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Introduction: Inspiratory muscle fatigue has been shown to have effects on the autonomic nervous system and physical condition. This study aimed to evaluate the influence of an inspiratory muscle fatigue protocol on respiratory muscle strength and heart rate variability in healthy youths. Materials and Methods: A randomized controlled clinical trial, employing double-blinding, was conducted with twenty-seven participants aged 18-45 years, non-smokers and engaged in sports activity at least three times a week for a minimum of 1 year. Participants were randomly assigned to three groups: Inspiratory Muscle Fatigue group, Activation group, and Control group. Measurements of heart rate variability, diaphragmatic ultrasound, and maximum inspiratory pressure were taken at two stages: before the intervention and immediately after treatment. Results: In our results with respect to baseline to post-treatment, the inspiratory muscle fatigue group showed lower values in the Sniff contraction velocity variable (10.96 cm/s ± 1.99-8.34 cm/s ± 1.23; p < 0.01) and higher values in the activation group (10.59 cm/s ± 0.89-12.66 cm/s ± 1.15; p < 0.01) with respect to the control group (10.27 cm/s ± 1.48-9.97 cm/s ± 1.42). On the other hand, the inspiratory muscle fatigue group showed higher values in the Low frequency variable (49.37 n.u. ± 13.91 to 69.48 n.u. ± 8.22; p < 0.01) and lower values in the activation group (57.92 n.u. ± 8.37 to 41.59 n.u. ± 11.21; p < 0.01) with respect to the control group (50.83 n.u. ± 17.30 to 52.10 n.u. ± 20.64). Additionally, significant correlations were found between respiratory variables and heart rate variability variables. Conclusion: Acute fatigue of the inspiratory musculature appears to negatively impact heart rate variability and inspiratory muscle strength in healthy youths. Clinical Trial Registration: https://clinicaltrials.gov/study/NCT06278714; Identifier: NCT06278714.

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Introduction: The influence of vagus nerve stimulation (VNS) parameters on provoked cardiac effects in different levels of cardiac innervation is not well understood yet. This study examines the effects of VNS on heart rate (HR) modulation across a spectrum of cardiac innervation states, providing data for the potential optimization of VNS in cardiac therapies. Materials and Methods: Utilizing previously published data from VNS experiments on six sheep with intact innervation, and data of additional experiments in five rabbits post bilateral rostral vagotomy, and four isolated rabbit hearts with additionally removed sympathetic influences, the study explored the impact of diverse VNS parameters on HR. Results: Significant differences in physiological threshold charges were identified across groups: 0.09 ± 0.06 µC for intact, 0.20 ± 0.04 µC for vagotomized, and 9.00 ± 0.75 µC for isolated hearts. Charge was a key determinant of HR reduction across all innervation states, with diminishing correlations from intact (r = 0.7) to isolated hearts (r = 0.44). An inverse relationship was observed for the number of pulses, with its influence growing in conditions of reduced innervation (intact r = 0.11, isolated r = 0.37). Frequency and stimulation delay showed minimal correlations (r < 0.17) in all conditions. Conclusion: Our study highlights for the first time that VNS parameters, including stimulation intensity, pulse width, and pulse number, crucially modulate heart rate across different cardiac innervation states. Intensity and pulse width significantly influence heart rate in innervated states, while pulse number is key in denervated states. Frequency and delay have less impact impact across all innervation states. These findings suggest the importance of customizing VNS therapy based on innervation status, offering insights for optimizing cardiac neuromodulation.

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Studies have shown that Trait Emotional Awareness (TEA) - the ability to recognize one's emotions - and Heart Rate Variability (HRV) are both negatively associated with psychological disorders. Although these studies imply that TEA is related to HRV and may explain the association between HRV and psychological disorders, there is limited research investigating this implication. Such investigation is essential to illuminate the psychophysiological processes linked to psychological disorders. The present study aims to investigate a) the association between TEA and HRV, b) the association between HRV and psychological disorders, and c) whether TEA explains the association between HRV and psychological disorders. A sample of 41 German students completed self-report questionnaires as indicators of psychological disorders, including the Hospital Anxiety and Depression Scale (HADS; Snaith & Zigmond, 1983) for anxiousness and depressiveness, as well as the somatization scale of the Hopkins Symptom Checklist (HSCL; Derogatis et al., 1976) for physical complaints. HRV was measured at baseline (resting HRV) and during exposure to a fear-provoking movie clip (reactive HRV). As hypothesized, a) TEA showed a positive association with reactive HRV, b) HRV showed negative associations with anxiousness and physical complaints, and c) TEA explained the relationships between reactive HRV and anxiousness, as well as physical complaints. Contrary to our hypothesis, we did not find any association between HRV and depressiveness. We discussed the contribution of TEA to psychophysiological health, limited generalizability of the current study, and direct future research to explore the underlying mechanisms linking TEA to health.

