FROM AUTHOR]

Objective: Stress system dysregulation is considered to have an important role in the aetiology of paediatric functional neurological (conversion) disorder. This study examined salivary cortisol and α-amylase awakening responses in children with functional neurological disorder to determine activation patterns of the hypothalamic–pituitary–adrenal axis and sympathetic system. A healthy cortisol awakening response involves a robust increase in cortisol within 30 minutes of awakening. Alpha-amylase awakening response is variable in children. Methods: Cortisol and α-amylase were measured in saliva from 32 patients with functional neurological disorder (26 girls and 6 boys, aged 11.3−16.1 years) and 31 healthy controls (23 girls and 8 boys, aged 8.6–17.7 years). Saliva samples were collected using a Salivette sampling device at two time points – upon awakening and 30 minutes after awakening. Results: Patients with functional neurological disorder showed a decrease in cortisol awakening response (–4 nmol.min/L) and controls showed an increase (107 nmol.min/L), t (55) = –.4.6, p < 0.001. Within the functional neurological disorder group, 57% showed an attenuated cortisol awakening response and 43% showed an obliterated/reversed cortisol awakening response: Cortisol awakening response was negatively correlated with adverse childhood experiences, r (58) = –0.6, p = 0.002, and subjective distress (total Depression Anxiety and Stress Scales score), r (58) = –0.4, p = 0.050. In controls, cortisol awakening response showed no correlation with adverse childhood experiences and a positive correlation with subjective distress, r (56) = 0.4, p = 0.023. Total cortisol remained similar between the functional neurological disorder and control group. No significant differences were observed between the functional neurological disorder and control group in any of the α-amylase analyses. Discussion: The results suggest dysregulation of the hypothalamic–pituitary–adrenal axis in children with functional neurological disorder. Hypothalamic–pituitary–adrenal dysregulation in children with functional neurological disorder may contribute to comorbid symptoms of fatigue, sleep disturbance and subjective loss of well-being because circadian rhythms and energy metabolism are disrupted. Hypothalamic–pituitary–adrenal dysregulation – and changes in glucocorticoid (cortisol) signalling at the molecular level – may also contribute to increased vulnerability for functional neurological disorder symptoms because of epigenetically mediated changes to neural networks implicated in functional neurological disorder. [ABSTRACT FROM AUTHOR]

Affective processing, including induction and regulation of emotion, activates neural networks, induces physiological responses, and generates subjective experience. Dysregulation of these processes can lead to maladaptive behavior and even psychiatric morbidity. Multimodal studies of emotion thus not only help elucidate the nature of emotion, but also contribute to important clinical insights. In the present study, we compared the induction (EI) and effortful regulation (ER) with reappraisal of fear and disgust in healthy subjects using functional near infrared spectroscopy (fNIRS) in conjunction with electrodermal activity (EDA). During EI, there was significant activation in medial prefrontal cortex (PFC) for fear and more widespread activation for disgust, with right lateral PFC significantly more active during disgust compared to fear. ER was equally effective for fear and disgust reducing subjective emotion rating by roughly 45%. Compared to baseline, there was no increased PFC activity for fear during ER, while for disgust lateral PFC was significantly more active. Significant differences between the two negative emotions were also observed in sympathetic nerve activity as reflected in EDA during EI, but not during ER. Lastly, compared to men, women had higher emotion rating for both fear and disgust without corresponding differences in EDA. In conclusion, in the present study we show that emotion induction was associated with differential activation in both PFC and sympathetic nerve activity for fear and disgust. These differences were however less prominent during emotion regulation. We discuss the potential interpretation of our results and their implications regarding our understanding of negative emotion processing. [ABSTRACT FROM AUTHOR]

We investigated pupillary responses to the world's shortest fixed verses, Japanese haiku as aesthetic poetry (AP) and senryu as comic poetry (CP), in comparison with non-poetry control stimuli (NP) comprised of slogans that had the same rhythm patterns. Native Japanese speakers without literary training listened to these stimuli while we recorded their pupil diameters. We found that participants' pupils were significantly dilated for CP compared to NP in an early time window. While AP also evoked larger dilations than NP, the latency for AP-related pupil dilation was relatively long. Thus, lay people experience quick and intense arousal in response to funny and humorous words, while aesthetic properties of words may also elicit intense but slower changes in listeners' arousal levels, presumably because they evoke more implicit and subtle emotional effects. This study is the first to provide evidence that poetic language elicits human pupillary dilation. A better understanding of the cognitive and neural substrates for the sensitive awareness of pleasures expressed via poetic language will provide insights for improving mental and physical health. Hence, pupillometry can act as a useful convenient measurement to delineate the sympathetic activation of emotional contexts via language. [ABSTRACT FROM AUTHOR]

A low-frequency to a high-frequency component ratio (LF/HF) in heart rate variability (HRV) may not accurately reflect sympathetic nervous activity during exercise. Thus, a valid HRV-based index of sympathetic nervous activity is needed. Therefore, the heart rate to LF ratio (Heart rate/LF) was evaluated as sympathetic nervous activity index which is reflected by catecholamine levels during incremental exercise. In this study, 15 healthy adults performed an incremental exercise test using a cycle ergometer. HRV was derived from electrocardiography and HRV components related to the autonomic nervous system were obtained using frequency analysis. Heart rate/LF was calculated using the heart rate and LF component produced by HRV analysis. Catecholamine, blood lactate levels and respiratory gas were also measured throughout the exercise test. While LF/HF did not increase with increasing exercise intensity, Heart rate/LF non-linearly increased during the incremental exercise test, as did noradrenaline and blood lactate. Interestingly, Heart rate/LF values were positively correlated with noradrenaline (ρ = 0.788, p < 0.05) and blood lactate (ρ = 0.802, p < 0.05) levels and carbon dioxide production (ρ = 0.903, p < 0.05) from at rest through the exercise stages. Heart rate/LF reflects sympathetic nervous activity and metabolic responses during incremental cycling exercise and has potential as an HRV index of sympathetic nervous activity during exercise. Trial registration: UMIN Japan identifier: UMIN000039639. [ABSTRACT FROM AUTHOR]

