To compare Functional Disability Inventory (FDI) between adolescents with chronic orthostatic intolerance (COI) and postural orthostatic tachycardia syndrome (POTS). This cross-sectional study included adolescents ≤19 years with orthostatic symptoms >3 months referred to a tertiary pediatric autonomic clinic (August 2024-March 2025) and classified as POTS or COI based upon active stand testing. Self- and parent-reported FDI scores were collected. Group comparisons used chi-square and Wilcoxon-Mann-Whitney tests. Univariable and multivariable linear regression models compared FDI scores, adjusting for age, sex, and body mass index. Adjusted means were estimated using post-fit marginal estimation. Ninety-two adolescents were included (46 POTS, 46 COI). Groups were similar in age, sex, and body mass index, but differed in heart rate response by definition. Self-reported FDI scores did not differ between COI and POTS in unadjusted (22.9 vs 22.4; P = .81) or adjusted analyses (adjusted mean difference 1.0, 95% CI -3.0 to 4.9; P = .63). Parent-reported FDI scores were also comparable in unadjusted (23.1 vs 22.3; P = .70) and adjusted analyses (adjusted mean difference 0.4, 95% CI -3.4 to 4.2; P = .85). Differences were well below the prespecified threshold for clinical significance. There was no evidence for a difference in functional disability in adolescents with COI, regardless of tachycardia-based POTS classification. This suggests that heart rate response is not associated with functional differences in pediatric orthostatic intolerance.

Highly sensitive persons' responses to acute and post-earthquake stress: Exploratory insights into genetic moderation.

This exploratory study examined the effects of player number and pitch size on internal and external load during small-sided Ultimate Frisbee games (SSGs) in elite male athletes and explored associations between playing density, expressed as area per player, and selected load indicators. Eight elite male Ultimate Frisbee players participated in SSGs across eight different configurations involving different player numbers (2v2, 3v3, 4v4) and pitch sizes (small, medium, and large). The 2v2 large-pitch was excluded because it was considered poorly representative of typical small-sided Ultimate Frisbee practice. Internal load was assessed as percentage of individual maximum heart rate (%HRmax), while external load was quantified using GPS-derived total distance, maximum speed, high-intensity running distance, and high-intensity accelerations/decelerations. Linear mixed-effects models examined the effects of player number and pitch size. LOESS curves were used only as descriptive visualizations of potential density-load patterns. Pitch size was associated with differences in locomotor variables, with larger pitches generally eliciting greater total and high-intensity running distances. Smaller formats, particularly 2v2 and 3v3, elicited higher HR responses and greater acceleration/deceleration demands than 4v4. Descriptive density analyses suggested outcome-specific tendencies, with locomotor variables generally greater in configurations providing medium-to-large relative areas per player, whereas acceleration/deceleration responses appeared less consistently related to density alone and may depend on both available space and player number. In this small homogeneous sample of elite male Ultimate Frisbee players, player number and pitch size appeared to modulate acute internal and external load responses during SSGs. However, given the limited sample size and the sparse number of density values, these findings should be interpreted as preliminary and hypothesis-generating rather than as stable effects, definitive thresholds, or practical prescription targets.

The common ACTN3 R577X polymorphism leads to α-actinin-3 deficiency in ~20% of the human population and may be detrimental to their muscle power. However, the impact of ACTN3R577X on metabolic health and exercise capacity in the general population remains unclear. The objective of the current study was to compare metabolic health markers, musculoskeletal traits, and cardiorespiratory capacity between untrained overweight α-actinin-3-deficient (XX; 20 men and 19 women) and α-actinin-3 expressing (RR; 20 men and 21 women) individuals. The participants were aged 43 ± 7 years and had a BMI of 28.6 ± 3.2 kg·m-2. Various metabolic health and exercise capacity aspects encompassing segmental body composition, bone density, systemic low-grade inflammation, blood lipid profile, whole-body glucose tolerance and insulin sensitivity, resting and exercise metabolism, and exercise capacity were evaluated. While XX groups had lower fat-free mass than RR groups, other anthropometrical and body composition features, including bone mineral content, did not differ between the genotype groups in either women or men. We found no significant differences between XX and RR individuals for blood lipid profile, markers of systemic inflammation, glucose tolerance, resting metabolism, and leg strength. Moreover, no clear genotype-related differences were observed in markers of insulin resistance and sensitivity, although XX women exhibited a slightly smaller increase in insulin concentration than RR women during an oral glucose tolerance test. An incremental cardiopulmonary cycling test revealed no differences in metabolic and heart rate responses, maximal fat oxidation, or exercise capacity. In conclusion, we observed no associations between α-actinin-3 deficiency and metabolic health, body composition, muscle function, or cardiorespiratory capacity in untrained overweight men and women.