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Introduction: Joint symbolic analysis (JSA) can be utilized to describe interactions between time series while accounting for time scales and nonlinear features. JSA is based on the computation of the rate of occurrence of joint patterns built after symbolization. Lagged JSA (LJSA) is obtained from the more classical JSA by introducing a delay/lead between patterns built over the two series and combined to form the joint scheme, thus monitoring coordinated patterns at different lags. Methods: In the present study, we applied LJSA for the assessment of cardiorespiratory coupling (CRC) from heart period (HP) variability and respiratory activity (R) in 19 healthy subjects (age: 27-35 years; 8 males, 11 females) during spontaneous breathing (SB) and controlled breathing (CB). The R rate of CB was selected to be indistinguishable from that of SB, namely, 15 breaths·minute-1 (CB15), or slower than SB, namely, 10 breaths·minute-1 (CB10), but in both cases, very rapid interactions between heart rate and R were known to be present. The ability of the LJSA approach to follow variations of the coupling strength was tested over a unidirectionally or bidirectionally coupled stochastic process and using surrogate data to test the null hypothesis of uncoupling. Results: We found that: i) the analysis of surrogate data proved that HP and R were significantly coupled in any experimental condition, and coupling was not more likely to occur at a specific time lag; ii) CB10 reduced CRC strength at the fastest time scales while increasing that at intermediate time scales, thus leaving the overall CRC strength unvaried; iii) despite exhibiting similar R rates and respiratory sinus arrhythmia, SB and CB15 induced different cardiorespiratory interactions; iv) no dominant temporal scheme was observed with relevant contributions of HP patterns either leading or lagging R. Discussion: LJSA is a useful methodology to explore HP-R dynamic interactions while accounting for time shifts and scales.

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Nonlinear markers of coupling strength are often utilized to typify cardiorespiratory and cerebrovascular regulations. The computation of these indices requires techniques describing nonlinear interactions between respiration (R) and heart period (HP) and between mean arterial pressure (MAP) and mean cerebral blood velocity (MCBv). We compared two model-free methods for the assessment of dynamic HP-R and MCBv-MAP interactions, namely the cross-sample entropy (CSampEn) and k-nearest-neighbor cross-unpredictability (KNNCUP). Comparison was carried out first over simulations generated by linear and nonlinear unidirectional causal, bidirectional linear causal, and lag-zero linear noncausal models, and then over experimental data acquired from 19 subjects at supine rest during spontaneous breathing and controlled respiration at 10, 15, and 20 breaths·minute-1 as well as from 13 subjects at supine rest and during 60° head-up tilt. Linear markers were computed for comparison. We found that: (i) over simulations, CSampEn and KNNCUP exhibit different abilities in evaluating coupling strength; (ii) KNNCUP is more reliable than CSampEn when interactions occur according to a causal structure, while performances are similar in noncausal models; (iii) in healthy subjects, KNNCUP is more powerful in characterizing cardiorespiratory and cerebrovascular variability interactions than CSampEn and linear markers. We recommend KNNCUP for quantifying cardiorespiratory and cerebrovascular coupling.

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The aim of this study was to assess cardiorespiratory coupling (CRC) in type 2 diabetes mellitus patients (T2DM) and apparently healthy individuals, in order to test the hypothesis that this method can provide additional knowledge to the information obtained through the heart rate variability (HRV). A cross-sectional study was conducted in T2DM patients(T2DMG=32) and health controls (CON=32). For CRC analysis, the electrocardiogram, arterial pressure, and thoracic respiratory movement were recorded at rest in supine position and during active standing. Beat-to-beat series of heart period and systolic arterial pressure were analyzed with the respiratory movement signal via a traditional non-causal approach, such as squared coherence function. In this sample of T2DM, no differences in HRV were observed when compared to the CON, but the T2DMG showed a reduction in resting CRC. We conclude that in CRC in T2DM, reflected by the squared coherence may already be compromised even before HRV changes.