Introduction: Autonomic nervous system functioning is theorised to underpin individual differences in sensory processing, with a small amount of supporting evidence. Despite recognition of the need to measure the balance between sympathetic and parasympathetic activity, most studies have measured only one of these systems. This study investigated whether sensory processing patterns are related to autonomic balance for young adults at rest and in response to a sensory-based stressor. Method: In this cross-sectional laboratory study, 100 young adults completed the adolescent/adult sensory profile. Heart rate variability and pre-ejection period were recorded before, during and after a coldpressor task. Results: Relationships between sensory processing patterns and autonomic balance varied by gender. In males, low sensory thresholds were generally related to a state of reciprocal sympathetic activation. In females, low thresholds were associated with greater autonomic reactivity in response to the coldpressor. Conclusion: This study showed, for the first time in young adults, that sensory processing patterns may be linked to patterns of autonomic balance. Therapists should be aware that young men with low sensory thresholds may be more likely than others to exhibit a resting state of sympathetic hyperarousal and further research should investigate whether this impacts their daily functioning and wellbeing. [ABSTRACT FROM AUTHOR]

The sympathetic and renin-angiotensin systems (RAS) are two critical regulatory systems in the kidney which affect renal hemodynamics and function. These two systems interact with each other so that angiotensin II (Ang II) has the presynaptic effect on the norepinephrine secretion. Another aspect of this interaction is that the sympathetic nervous system affects the function and expression of local RAS receptors, mainly Ang II receptors. Therefore, in many pathological conditions associated with an increased renal sympathetic tone, these receptors' expression changes and renal denervation can normalize these changes and improve the diseases. It seems that the renal sympathectomy can alter Ang II receptors expression and the distribution of RAS receptors in the kidneys, which influence renal functions. [ABSTRACT FROM AUTHOR]

We explore complex dynamic patterns of autonomic physiological linkage (i.e., statistical interdependence of partner's physiology; PL), within the sympathetic and parasympathetic nervous systems (SNS and PNS), as potential correlates of emotional and regulatory dynamics in close relationships. We include electrodermal activity (EDA) as an indicator of SNS activation and respiratory sinus arrhythmia (RSA) as an indicator of regulatory and/or homeostatic processes within the PNS. Measures of EDA and RSA were collected in 10-second increments from 53 heterosexual couples during a mixed-emotion conversation in the laboratory. We used the R statistical package, rties (Butler & Barnard, 2019), to model the dynamics of EDA and RSA with a coupled oscillator model and then categorized couples into qualitatively distinct profiles based on the set of parameters that emerged. We identified two patterns for EDA and three patterns for RSA. We then investigated associations between the PL patterns and self-report measures of relationship and conversation quality and emotional valence using Bayesian multilevel and logistic regression models. Overall, we found robust results indicating that PL profiles were credibly predicted by valence and relationship quality reported prior to the conversations. In contrast, we found very little evidence suggesting that PL patterns predict self-reported conversation quality or valence following the conversation. Together, these results suggest that PL across autonomic subsystems may reflect different processes and therefore have different implications when considering interpersonal dynamics. [ABSTRACT FROM AUTHOR]

Acute mental fatigue, characterized by a transient decline in cognitive efficiency during or following prolonged cognitive tasks, can be managed through adaptive effort deployment. In response to mental fatigue, individuals can employ two main behavioral patterns: engaging a compensatory effort to limit performance decrements, or disengaging effort, leading to performance deterioration. This study investigated the behavioral pattern used by participants in mental fatigue conditions. Fifty participants underwent a sequential-task protocol with counterbalanced sessions who took place in two separate sessions: a 30-min incongruent Stroop task (fatiguing session) or a 30-min documentary viewing task (control session), followed by a time-to-exhaustion (TTE) handgrip task at 13 % of maximal voluntary contraction. Psychophysiological measures included the preejection period, heart rate variability, blood pressure, and respiration. Behavioral results showed deteriorated TTE handgrip performance after the Stroop task compared to after the documentary viewing task. During the Stroop task participants were more conservative and prioritized accuracy over speed. Self-reported fatigue was greater after the Stroop task. Psychophysiological data revealed a gradual decrease in sympathetic activity over time in both tasks, with the Stroop task showing a more pronounced decrease. Taken together, these findings suggest a disengagement of effort for a large proportion of participants (49 %) that could be partly attributed to a habituation to the demands of the Stroop task. This study illustrates the interplay of behavioral patterns of effort investment in the context of mental fatigue and underscores the role of disengagement as a dominant response to this phenomenon among healthy participants. • A conservative strategy favoring accuracy was adopted during a cognitive task that induced mental fatigue. • Mental fatigue during a cognitive task leads to a decrease in sympathetic activity with increasing time-on task. • Mental fatigue induced by a 30-min effortful cognitive task impairs the performance in a subsequent endurance physical task. [ABSTRACT FROM AUTHOR]

An unannounced balance loss during walking, i.e., balance perturbation, is a stressful event, which changes the activity of the sympathetic nervous system (SNS). We examined SNS response to unannounced balance perturbation during walking, simulating real-life condition of balance loss. We asked: do laboratory-induced unannounced balance losses during walking cause a sympathetic response, and-if so-does it habituate after a series of perturbations? Thirty-four young adults underwent a series of six successive unannounced balance perturbations while walking on a treadmill. Sympathetic activity was monitored continuously using electrodermal activity and compared before and immediately after each unannounced perturbation. All perturbations elicited a significant increase of electrodermal activity ( P < 0.001), indicating a phasic increase in the sympathetic drive. The relative phasic increase of electrodermal activity caused by the first perturbation was significantly higher than the last perturbation ( P < 0.05). Three different types of electrodermal activity behavior were observed: steady-level tonic SNS activity, increased SNS activity, and decreased SNS activity. Balance loss during walking triggers phasic SNS response, this response habituates after a series of unannounced balance perturbations. In addition, three distinct patterns of tonic sympathetic activity may imply variations in the ability of the SNS response to habituate across individuals. NEW & NOTEWORTHY Up to date, the literature typically provides information about sympathetic nervous system activity and relatively static balance. We believe that exposing participants to a balance loss during walking, i.e., unexpected perturbation, provides a more ecologically valid situation to measure sympathetic nervous system response; this provides new and vital knowledge that can have a significant impact and understanding of how the SNS responds to a loss of balance in a real-life situation.