Study Objectives: Chronic short sleep duration is associated with cardiovascular disease (CVD) risk, especially in females. The impact of biological sex on hemodynamic reactivity to spontaneous nocturnal arousals following experimental sleep restriction remains largely unknown. We therefore investigated the effect of nine-day four-hour sleep restriction on heart rate (HR) and pulse transit time (PTT) changes following spontaneous arousals in healthy males and females. We hypothesized that HR and PTT reactivity would be augmented following sleep restriction, and these responses would be more robust in females. Methods: Nineteen participants (8 females; 23±5 years) were enrolled into this study, which included two 16-day in-patient studies comprised of sleep restriction (four-hour sleep opportunity) and normal sleep (nine-hour sleep opportunity) study arms. Overnight polysomnography on days 2 (acclimation), 5 (early experimental), 11 (late experimental), and 14 (recovery) of each sleep intervention was used to analyze HR and PTT responses to spontaneous arousals. Results: Sleep restriction did not alter HR or PTT reactivity in males or females during the early experimental phase (Day 5; interaction: p>0.05). The HR response to arousal was altered in a sex-dependent manner following sleep restriction during the late experimental phase (Day 11, interaction: p=0.013). Continued sleep loss resulted in greater PTT reduction following spontaneous arousals in females, but not in males (Day 11, interaction: p=0.007) Conclusions: Sustained sleep curtailment disrupts nocturnal vascular responsiveness to spontaneous arousals, more evident in females than males. These findings provide mechanistic insight into the sex-specific relationship between shortened sleep duration and CVD risk in females.

This study aimed to examine the acute and chronic effects of a standard race load and an eight-week training period on heart rate and respiratory function parameters in short-, middle-, and long-distance runners. The study was designed as a quasi-experimental study with a repeated-measures design. The research group consisted of short-distance (n = 11), middle-distance (n = 13), and long-distance (n = 10) female runners who were actively engaged in athletics. Resting, post-race, and recovery heart rate values (1 and 15min post-exercise) were measured. Respiratory function parameters (FVC, FEV1, and PEF) were assessed before and immediately after exercise. Measurements were conducted at baseline and repeated after an eight-week training period. A mixed-design repeated-measures ANOVA was used to examine the effects of group, time, and period on physiological variables. Resting heart rate values were similar in short- and middle-distance runners, whereas long-distance runners exhibited lower values. Heart rate responses during post-race and recovery periods differed across disciplines, with short-distance runners showing a faster decline in the early recovery phase and long-distance runners reaching lower levels during the later recovery stage. Regarding respiratory function, post-exercise increases in FVC were observed in short- and middle-distance runners during the second measurement period, while FEV1 remained unchanged. PEF values increased only in short-distance runners during the same period. The eight-week training period did not significantly affect heart rate, and a significant increase was observed in FVC, whereas FEV1 remained unchanged. Recovery patterns also differed between disciplines, with short-distance runners showing a faster decline in heart rate during the early recovery phase, whereas long distance runners reached lower heart rate values during the later stages of recovery. These findings indicate that the changes observed following an 8-week period differ across running disciplines and exhibit a discipline-specific pattern. Not applicable, as this study is not a clinical trial.

Cardioventilatory failure is the leading mechanism proposed to underlie sudden unexpected death in epilepsy (SUDEP), which occurs predominantly at night in patients with generalized tonic-clonic seizures. Interictal hypercapnic cardioventilatory responses are suggested to be involved, as they are ablated in chronically epileptic kainic acid (KA) rats, a temporal lobe epilepsy model with focal to bilateral tonic-clonic seizures. However, how this impairment emerges during epileptogenesis and whether it is influenced by day/night period remain unclear. Here, we aimed to investigate the progress of hypercapnic cardioventilatory responses through the epileptogenesis of KA rats and whether it is affected by day or night. Ventilatory or breathing frequency (fB) and heart rate (HR) were measured before, during, and after a 1-h exposure to acute hypercapnia (10% CO2) using photoplethysmography in KA and healthy rats. Measurements were performed monthly for 6 months, with additional nocturnal hypercapnia recordings at month 6 to assess day/night modulation. To control for repeated CO2 exposure, an independent cohort of age-matched KA and healthy rats underwent a single hypercapnia exposure at month 6. In healthy rats, cardioventilatory responses to hypercapnia remained stable over time, with increased fB and reduced HR. Conversely, KA rats displayed an abrupt blunting of the fB response at month 4, followed by blunting of the HR response at month 6. Correlation analyses revealed a loss of correlation between fB and HR following KA injection, which reemerged when the cardioventilatory response to CO2 was fully ablated. No association was observed between seizure severity and cardioventilatory impairment. KA rats displayed similar deficits regardless of CO2 exposure frequency, and no day-night differences were detected in either group. These findings indicate that cardioventilatory responses are decreased during epileptogenesis in the KA model, suggesting their potential utility for evaluating SUDEP risk.