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Stellate ganglia within the intrathoracic cardiac control system receive and integrate central, peripheral, and cardiopulmonary information to produce postganglionic cardiac sympathetic inputs. Pathological anatomical and structural remodeling occurs within the neurons of the stellate ganglion (SG) in the setting of heart failure (HF). A large proportion of SG neurons function as interneurons whose networking capabilities are largely unknown. Current therapies are limited to targeting sympathetic activity at the cardiac level or surgical interventions such as stellectomy, to treat HF. Future therapies that target the SG will require understanding of their networking capabilities to modify any pathological remodeling. We observe SG networking by examining cofluctuation and specificity of SG networked activity to cardiac cycle phases. We investigate network processing of cardiopulmonary transduction by SG neuronal populations in porcine with chronic pacing-induced HF and control subjects during extended in-vivo extracellular microelectrode recordings. We find that information processing and cardiac control in chronic HF by the SG, relative to controls, exhibits: (i) more frequent, short-lived, high magnitude cofluctuations, (ii) greater variation in neural specificity to cardiac cycles, and (iii) neural network activity and cardiac control linkage that depends on disease state and cofluctuation magnitude.

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The estimation of cardiorespiratory coupling (CRC) is attracting interest in sports physiology as an important tool to characterize cardiac neural regulation genuinely driven by respiration. When applied in sports medicine, cardiorespiratory coupling measurements can provide information on the effects of training, pre-competition stress, as well as cardiovascular adjustments during stressful stimuli. Furthermore, since the cardiorespiratory coupling is strongly affected by physical activity, the study of the cardiorespiratory coupling can guide the application of specific training methods to optimize the coupling between autonomic activity and heart with possible effects on performance. However, a consensus about the physiological mechanisms, as well as methodological gold standard methods to quantify the cardiorespiratory coupling, has not been reached yet, thus limiting its application in experimental settings. This review supports the relevance of assessing cardiorespiratory coupling in the sports medicine, examines the possible physiological mechanisms involved, and lists a series of methodological approaches. cardiorespiratory coupling strength seems to be increased in athletes when compared to sedentary subjects, in addition to being associated with positive physiological outcomes, such as a possible better interaction of neural subsystems to cope with stressful stimuli. Moreover, cardiorespiratory coupling seems to be influenced by specific training modalities, such as inspiratory muscle training. However, the impact of cardiorespiratory coupling on sports performance still needs to be better explored through ad hoc physical exercise tests and protocols. In addition, this review stresses that several bivariate and multivariate methods have been proposed to assess cardiorespiratory coupling, thus opening new possibilities in estimating cardiorespiratory interactions in athletes.

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BACKGROUND: Systemic arterial hypertension (SAH), type 2 diabetes mellitus (T2DM), and Parkinson's disease (PD) are highly prevalent chronic diseases that can significantly impact the cardiovascular system. AIM: The aim of this study was to compare hemodynamic and autonomic variables at rest in individuals with SAH, T2DM, or PD. METHODS: Fifty sedentary or insufficiently active individuals (22 men) with SAH (age = 66 ± 5.0 yr), T2DM (age = 52 ± 10 yr) or PD (age = 68 ± 8.0 yr) had their resting blood pressure (BP), arterial stiffness, endothelial function, and heart rate variability (HRV) assessed and compared. RESULTS: Systolic and diastolic BP were higher in SAH (130 ± 10 / 80 ± 10 mmHg) than T2DM (110 ± 14 / 75 ± 11 mmHg) and PD, and (123 ± 20 / 70 ± 11 mmHg) respectively. T2DM individuals showed lower arterial stiffness (8.4 ± 1.1 m/s), when compared to SAH (10.3 ± 2.3 m/s) and PD (10.6 ± 3.0 m/s). T2DM had greater resting tachycardia showed by the mean RR (759 ± 79 ms), than SAH (962 ± 169 ms) and PD (976 ± 134 ms), which was accompanied by higher sympathetic modulation (low frequency [LF]: 62 ± 19 nu) and lower parasympathetic modulation (high frequency [HF]: 32 ± 16 nu) when compared to SAH (LF: 40 ± 16 nu; HF: 61 ± 33 nu). No differences among groups were found on non-linear HRV markers and endothelial reactivity indexes. CONCLUSIONS: Individuals with T2DM showed impaired levels of cardiac autonomic markers when compared to individuals with SAH and PD, despite of having lower levels of BP and arterial stiffness.