Chemerin is an adipokine that contributes to metabolism regulation. Nucleus tractus solitarius (NTS) is the first relay station in the brain for accepting various visceral afferent activities for regulating cardiovascular activity. However, the roles of chemerin in the NTS in regulating sympathetic activity and blood pressure are almost unknown. This study aimed to determine the role and potential mechanism of chemerin in the NTS in modulating sympathetic outflow and blood pressure. Bilateral NTS microinjections were performed in anaesthetized adult male Sprague-Dawley rats. Renal sympathetic nerve activity (RSNA), mean arterial pressure (MAP) and heart rate (HR) were continuously recorded. Chemerin and its receptor chemokine-like receptor 1 (CMKLR1) were highly expressed in caudal NTS (cNTS). Microinjection of chemerin-9 to the cNTS increased RSNA, MAP and HR, which were prevented by CMKLR1 antagonist α-NETA, superoxide scavenger tempol or N-acetyl cysteine, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitors diphenyleneiodonium or apocynin. Chemerin-9 increased superoxide production and NADPH oxidase activity in the cNTS. The increased superoxide production induced by chemerin-9 was inhibited by α-NETA. The effects of cNTS microinjection of chemerin-9 on the RSNA, MAP and HR were attenuated by the pretreatment with paraventricular nucleus (PVN) microinjection of NMDA receptor antagonist MK-801 rather than AMPA/kainate receptor antagonist CNQX. These results indicate that chemerin-9 in the NTS increases sympathetic outflow, blood pressure and HR via CMKLR1-mediated NADPH oxidase activation and subsequent superoxide production in anaesthetized normotensive rats. Glutamatergic inputs in the PVN are needed for the chemerin-9-induced responses., (© 2024 Federation of European Neuroscience Societies and John Wiley & Sons Ltd.)

Aim: To show that electroacupuncture stimulation (ES) remodels sympathetic innervation in brown adipose tissue (BAT) via the bone morphogenic protein 8B (BMP8B)-neuregulin 4 (NRG4)-ErbB4 axis, with somatotopic dependence., Materials and Methods: We established a high-fat diet (HFD) model with C57BL/6J mice to measure the thermogenesis and metabolism of BAT. In addition, the sympathetic nerve activity (SNA) was measured with the electrophysiological technique, and the immunostaining of c-Fos was used to detect the central nervous system sources of sympathetic outflows. Finally, the key role of the BMP8B-NRG4-ErbB4 axis was verified by peripheral specific antagonism of ErbB4., Results: ES at the forelimb and abdomen regions significantly up-regulate SNA, whereas ES at the hindlimb region has a limited regulatory effect on SNA but still partially restores HFD-induced BAT dysfunction. Mechanistically, ES at the forelimb and abdomen regions driving catecholaminergic signals in brown adipocytes depends on neural activities projected from the ventromedial nucleus of the hypothalamus (VMH) to the spinal cord intermediolateral column (IML). Notably, the peripheral suppression of ErbB4 in BAT inhibits the thermogenesis and metabolic function of BAT, as well as significantly hindering the SNA activation and metabolic benefits induced by ES., Conclusion: These results suggest that ES appears to be an effective approach for remodeling sympathetic innervation in BAT, which is closely related to neuronal activity in the VMH and the NRG4-ErbB4 signaling pathway., (© 2024 John Wiley & Sons Ltd.)

Depressed individuals exhibit altered sensitivity to both positive and negative social contact, and may not reap the same psychological and emotional benefits to socializing as non-depressed individuals. Although depressive symptoms and loneliness predict social withdrawal and decreased pleasure, little is currently understood about immediate affective arousal dynamics during real-time socializing. Using a novel ambulatory protocol that tracked both objective features of affective arousal (electrodermal activity) and subjective valence (self-reported) during college students' social interactions, we evaluated the moderating role of depression and loneliness symptoms on the associations between socializing with others (specifically, with a romantic partner, a close friend, or a group of friends) and the arousal and valence dimensions of affect. Among a racially and ethnically diverse sample of 118 college students (64% African American/Black/Continental African, 20% Latinx, 8% Asian, and 8% White) recruited from a large, predominantly White Midwestern university, those lower in depression and loneliness symptomatology evinced decreased average arousal (Β = -0.10, SE = 0.04, p < .01) when in relaxed and intimate socializing contexts (e.g., with a romantic partner and a close friend), consistent with the idea that these contexts facilitate important opportunities for psychological rest and recovery. Those lower in depression and loneliness symptoms also showed higher average arousal when socializing in the energizing context of being with a group of friends. Overall, the results suggest psychopathology is reflected in patterns of sympathetic arousal when socializing, with more depressed and lonely individuals generally feeling worse while receiving fewer psychophysiological rewards in multiple socializing contexts., (© 2024 Society for Psychophysiological Research.)

Type 2 diabetes (T2D) is often accompanied by hypertension, exaggerated blood pressure (BP) responses to sympatho-excitatory stressors, and raised cardiovascular disease risk. Appropriate respiratory-sympathetic coupling and sympathetic transduction to BP are important for short- and longer-term BP control. We tested the hypotheses that respiratory modulation of muscle sympathetic nerve activity (MSNA) and its transduction to BP would be impaired in T2D and associated with higher BP and respiratory-coupled BP variability. Resting MSNA, respiration and beat-to-beat BP were recorded in 20 T2D (49.1 ± 7.4 years; mean ± SD) and 13 healthy control (46.3 ± 9.4 years) participants. MSNA and the transduction of sympathetic bursts (signal-averaging) to mean arterial pressure (MAP) were compared at low and high lung volume phases. The peak MAP response following a sympathetic burst was lower during the high lung volume than low lung volume phase in controls (P = 0.005), whereas it was unchanged with phase in T2D participants (P = 0.522). Respiratory modulation of MSNA was impaired in T2D participants, who had an attenuated reduction in burst incidence from low to the high lung volume phase, versus controls (27.8 ± 38.4% vs. 49.4 ± 24.6%, respectively; P = 0.043). The T2D participants were grouped into unimpaired respiratory modulators (burst incidence modulation median or above) or impaired respiratory modulators (below median). Impaired modulators had higher systolic BP (133 ± 14 vs. 121 ± 11 mmHg, P = 0.046), greater Traube-Hering wave amplitudes (6.3 ± 2.4 vs. 4.6 ± 1.1 mmHg; P = 0.028) and higher BP variability (MAP average real variability, 2.0 ± 0.7 vs. 1.4 ± 0.3, P = 0.033). Respiratory modulation of MSNA and sympathetic transduction to BP are altered in T2D patients and may contribute to their increased hypertension and cardiovascular risk. KEY POINTS: Respiratory-sympathetic coupling and sympathetic transduction to blood pressure (BP) contribute to short- and longer-term BP control. Our understanding of these processes in health and type 2 diabetes (T2D), a condition with high prevalence of hypertension and cardiovascular risk, is incomplete. We found that respiration and sympathetic transduction to BP are coupled in healthy individuals. The mean arterial pressure response to a sympathetic burst was reduced during the high lung volume compared to the low lung volume phase. This coupling was absent in T2D. Respiratory modulation of muscle sympathetic nerve activity (MSNA) is impaired in T2D, with a blunted reduction of MSNA observed during the high lung volume phase. T2D patients with impaired respiratory MSNA modulation had augmented systolic BP, respiratory-related BP excursions (Traube-Hering waves) and BP variability. Abnormal respiratory modulation of MSNA and sympathetic transduction to BP in T2D may contribute to altered blood pressure control and cardiovascular risk in this population., (© 2024 The Author(s). The Journal of Physiology published by John Wiley & Sons Ltd on behalf of The Physiological Society.)