Heart rate (HR) in vertebrates is determined by the discharge frequency of cardiac pacemaker cells, which are innervated by the autonomic nervous system. The portion of this system located within the heart, the intracardiac nervous system (ICNS), transmits impulses to cardiac effectors for control of cardiac output. Central autonomic neurons modulate the heart through sympathetic (acceleratory) and parasympathetic (inhibitory) axons in the vagosympathetic trunks. In the classical model of cardiac control, the balance between sympathetic and parasympathetic efferent signals determines HR. Recent evidence of spontaneous neural activity within the ICNS in isolated hearts suggests a local regulatory element incardiac control. We examined the potential for ICNS modulation of HR in the isolated zebrafish heart, using atropine to block parasympathetic drive to the pacemaker, and timolol to block sympathetic drive. Atropine (3, 10, 30 µM) evoked tachycardia of similar magnitude at 22 and 28 ° C. Timolol (3, 10 and 30 µM) caused bradycardia at both temperatures, with greater proportional HR responses to all doses at the higher temperature. Our results suggest that both sympathetic and parasympathetic outputs from the ICNS influence the pacemaker, with the degree of sympathetic drive being temperature-sensitive. Intrinsic HR, obtained after dual antagonist application, was not significantly different from HR before drug application so the effects of sympathetic and parasympathetic drive on pacemaker rate appeared to be evenly balanced. We propose that the ICNS in the isolated zebrafish heart is capable of modulating HR in the absence of extracardiac autonomic inputs.

Group-level averaging of psychophysiological data often obscures meaningful individual differences, masking response patterns that may explain variability in behavior and central nervous system activity. Identifying such patterns is particularly relevant in heart rate (HR) responses to threat, where subtle variations may reflect distinct coping mechanisms such as orienting or defense. Machine learning techniques that learn latent representations, particularly variational autoencoders (VAEs), offer powerful tools for revealing such hidden structures. This methodological report introduces a simple VAE-based approach for characterizing HR responses to threat pictures in 165 participants. To validate the method, simulations first demonstrated that the model accurately separated simulated HR waveforms. The VAE was then applied to empirical HR responses, mapping them into a three-dimensional latent space for subsequent cluster analysis, which was compared to clustering based directly on raw HR waveforms. The VAE revealed three distinct response profiles: (1) strong decelerators (cardiac orienting response), (2) weak decelerators with late acceleration, and (3) immediate accelerators without a decelerative phase. In contrast, clustering raw HR waveforms identified only two groups. Clusters derived from the latent space were more coherent and exhibited greater within-group consistency. Finally, applying the pre-trained autoencoder to a small fear-conditioning dataset enabled characterization of distinct HR response patterns despite limited sample size. These findings show that even a basic autoencoder enhances the categorization of psychophysiological response patterns, offering a framework for linking individual autonomic variability to broader models of affective and defensive behavior.

This study examined whether multiple group membership (MGM) predicted future cardiovascular reactivity (CVR) in women and whether this relationship was moderated by the number of social group memberships they perceived to be the basis for their discrimination. Using a longitudinal design, data were drawn from Waves 2 and 3 of the Midlife in the United States (MIDUS) study. The sample included 179 women for diastolic and systolic blood pressure (DBP, SBP) reactivity and 200 women for heart rate (HR) reactivity (ages 47-94, M = 63.66, SD = 8.90). Greater MGM at Time 1 was associated with lower HR responses to stress at Time 2, indicating reduced cardiovascular responding during the stress tasks. Moderation analyses revealed that among women who attributed discrimination to one group, higher MGM predicted higher HR reactivity suggesting a more engaged stress response. In contrast, among women who did not attribute discrimination to any group, higher MGM was significantly associated with lower HR reactivity. No significant effects were found for SBP and DBP reactivity. Together, these findings suggest that MGM does not uniformly confer stress-buffering benefits and may, in some contexts, reflect cumulative social burden rather than protection. The results highlight the importance of considering the social meaning and context of group memberships, particularly experiences of discrimination, when evaluating their implications for women's stress-related health.