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We propose a procedure suitable for automated synchrogram analysis for setting the threshold below which phase variability between two marker event series is of such a negligible amount that the null hypothesis of phase desynchronization can be rejected. The procedure exploits the principle of maximizing the likelihood of detecting phase synchronization epochs and it is grounded on a surrogate data approach testing the null hypothesis of phase uncoupling. The approach was applied to assess cardiorespiratory phase interactions between heartbeat and inspiratory onset in amateur cyclists before and after 11-week inspiratory muscle training (IMT) at different intensities and compared to a more traditional approach to set phase variability threshold. The proposed procedure was able to detect the decrease in cardiorespiratory phase locking strength during vagal withdrawal induced by the modification of posture from supine to standing. IMT had very limited effects on cardiorespiratory phase synchronization strength and this result held regardless of the training intensity. In amateur athletes training, the inspiratory muscles did not limit the decrease in cardiorespiratory phase synchronization observed in the upright position as a likely consequence of the modest impact of this respiratory exercise, regardless of its intensity, on cardiac vagal control. This article is part of the theme issue 'Advanced computation in cardiovascular physiology: new challenges and opportunities'.

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Cardiac autonomic control is commonly assessed via the analysis of fluctuations of the temporal distance between two consecutive R-waves (RR). Cardiac regulation assessment following high intensity physical exercise is difficult due to RR non-stationarities. The very short epoch following maximal sprint exercise when RR remains close to its lowest value, i.e., the PLATEAU, provides the opportunity to evaluate cardiac regulation from stationary RR sequences. The aim of the study is to evaluate cardiac autonomic control during PLATEAU phase following 60-m maximal sprint and compare the results to those derived from sequences featuring the same length as the PLATEAU and derived from pre-exercise and post-exercise periods. These sequences were referred to as PRE and POST sequences. RR series were recorded in 21 subjects (age: 24.9 ± 5.1 years, 15 men and six women). We applied a symbolic approach due to its ability to deal with very short RR sequences. The symbolic approach classified patterns formed by three RRs according to the sign and number of RR variations. Symbolic markers were compared to more classical time and frequency domain indexes. Comparison was extended to simulated signals to explicitly evaluate the suitability of methods to deal with short variability series. A surrogate test was applied to check the null hypothesis of random fluctuations. Over simulated data symbolic analysis was able to separate dynamics with different spectral profiles provided that the frame length was longer than 10 cardiac beats. Over real data the surrogate test indicated the presence of determinism in PRE, PLATEAU, and POST sequences. We found that the rate of patterns with two variations with unlike sign increased during PLATEAU and in POST sequences and the frequency of patterns with no variations remained unchanged during PLATEAU and decreased in POST compared to PRE sequences. Results indicated a sustained sympathetic control along with an early vagal reactivation during PLATEAU and a shift of the sympathovagal balance toward vagal predominance in POST compared to PRE sequences. Time and frequency domains markers were less powerful because they were dominated by the dramatic decrease of RR variance during PLATEAU.

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Optogenetics is a new approach using light intensity to modulate the electrical activity of excitable cells by the interaction of light-sensitive proteins. This method has been widely and enthusiastically utilized in some fields over the last decade. Localizing a photosensitive protein to a specific place in the membrane of cardiomyocytes at a specific time is essential for most biological processes. In this case, vectors are injected into the circulation to allow them to spread throughout the whole heart. The aim of this protocol is to perform different illumination modes with blue laser to investigate optical control of Langendorff-perfused mice hearts which were systematically injected with adeno-associated virus (AAV) for ChR2(H134R) gene transfer. Electrograms (EGs) and epicardium monophasic action potential (MAP) showed that ChR2 expression in the heart can be flexibly controlled by blue light across different illumination sites with corresponding triggered ectopic rhythm. Illumination intensity, pulse duration, and impulse frequency were associated with the light capture rate. Flexible control of the cardiac rhythm with optogenetics provides an innovative approach to cardiac research and therapy.