The present study investigated the impact of central α 2 -adrenergic mechanisms on sympathetic action potential (AP) discharge, recruitment and latency strategies. We used the microneurographic technique to record muscle sympathetic nerve activity and a continuous wavelet transform to investigate postganglionic sympathetic AP firing during a baseline condition and an infusion of a α 2 -adrenergic receptor agonist, dexmedetomidine (10 min loading infusion of 0.225 µg kg -1 ; maintenance infusion of 0.1-0.5 µg kg h -1 ) in eight healthy individuals (28 ± 7 years, five females). Dexmedetomidine reduced mean pressure (92 ± 7 to 80 ± 8 mmHg, P < 0.001) but did not alter heart rate (61 ± 13 to 60 ± 14 bpm; P = 0.748). Dexmedetomidine reduced sympathetic AP discharge (126 ± 73 to 27 ± 24 AP 100 beats -1 , P = 0.003) most strongly for medium-sized APs (normalized cluster 2: 21 ± 10 to 5 ± 5 AP 100 beats -1 ; P < 0.001). Dexmedetomidine progressively de-recruited sympathetic APs beginning with the largest AP clusters (12 ± 3 to 7 ± 2 clusters, P = 0.002). Despite de-recruiting large AP clusters with shorter latencies, dexmedetomidine reduced AP latency across remaining clusters (1.18 ± 0.12 to 1.13 ± 0.13 s, P = 0.002). A subset of six participants performed a Valsalva manoeuvre (20 s, 40 mmHg) during baseline and the dexmedetomidine infusion. Compared to baseline, AP discharge (Δ 361 ± 292 to Δ 113 ± 155 AP 100 beats -1 , P = 0.011) and AP cluster recruitment elicited by the Valsalva manoeuvre were lower during dexmedetomidine (Δ 2 ± 1 to Δ 0 ± 2 AP clusters, P = 0.041). The reduction in sympathetic AP latency elicited by the Valsalva manoeuvre was not affected by dexmedetomidine (Δ -0.09 ± 0.07 to Δ -0.07 ± 0.14 s, P = 0.606). Dexmedetomidine reduced baroreflex gain, most strongly for medium-sized APs (normalized cluster 2: -6.0 ± 5 to -1.6 ± 2 % mmHg -1 ; P = 0.008). These data suggest that α 2 -adrenergic mechanisms within the central nervous system modulate sympathetic postganglionic neuronal discharge, recruitment and latency strategies in humans. KEY POINTS: Sympathetic postganglionic neuronal subpopulations innervating the human circulation exhibit complex patterns of discharge, recruitment and latency. However, the central neural mechanisms governing sympathetic postganglionic discharge remain unclear. This microneurographic study investigated the impact of a dexmedetomidine infusion (α 2 -adrenergic receptor agonist) on muscle sympathetic postganglionic action potential (AP) discharge, recruitment and latency patterns. Dexmedetomidine infusion inhibited the recruitment of large and fast conducting sympathetic APs and attenuated the discharge of medium sized sympathetic APs that fired during resting conditions and the Valsalva manoeuvre. Dexmedetomidine infusion elicited shorter sympathetic AP latencies during resting conditions but did not affect the reductions in latency that occurred during the Valsalva manoeuvre. These data suggest that α 2 -adrenergic mechanisms within the central nervous system modulate sympathetic postganglionic neuronal discharge, recruitment and latency strategies in humans., (© 2024 The Author(s). The Journal of Physiology published by John Wiley & Sons Ltd on behalf of The Physiological Society.)

The sympathetic nervous system is critical for regulating blood pressure (BP) via the arterial baroreflex and sympathetic transduction in the peripheral vasculature. These mechanisms interact, and both may be altered with aging and impacted by menopause. Although age-related decreases in sympathetic transduction have been demonstrated in women, it remains unclear whether sympathetic baroreflex sensitivity (BRS) is impaired in postmenopausal women (POST). We tested the hypothesis that sympathetic BRS would be enhanced in POST compared with premenopausal women (PRE). We examined beat-by-beat BP and muscle sympathetic nerve activity (MSNA) in 19 PRE (22 ± 2 yr, 22 ± 3 kg/m 2 ) and 12 POST (57 ± 5 yr, 24 ± 2 kg/m 2 ) during 10 min of rest. Spontaneous sympathetic BRS was quantified as the slope of a linear regression between MSNA burst incidence and diastolic BP. Sympathetic transduction to mean arterial pressure (MAP) for the 10 cardiac cycles following spontaneous MSNA bursts was assessed via signal averaging method. Resting MAP was similar (PRE: 82 ± 8 vs. POST: 85 ± 8 mmHg, P = 0.43), whereas resting MSNA was elevated in POST (PRE: 10 ± 6 vs. POST: 45 ± 16 bursts/100 heart beats, P < 0.0001). Spontaneous sympathetic BRS was enhanced in POST (PRE: -2.0 ± 1.2 vs. POST: -5.2 ± 1.9 bursts/beat/mmHg, P < 0.0005). Sympathetic transduction to MAP was attenuated in POST (time: P < 0.001, group: P < 0.001, interaction: P < 0.01). These data suggest that sympathetic BRS may be enhanced in POST. Consistent with recent hypotheses, enhanced sensitivity of the arterial baroreflex's neural arc may signify a compensatory response to reduced efficiency of the peripheral arterial baroreflex arc (i.e., sympathetic transduction) to preserve BP buffering capacity. NEW & NOTEWORTHY Studies examining sympathetic baroreflex function with aging remain equivocal, with some studies showing an increase, decrease, or no change in sympathetic baroreflex sensitivity (BRS) in older adults compared with younger adults. With aging, women experience unique physiological changes due to menopause that influence autonomic function. For the first time, we show that postmenopausal women exhibit a greater sympathetic BRS compared with young premenopausal women.