Influence of resilience on autonomic nervous system habituation to repeated stress exposure: Insights from heart rate variability and heart rate response.

How does subjective social status get under the skin? A scoping review of associations with biomarkers of the primary stress systems.

The effects of rumination and reappraisal on repeated exposure to stress.

The growing use of synthetic materials in aquaculture, such as polyvinyl chloride (PVC) and fibre reinforced plastic (FRP), has prompted concerns regarding their environmental and biological safety. Despite their durability and cost-effectiveness, the ecological impact of these materials, especially when colonized by periphyton, remains underexplored. This study investigates the developmental and physiological responses of zebrafish embryos (Danio rerio) exposed to water containing periphyton-covered PVC and FRP sheets. Survivability, morphological development, hatching success, heart rate, and cellular responses were evaluated to understand potential toxic effects. While periphyton biofilms were expected to promote ecological compatibility, findings revealed that both periphyton-inhabited PVC and FRP adversely affected embryonic development. Notable effects included delayed hatching, elevated mortality, and increased oxidative stress. However, PVC exhibited relatively higher biocompatibility, causing fewer disruptions to embryo viability and cellular function compared to FRP. At the molecular level, FRP induced stronger toxic responses, likely due to its chemical composition and more aggressive interaction with developing embryos. In contrast, PVC's material characteristics and associated biofilm interactions were less harmful. The study highlights the importance of assessing both material type and biofilm dynamics in aquaculture systems and supports the shift toward eco-compatible infrastructure for sustainable aquatic practices.

Cardiac Dynamics During Social Evaluative Feedback: Evidence from Intersubject Representational Similarity Analysis.

Measuring approach-avoidance behavior in patients with panic disorder using the human elevated plus maze in mixed reality.

Exercising blood pressure (BP) and heart rate (HR) responses were recorded during graded exercise testing and ACFE exposure was assessed among 3,417 young adults (mean age = 25 ± 4 y; 44% female; 46% Black). Linear mixed-effects models that included participant-specific random intercepts and random slopes were used to assess the relation between ACFE exposure and exercising systolic (SBP), diastolic, and mean BP, pulse pressure (PP), pulse pressure index (PPI), heart rate (HR), and rate pressure product (RPP). All models were adjusted for resting values of the hemodynamic outcome, as well as age, sex, race, study center, body mass index, current hypertension medication use, smoking status, and alcohol consumption. Graded exercise hemodynamic responses were analyzed in 3,346-3,417 participants in the final models, providing 15,372-17,481 observations. Higher ACFE exposure was associated with lower SBP (β = -0.304 mmHg/ACFE, p = 0.033), HR (β = -0.485 bpm/ACFE, p <0.001), and RPP (β = -83.404 bpm·mmHg/ACFE, p =0.002) at the lowest workload, but steeper workload-related increases in SBP (interaction β = 0.044 mmHg·MET⁻¹·ACFE⁻¹, p =0.029), HR (β = 0.061 bpm·MET⁻¹·ACFE⁻¹, p <0.001), RPP (β = 10.16 bpm·mmHg·MET⁻¹·ACFE⁻¹, p =0.025), and PP (β = 0.052 mmHg·MET⁻¹·ACFE⁻¹, p =0.038) and PPI (β = 0.000232 units·MET⁻¹·ACFE⁻¹, p =0.018). These findings were robust to additional adjustment for central adiposity, exercise capacity, and maximal heart rate and heart rate recovery. Our findings add nuanced evidence revealing that early adversity is associated with a demand-dependent shift in cardiovascular regulation, with attenuated responses at low demand, but more dramatic increases in pulsatile and myocardial load responses during progressive physiological stress.

The underwater environment triggers the autonomic nervous system (ANS) responses during self-contained underwater breathing apparatus (SCUBA) diving, which aims to conserve oxygen during submersion. The aim of the study is to evaluate cardiovascular responses in professional SCUBA divers by analysing heart rate dynamics across dive phases and comparing responses between novice and experienced divers in a real-world setting. Twenty certified divers performed standard dives to a minimum depth of 66 feet and remained there for 5 minutes as part of the protocol. The dive was divided into six phases: rest, pre-dive, descent, bottom, ascent, and post-dive. The heart rate across different dive phases and cardiovascular reflex indices, such as heart rate drop and the minimum heart rate, is calculated. Statistical analysis was performed to comprehend the differences across phases and changes in cardiovascular reflex indices between diving experience groups. The statistical analysis shows noteworthy differences in heart rate across dive phases. The notable variations were between the pre-dive and bottom phases (p<0.05) and between the descent and bottom phases(p<0.05). The study highlights the persistence of bradycardia even when depth remained constant, and a difference of 7.71 percentage points in the percentage drop in heart rate between experienced and novice divers. Experienced divers showed a pattern of lower heart-rate responses than novice divers across selected phases of the dive. The findings point to the value of further work on diver health monitoring, training, and cardiovascular adaptation in larger samples. Experienced divers should be regularly screened for cardiovascular disease to avoid any adverse events.