The purpose of this systematic review and meta-analysis was to examine the effects of exercise training on muscle sympathetic nerve activity (MSNA) in humans. Studies included exercise interventions [randomized controlled trials (RCTs), nonrandomized controlled trials (non-RCTs), or pre-to-post intervention] that reported on adults (≥18 yr) where MSNA was directly assessed using microneurography, and relevant outcomes were assessed [MSNA (total activity, burst frequency, burst incidence, amplitude), heart rate, blood pressure (systolic blood pressure, diastolic blood pressure, or mean blood pressure), and aerobic capacity (maximal or peak oxygen consumption)]. Forty intervention studies ( n = 1,253 individuals) were included. RCTs of exercise compared with no exercise illustrated that those randomized to the exercise intervention had a significant reduction in MSNA burst frequency and incidence compared with controls. This reduction in burst frequency was not different between individuals with cardiovascular disease compared with those without. However, the reduction in burst incidence was greater in those with cardiovascular disease [9 RCTs studies, n = 234, mean difference (MD) -21.08 bursts/100 hbs; 95% confidence interval (CI) -16.51, -25.66; I 2 = 63%] compared with those without (6 RCTs, n = 192, MD -10.92 bursts/100 hbs; 95% CI -4.12, -17.73; I 2 = 76%). Meta-regression analyses demonstrated a dose-response relationship where individuals with higher burst frequency and incidence preintervention had a greater reduction in values post-intervention. These findings suggest that exercise training reduces muscle sympathetic nerve activity, which may be valuable for improving cardiovascular health. NEW & NOTEWORTHY This systematic review and meta-analysis suggests exercise training reduces muscle sympathetic nerve activity (MSNA), which may be valuable for improving cardiovascular health. The reduction in burst incidence was greater among individuals with cardiovascular disease when compared with those without; exercise training may be particularly beneficial for individuals with cardiovascular disease. Meta-regression analyses demonstrated a dose-response relationship, where individuals with higher sympathetic activity preintervention had greater reductions in sympathetic activity post-intervention.

Body posture and biological sex exhibit independent effects on the sympathetic neural responses to dynamic exercise. However, the neural mechanisms (e.g., baroreflex) by which posture impacts sympathetic outflow during rhythmic muscular contractions, and whether biological sex affects posture-mediated changes in efferent sympathetic nerve traffic during exercise, remain unknown. Thus, we tested the hypotheses that increases in muscle sympathetic nerve activity (MSNA) would be greater during upright compared with supine rhythmic handgrip (RHG) exercise, and that females would demonstrate smaller increases in MSNA during upright RHG exercise than males. Twenty young (30 [6] yr; means [SD]) individuals (9 males, 11 females) underwent 6 min of supine and upright (head-up tilt 45°) RHG exercise at 40% maximal voluntary contraction with continuous measurements of MSNA (microneurography), blood pressure (photoplethysmography), and heart rate (electrocardiogram). In the pooled group, absolute MSNA burst frequency ( P < 0.001), amplitude ( P = 0.009), and total MSNA ( P < 0.001) were higher during upright compared with supine RHG exercise. However, body posture did not impact the peak change in MSNA during RHG exercise (range: P = 0.063-0.495). Spontaneous sympathetic baroreflex gain decreased from rest to RHG exercise ( P = 0.006) and was not impacted by posture ( P = 0.347). During upright RHG exercise, males demonstrated larger increases in MSNA burst amplitude ( P = 0.002) and total MSNA ( P = 0.001) compared with females, which coincided with greater reductions in sympathetic baroreflex gain among males ( P = 0.004). Collectively, these data indicate that acute attenuation of baroreflex-mediated sympathoinhibition permits increases in MSNA during RHG exercise and that males exhibit a greater reserve for efferent sympathetic neural recruitment during orthostasis than females. NEW & NOTEWORTHY The impact of posture and sex on cardiovascular control during rhythmic handgrip (RHG) exercise is unknown. We show that increases in muscle sympathetic nerve activity (MSNA) during RHG are partly mediated by a reduction in sympathetic baroreflex gain. In addition, males demonstrate larger increases in total MSNA during upright RHG than females. These data indicate that the baroreflex partly mediates increases in MSNA during RHG and that males have a greater sympathetic vasoconstrictor reserve than females.

Purpose: The nadir pressure responses to cardiac cycles absent of muscle sympathetic nerve activity (MSNA) bursts (or non-bursts) are typically reported in studies quantifying sympathetic transduction, but the information gained by studying non-bursts is unclear. We tested the hypothesis that longer sequences of non-bursts (≥8 cardiac cycles) would be associated with a greater nadir diastolic blood pressure (DBP) and that better popliteal artery function would be associated with an augmented reduction in DBP., Methods: Resting beat-by-beat DBP (via finger photoplethysmography) and common peroneal nerve MSNA (via microneurography) were recorded in 39 healthy, adults (age 23.4 ± 5.3 years; 19 females). For each cardiac cycle absent of MSNA bursts, the mean nadir DBP (ΔDBP) during the 12 cardiac cycles following were determined, and separate analyses were conducted for ≥8 or < 8 cardiac cycle sequences. Popliteal artery endothelial-dependent (via flow-mediated dilation; FMD) and endothelial-independent vasodilation (via nitroglycerin-mediated dilation; NMD) were determined., Results: The nadir DBP responses to sequences ≥8 cardiac cycles were larger (-1.40 ± 1.27 mmHg) than sequences <8 (-0.38 ± 0.46 mmHg; p < 0.001). In adjusting for sex and burst frequency (14 ± 8 bursts/min), larger absolute or relative FMD (p < 0.01), but not NMD (p > 0.53) was associated with an augmented nadir DBP. This overall DBP-FMD relationship was similar in sequences ≥8 (p = 0.04-0.05), but not <8 (p > 0.72)., Conclusion: The DBP responses to non-bursts, particularly longer sequences, were inversely associated with popliteal endothelial function, but not vascular smooth muscle sensitivity. This study provides insight into the information gained by quantifying the DBP responses to cardiac cycles absent of MSNA., (Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.)

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 yr, body mass index (BMI): 26 ± 4 kg/m 2 ]. 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 burst 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. NEW & NOTEWORTHY The present study investigated the independent association between actigraphy-based sleep duration, efficiency, and measures of blood pressure, heart rate, and muscle sympathetic nerve activity (MSNA) in adult males and females. Contrary to our hypothesis, the findings do not support an independent association between habitual sleep and cardiovascular or sympathetic neural activity. However, these findings do not preclude a potential association between these parameters in populations with sleep disorders and/or cardiovascular disease.

Background: Para-sympathetic vagal activation has profound influence on heart rate and other cardiovascular parameters. We tested the hypothesis that transcutaneous Vagal Nerve Stimulation (tVNS) through the auricular branch of the vagus nerve would attenuate the normal sympathetic response to central blood volume reduction by lower body negative pressure (LBNP)., Method: 10 healthy volunteers (6 female; age 21 ± 2 years; weight 62 ± 13 kg; height 167 ± 12 cm) were included in this cross-over design trial. After 15 min rest in supine position, subjects underwent three 15-min periods of 30 mmHg LBNP intervention with and without cyclic tVNS stimulation. Continuous cardiovascular parameters (Nexfin) were recorded., Results: Overall tVNS did not convincingly attenuate sympathetic response to central hypovolemia. Deactivation of the tVNS during LBNP resulted in increased MAP at 2.3 ± 0.5 mmHg (P < 0.001). Comparing the cyclic actual active stimulation periods to periods with pause during tVNS intervention showed a decrease in HR by 72.9 ± 11.2 to 70.2 ± 11.6 bpm (mean ± SD; P < 0.05), and concomitant increases in SV (86.0 ± 12.1 to 87.2 ± 12.6 mL; P < 0.05), MAP (82.9 ± 6.3 to 84.0 ± 6.2 mmHg; P < 0.05) and TPR (1116.0 ± 111.1 to 1153 ± 104.8 dyn*s/cm5; P < 0.05)., Conclusion: tVNS in 30 s cycles during LBNP can selectively attenuate HR, prompting a compensatory augmented sympathetic response. It would appear the method used in this study at least, has an isolated cardiac inhibitory effect probably mediated by augmented vagal activity on the sinoatrial or atrio-ventricular node, possibly in combination with reduced activity in the sympathetic cardiac nerve., Competing Interests: Declaration of competing interest The authors have no competing interests., (Copyright © 2024 Elsevier B.V. All rights reserved.)

There is clear evidence that the sympathetic nervous system (SNS) mediates bone metabolism. Histological studies show abundant SNS innervation of the periosteum and bone marrow-these nerves consist of noradrenergic fibers that immunostain for tyrosine hydroxylase, dopamine beta-hydroxylase, or neuropeptide Y. Nonetheless, the brain sites that send efferent SNS outflow to the bone have not yet been characterized. Using pseudorabies (PRV) viral transneuronal tracing, we report, for the first time, the identification of central SNS outflow sites that innervate bone. We find that the central SNS outflow to bone originates from 87 brain nuclei, sub-nuclei, and regions of six brain divisions, namely the midbrain and pons, hypothalamus, hindbrain medulla, forebrain, cerebral cortex, and thalamus. We also find that certain sites, such as the raphe magnus (RMg) of the medulla and periaqueductal gray (PAG) of the midbrain, display greater degrees of PRV152 infection, suggesting that there is considerable site-specific variation in the levels of central SNS outflow to the bone. This comprehensive compendium illustrating the central coding and control of SNS efferent signals to bone should allow for a greater understanding of the neural regulation of bone metabolism, and importantly and of clinical relevance, mechanisms for central bone pain., Competing Interests: VR, DL, KG, SK Reviewing editor, eLife, AG, RW, FK, LC, HK, OM, OB, SS No competing interests declared, TY Senior editor, eLife, MZ consults for Gershon Lehmann, Guidepoint and Coleman groups, (© 2024, Ryu et al.)

Na V 1.7 plays a crucial role in inducing and conducting action potentials in pain-transducing sensory nociceptor fibres, suggesting that Na V 1.7 blockers could be effective non-opioid analgesics. While SCN9A is expressed in both sensory and autonomic neurons, its functional role in the autonomic system remains less established. Our single neuron rt-PCR analysis revealed that 82% of sympathetic neurons isolated from guinea-pig stellate ganglia expressed Na V 1.7 mRNA, with Na V 1.3 being the only other tetrodotoxin-sensitive channel expressed in approximately 50% of neurons. We investigated the role of Na V 1.7 in conducting action potentials in postganglionic sympathetic nerves and in the sympathetic adrenergic contractions of blood vessels using selective Na V 1.7 inhibitors. Two highly selective Na V 1.7 blockers, GNE8493 and PF 05089771, significantly inhibited postganglionic compound action potentials by approximately 70% (P < 0.01), with residual activity being blocked by the Na V 1.3 inhibitor, ICA 121431. Electrical field stimulation (EFS) induced rapid contractions in guinea-pig isolated aorta, pulmonary arteries, and human isolated pulmonary arteries via stimulation of intrinsic nerves, which were inhibited by prazosin or the Na V 1 blocker tetrodotoxin. Our results demonstrated that blocking Na V 1.7 with GNE8493, PF 05089771, or ST2262 abolished or strongly inhibited sympathetic adrenergic responses in guinea-pigs and human vascular smooth muscle. These findings support the hypothesis that pharmacologically inhibiting Na V 1.7 could potentially reduce sympathetic and parasympathetic function in specific vascular beds and airways. KEY POINTS: 82% of sympathetic neurons isolated from the stellate ganglion predominantly express Na V 1.7 mRNA. Na V 1.7 blockers inhibit action potential conduction in postganglionic sympathetic nerves. Na V 1.7 blockade substantially inhibits sympathetic nerve-mediated adrenergic contractions in human and guinea-pig blood vessels. Pharmacologically blocking Na V 1.7 profoundly affects sympathetic and parasympathetic responses in addition to sensory fibres, prompting exploration into the broader physiological consequences of Na V 1.7 mutations on autonomic nerve activity., (© 2024 The Authors. The Journal of Physiology © 2024 The Physiological Society.)

In resistant hypertensive patients acute carotid baroreflex stimulation is associated with a blood pressure (BP) reduction, believed to be mediated by a central sympathoinhbition.The evidence for this sympathomodulatory effect is limited, however. This meta-analysis is the first to examine the sympathomodulatory effects of acute carotid baroreflex stimulation in drug-resistant and uncontrolled hypertension, based on the results of microneurographic studies. The analysis included 3 studies assessing muscle sympathetic nerve activity (MSNA) and examining 41 resistant uncontrolled hypertensives. The evaluation included assessment of the relationships between MSNA and clinic heart rate and BP changes associated with the procedure. Carotid baroreflex stimulation induced an acute reduction in clinic systolic and diastolic BP which achieved statistical significance for the former variable only [systolic BP: -19.98 mmHg (90% CI, -30.52, -9.43), P < 0.002], [diastolic BP: -5.49 mmHg (90% CI, -11.38, 0.39), P = NS]. These BP changes were accompanied by a significant MSNA reduction [-4.28 bursts/min (90% CI, -8.62, 0.06), P < 0.07], and by a significant heart rate decrease [-3.65 beats/min (90% CI, -5.49, -1.81), P < 0.001]. No significant relationship was detected beween the MSNA, systolic and diastolic BP changes induced by the procedure, this being the case also for heart rate. Our data show that the acute BP lowering responses to carotid baroreflex stimulation, although associated with a significant MSNA reduction, are not quantitatively related to the sympathomoderating effects of the procedure. This may suggest that these BP effects depend only in part on central sympathoinhibition, at least in the acute phase following the intervention., (© 2024. The Author(s), under exclusive licence to The Japanese Society of Hypertension.)