Type 1 diabetes (T1D) is associated with an increased risk of cardiovascular and autonomic complications. Although cardiopulmonary exercise testing (CPET) is a valuable tool for assessing cardiorespiratory function, data on physiological response to maximal exertion in adolescents with T1D remain limited and inconsistent. This study aimed to compare cardiovascular, respiratory, metabolic, and microvascular responses to CPET in adolescents with T1D and healthy peers. Sixteen participants aged 11-16 years (eight with T1D and eight healthy controls), matched for anthropometric characteristics, underwent CPET on a cycle ergometer. Respiratory gas exchange, heart rate, heart rate variability, blood pressure, blood glucose, lactate concentration, skin blood flow, skin temperature, and cutaneous vascular conductance were measured at predefined time points during rest, exercise, and recovery. Blood glucose, lactate concentration, and skin microvascular variables were assessed at rest and during recovery. Adolescents with T1D demonstrated a significantly lower V̇O2/power output slope and a higher ventilatory equivalent for oxygen at maximal effort, suggesting altered oxygen uptake efficiency. Maximal power output and maximal oxygen consumption did not differ between groups. Heart rate responses and heart rate variability were similar throughout testing. However, finger skin blood flow and cutaneous vascular conductance were significantly lower in the T1D group at rest and during recovery. Adolescents with T1D showed preserved cardiovascular function and comparable overall exercise capacity to healthy peers, despite subtle impairments in oxygen utilization and reduced skin microvascular function. These findings indicate that even at a young age, T1D is associated with altered metabolic, respiratory, and microvascular responses to maximal exercise. The results suggest that peripheral, rather than central mechanisms may underlie these differences, potentially involving glucose levels or synthetic insulin effects on vascular endothelium.

Implanted cervical vagus nerve stimulation (VNS) is used to treat refractory epilepsy, depression, stroke sequelae, and rheumatoid arthritis. It is necessary to understand the recruitment of different neural elements in response to VNS to uncover the therapeutic mechanisms for these therapies. We quantified VNS-evoked physiologic responses in participants who underwent VNS implant surgery: laryngeal muscle activation (electromyogram [EMG]; indicating side effects; mediated by activation of large-diameter myelinated A-fibers) and changes in heart rate (HR; mediated by activation of small-diameter myelinated B-fibers). Moreover, it is necessary to validate noninvasive measurements of laryngeal EMG. We recruited adult participants (seven females, three males) with treatment-resistant epilepsy who were receiving a new VNS implant ("acute") or replacement of an implanted VNS pulse generator ("chronic"). During these procedures, we delivered VNS across pulse widths (50, 250, and 1000 μs per phase) and stimulation amplitudes (0.05-28 mA) while recording laryngeal EMG and HR. The median stimulation amplitudes to evoke 50% of maximal laryngeal EMG response were 1.32, 0.49, and 0.34 mA for pulse widths of 50, 250, and 1000 μs per phase, respectively; thresholds were comparable between EMG electrodes placed endotracheally and subcutaneously. The median stimulation amplitudes to cause a 10% decrease in HR were 13.39 and 3.53 mA at 50 and 250 μs per phase, respectively-that is, approximately six to 63 times higher than the 50% EMG thresholds. We did not observe a qualitative difference in EMG or HR responses between sexes, acute/chronic, or stimulation polarities. For each subject in the chronic implant group, clinician-selected stimulation amplitudes were higher than the 50% EMG thresholds and lower than the 10% HR thresholds. Thresholds to evoke bradycardia were two times higher than clinician-selected stimulation amplitudes. This suggests that target fibers may not be activated by VNS (given low responder rates and confounds in clinical trials), target fibers of VNS for epilepsy may have a larger diameter than those projecting to the heart, and/or the therapeutic effect in refractory epilepsy may be evoked with less fiber activation than is required to produce bradycardia. The Clinicaltrials.gov registration number for the study is NCT05395026.