The purpose of the present study was to clarify the impact of age on the sympathoinhibitory response to cardiopulmonary baroreceptor loading in females. Nine older females (mean ± SD, 70 ± 6 yr) and 11 younger females (20 ± 1 yr) completed the study. A passive leg raising (PLR) test was performed wherein the participants were positioned supine (baseline, 0°), and their lower limbs were passively lifted at 10°, 20°, 30°, and 40° (3 min at each angle). Muscle sympathetic nerve activity (MSNA) was recorded via microneurography of the left radial nerve. The central venous pressure was estimated based on peripheral venous pressure (eCVP), which was monitored using a cannula in the right large antecubital vein. Baseline MSNA was higher in older females than in younger females. MSNA burst frequency (BF) decreased during the PLR test in both older and younger females, but the magnitude of the decrease in MSNA BF was smaller in older females than in younger females (older, -3.5 ± 1.5 vs. younger, -6.3 ± 1.5 bursts/min at 40° from baseline, P = 0.014). The eCVP increased during the PLR in both groups, and there was no difference in the changes in eCVP between the two groups (older, +1.07 ± 0.37 vs. younger, +1.12 ± 0.33 mmHg at 40° from baseline, P = 0.941). These results suggest that inhibition of sympathetic vasomotor outflow during cardiopulmonary baroreceptor loading could be blunted with advancing age in females. NEW & NOTEWORTHY There were no available data concerning the effect of age on the sympathoinhibitory response to cardiopulmonary baroreceptor loading in females. The magnitude of the decrease in muscle sympathetic nerve activity during passive leg raising (10°-40°) was smaller in older females than in young females. In females, inhibition of sympathetic vasomotor outflow during cardiopulmonary baroreceptor loading could be blunted with advancing age.

Sinusoidal galvanic vestibular stimulation (sGVS) induces robust modulation of muscle sympathetic nerve activity (MSNA) alongside perceptions of side-to-side movement, sometimes with an accompanying feeling of nausea. We recently showed that transcranial alternating current stimulation (tACS) of the dorsolateral prefrontal cortex (dlPFC) also modulates MSNA, but does not generate any perceptions. Here, we tested the hypothesis that when the two stimuli are given concurrently, the modulation of MSNA would be additive. MSNA was recorded from 11 awake participants via a tungsten microelectrode inserted percutaneously into the right common peroneal nerve at the fibular head. Sinusoidal stimuli (± 2 mA, 0.08 Hz, 100 cycles) were applied in randomised order as follows: (i) tACS of the dlPFC at electroencephalogram (EEG) site F4 and referenced to the nasion; (ii) bilateral sGVS applied to the vestibular apparatuses via the mastoid processes; and (iii) tACS and sGVS together. Previously obtained data from 12 participants supplemented the data for stimulation protocols (i) and (ii). Cross-correlation analysis revealed that each stimulation protocol caused significant modulation of MSNA (modulation index (paired data): 35.2 ± 19.4% for sGVS; 27.8 ± 15.2% for tACS), but there were no additive effects when tACS and sGVS were delivered concurrently (32.1 ± 18.5%). This implies that the vestibulosympathetic reflexes are attenuated with concurrent dlPFC stimulation. These results suggest that the dlPFC is capable of blocking the processing of vestibular inputs through the brainstem and, hence, the generation of vestibulosympathetic reflexes., (© 2024. The Author(s).)

During times of stress, we look to close others for support. Social support conversations are critical for relationship maintenance and well-being. Yet, certain ways of talking about problems-such as co-ruminating-can exacerbate stress. Since social support and co-rumination are both dyadic processes, it is important to examine physiological responses during these conversations in a dyadic manner. Little research has examined physiological synchrony of the sympathetic nervous system (SNS) during social support conversations or co-ruminative conversations. The current research capitalizes on an experimental manipulation of co-rumination using a sample of close friends (147 dyads) and romantic partners (113 dyads) to examine physiological covariation in the context of support. Across both samples, dyads exhibited significant physiological covariation in pre-ejection period reactivity (PEP). Contrary to our hypothesis, dyads in the co-rumination condition did not show more covariation. Close friend dyads did, however, exhibit more covariation as compared to romantic dyads. We also found significant variability in physiological covariation across dyads, with a minority of dyads exhibiting negative covariation of PEP reactivity. The homogeneity of the samples limits the generalizability of the findings and highlights the need for more diverse samples in future work. These findings underline the need for further exploration into the mechanisms that contribute to distinct patterns of physiological synchrony, the conditions in which negative synchrony occurs, and what predicts especially strong positive synchrony. This work extends our understanding of physiological synchrony of the sympathetic nervous system during support conversations and emphasizes the importance of considering heterogeneity in physiological processes., (© 2024 Society for Psychophysiological Research.)

Contemporary discussion of the baroreflex includes the efferent vascular-sympathetic and cardiovagal arms. Since sympathetic postganglionic neurons also innervate the left ventricle (LV), it is often assumed that the LV produces a sympathetically mediated increase in contractility during baroreceptor unloading, but this has not been characterized using a load-independent index of contractility. We aimed to determine 1 ) whether LV contractility increases in response to baroreceptor unloading and 2 ) whether such increases are mediated via the sympathetic or parasympathetic arm of the autonomic nervous system. Ten male Wistar rats were anesthetized (urethane) and instrumented with arterial and LV pressure-volume catheters to measure mean arterial pressure (MAP) and load-independent LV contractility [maximal rate of increase in pressure adjusted to end-diastolic volume (PAdP/d t max )], respectively. Rats were placed in a servo-controlled lower-body negative pressure (LBNP) chamber to reduce MAP by 10% for 60 s to mechanically unload baroreceptors under control conditions. LBNP was repeated in each animal following infusions of cardiac autonomic blockers using esmolol (sympathetic), atropine (parasympathetic), and esmolol + atropine. Under control conditions, PAdP/d t max increased during baroreceptor unloading (26 ± 6 vs. 31 ± 9 mmHg·s -1 ·μL -1 , P = 0.031). During esmolol, there was no increase in LV contractility during baroreceptor unloading (11 ± 2 vs. 12 ± 2, P = 0.125); however, during atropine, there was an increase in LV contractility during baroreceptor unloading (26 ± 6 vs. 31 ± 9, P = 0.019). During combined esmolol and atropine, there was a small increase in contractility versus control (13 ± 3 vs. 15 ± 4, P = 0.046). Our results demonstrate that, in anesthetized rats, LV contractility increases in response to baroreceptor unloading, which is largely sympathetically mediated. NEW & NOTEWORTHY This study empirically demonstrates a sympathetically mediated increase in LV contractility in response to baroreceptor unloading using a load-independent index of cardiac contractility in the anesthetized rat.

Intense inspiratory muscle work can evoke a metabolite-stimulated pressor reflex, commonly referred to as the respiratory muscle metaboreflex. When completing similar relative and absolute levels of inspiratory work, females have an attenuated blood pressure response. We sought to test the hypothesis that the lower blood pressure response to the respiratory muscle metaboreflex in females is associated with a reduced sympathetic response. Healthy young (26 ± 4 yr) males ( n = 9) and females ( n = 7) completed two experimental days. On day 1 , participants completed pulmonary function testing and became familiarized with an inspiratory pressure-threshold loading (PTL) task. On the second day, balloon-tipped catheters were placed in the esophagus and stomach to measure pleural and gastric pressures, and transdiaphragmatic pressure was calculated. A microelectrode was inserted into the fibular nerve to quantify muscle sympathetic nerve activity (MSNA), and participants then completed isocapnic PTL to task failure. There was a significant sex-by-time interaction in the mean arterial pressure (MAP, P = 0.015) and burst frequency ( P = 0.039) response to PTL. Males had a greater rise in MAP (Δ21 ± 9 mmHg) than females (Δ13 ± 5 mmHg, P = 0.026). Males also demonstrated a greater rise in MSNA burst frequency (Δ18 ± 7 bursts/min) than females (Δ10 ± 5 bursts/min, P = 0.015). The effect of sex was observed despite females and males completing the same magnitude of diaphragm work throughout the task ( P = 0.755). Our findings provide novel evidence that the lower blood pressure response to similar relative and absolute inspiratory muscle work in females is associated with lower sympathetic activation. NEW & NOTEWORTHY The blood pressure response to high levels of inspiratory muscle work is lower in females and occurs alongside a reduced sympathetic response. The reduced blood pressure and sympathetic response occur despite males and females performing similar levels of absolute inspiratory work. Our findings provide evidence that sex differences in the respiratory muscle metaboreflex are, in part, sympathetically mediated.

Emotion regulation (ER) is a multifaceted construct, involving behavioral, cognitive, and physiological processes. Although autonomic coordination is theorized to play a crucial role in adaptive functioning, few studies have examined how different individual and contextual factors together may contribute to such coordination. This study examined the joint influences of narrative processing and emotional negativity/lability (N/L) traits on the coordination of the sympathetic and parasympathetic nervous systems in a sample of 112 children, ages 8-12 years (M age  = 10.15 years, SD = 1.33). Children completed a stress-induction task followed by an interview about the task. Children's trait-level N/L was assessed via parent-report on the Emotion Regulation Checklist. Narrative processing was assessed and coded based on children's narrative accounts of the event (i.e., causal coherence, overall emotional tone). Indexes of sympathetic (skin conductance response, SCR) and parasympathetic (respiratory sinus arrhythmia, RSA) functioning were derived from physiological data obtained during the interview. Results revealed that children's trait-level N/L and narrative processing of the stressful event interacted to predict the RSA-SCR correlation. Specifically, children who were high on either N/L or narrative causal coherence, but not both, demonstrated significant RSA-SCR correlation. Similarly, children with high N/L and negative-to-neutral narratives, as well as those with low N/L and neutral-to-positive narratives, exhibited significant RSA-SCR correlation. This work provides empirical evidence that narrative processing and trait N/L, together with RSA-SCR correlation, work in tandem to regulate emotional arousal., (© 2024 Society for Psychophysiological Research.)

It has been suggested that intimate partner violence (IPV) against women perpetrators present emotional dysregulations when dealing with acute stress, which in turn could help to explain their proneness to violence. Emotional regulation can be objectively measured by means of psychophysiological parameters/variables/indicators of autonomic nervous system (ANS) activity, such as cardiorespiratory (heart rate [HR], pre-ejection period [PEP] and respiratory sinus arrythmia [RSA]) and electrodermal (skin conductance levels [SCL]) signals. Therefore, this study aims to assess whether IPV perpetrators (n = 107) present differential psychophysiological and psychological state changes when coping with an acute cognitive laboratory stressor (a set of cognitive tests performed in front of an expert committee) in comparison with nonviolent men (n = 87). Moreover, the study assesses whether psychological state variables foster the psychophysiological response to acute stress. Our results demonstrate that, compared to nonviolent controls, IPV perpetrators showed higher HR and SCL values, shorter PEP, and lower RSA values during recovery from stress. They also presented higher negative affect (i.e., more anger and worse mood) after stress. Thus, high baseline anger explained the increases in emotional arousal when measured as SCL increases. The present study contributes evidence showing that IPV perpetrators and nonviolent men cope differently with stress. These findings might help forensic science to identify characteristics of violent individuals to establish their therapeutic needs. Furthermore, it would be appropriate to combine psychophysiological measurements with self-reports, thus increasing the reliability of the assessment of violent individuals. [ABSTRACT FROM AUTHOR]

Explaining the onset and maintenance of pain can be challenging in many clinical presentations. Allostasis encompasses the mechanisms through which humans adapt to stressors to maintain physiological stability. Due to related neuro-endocrine-immune system effects, allostasis and allostatic load (the cumulative effects on the brain and body that develop through the maintenance of physiological stability) offer the potential to explain the development and maintenance of musculoskeletal pain in certain cases. This paper outlines the concept of allostatic load, highlights the evidence for allostatic load in musculoskeletal pain conditions to date, and discusses mechanisms through which allostatic load influences pain, with particular focus on hypothalamic–pituitary–adrenal axis and sympathetic nervous system function and central, brain-driven governance of these systems. Finally, through case examples, consideration is given as to how allostatic load can be integrated into clinical reasoning and how it can be used to help explain pain to individuals and guide clinical decision-making. Impact Awareness of the concept of allostatic load, and subsequent assessment of physical and psychological stressors potentially contributing to allostatic load, may facilitate a broader understanding of the multidimensional presentations of many people with pain, both acute and persistent. This may facilitate discussion between clinicians and their patients regarding broader influences on their presentations and drive more targeted and inclusive pain management strategies. [ABSTRACT FROM AUTHOR]