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The strength of cardiorespiratory interactions diminishes with age. Physical exercise can reduce the rate of this trend. Inspiratory muscle training (IMT) is a technique capable of improving cardiorespiratory interactions. This study evaluates the effect of IMT on cardiorespiratory coupling in amateur cyclists. Thirty male young healthy cyclists underwent a sham IMT of very low intensity (SHAM, n = 9), an IMT of moderate intensity at 60% of the maximal inspiratory pressure (MIP60, n = 10) and an IMT of high intensity at the critical inspiratory pressure (CIP, n = 11). Electrocardiogram, non-invasive arterial pressure, and thoracic respiratory movement (RM) were recorded before (PRE) and after (POST) training at rest in supine position (REST) and during active standing (STAND). The beat-to-beat series of heart period (HP) and systolic arterial pressure (SAP) were analyzed with the RM signal via a traditional non-causal approach, such as squared coherence function, and via a causal model-based transfer entropy (TE) approach. Cardiorespiratory coupling was quantified via the HP-RM squared coherence at the respiratory rate (K 2 HP-R M), the unconditioned TE from RM to HP (TER M → HP) and the TE from RM to HP conditioned on SAP (TER M → HP| SAP). In PRE condition we found that STAND led to a decrease of TER M → HP| SAP. After SHAM and CIP training this tendency was confirmed, while MIP60 inverted it by empowering cardiorespiratory coupling. This behavior was observed in presence of unvaried SAP mean and with usual responses of the baroreflex control and HP mean to STAND. TER M → HP and K 2 HP- RM were not able to detect the post-training increase of cardiorespiratory coupling strength during STAND, thus suggesting that conditioning out SAP is important for the assessment of cardiorespiratory interactions. Since the usual response of HP mean, SAP mean and baroreflex sensitivity to postural stressor were observed after MIP60 training, we conclude that the post-training increase of cardiorespiratory coupling during STAND in MIP60 group might be the genuine effect of some rearrangements at the level of central respiratory network and its interactions with sympathetic drive and vagal activity.

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The dynamic embodiment of psychological processes is evident in the association of health outcomes, behavioural traits and psychological functioning with Heart Rate Variability (HRV). The dominant high-frequency component of HRV is an index of the central neural control of heart rhythm, mediated via the parasympathetic vagus nerve. HRV provides a potential objective measure of action policies for the adaptive and predictive allostatic regulation of homeostasis within the cardiovascular system. In its support, a network of brain regions (referred to as the 'central autonomic network') maps internal state, and controls autonomic responses. This network includes regions of prefrontal cortex, anterior cingulate cortex, insula, amygdala, periaqueductal grey, pons and medulla. Human neuroimaging studies of neural activation and functional connectivity broadly endorse this architecture, and its link with cardiac regulation at rest and dysregulation in clinical states that include affective disorders. In this review, we appraise neuroimaging research and related evidence for HRV as an informative marker of autonomic integration with affect and cognition, taking a perspective on function and organisation. We consider evidence for the utility of HRV as a metric to inform targeted interventions to improve autonomic and affective dysregulation, and suggest research questions for further investigation.

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Heart failure (HF) is one of the most frequent heart diseases. It is usually characterized with structural and functional cardiac abnormalities followed by dysfunction of autonomic cardiac control. Current methods of heartbeat interval analysis are not capable to differentiate HF patients and some new differentiation of HF patients could be useful in the determination of the direction of their treatment. In this study, we examined potential of the ratio of the short-term and long-term scaling exponents (α 1 and α 2) to separate HF patients with similar level of reduced cardiac autonomic nervous system control and with no significant difference in age, left ventricular ejection fraction (LVEF) and NYHA class. Thirty-five healthy control subjects and 46 HF patients underwent 20 min of continuous supine resting ECG recording. The interbeat interval time series were analyzed using standardized power spectrum analysis, detrended fluctuation analysis method and standard Poincaré plot (PP) analysis with measures of asymmetry of the PP. Compared with healthy control group, in HF patients linear measures of autonomic cardiac control were statistically significantly reduced (p < 0.05), heart rate asymmetry was preserved (C up > C down, p < 0.01), and long-term scaling exponent α 2 was significantly higher. Cluster analysis of the ratio of short- and long-term scaling exponents showed capability of this parameter to separate four clusters of HF patients. Clusters were determined by interplay of presence of short-term and long-term correlations in interbeat intervals. Complementary measure, commonly accepted ratio of the PP descriptors, SD2/SD1, showed tendency toward statistical significance to separate HF patients in obtained clusters. Also, heart rate asymmetry was preserved only in two clusters. Finally, a multiple regression analysis showed that the ratio α 1/α 2 could be used as an integrated measure of cardiac dynamic with complex physiological background which, besides spectral components as measures of autonomic cardiac control, also involves breathing frequency and mechanical cardiac parameter, left ventricular ejection fraction.

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Optogenetics is an innovative method for precise control of biological function, which makes light manipulation displays more advantages than electric energy because of contactless spatial flexibility and cell-to-cell synchronous communication. The aim of this study was to perform different illumination modes with blue laser to investigate optical control of the mice hearts. In this study, we transfected the light sensitive protein ChR2(H134R) into mouse hearts, which were illuminated with a 473 nm laser on the Langendorff apparatus. We recorded all the signals of electrograms (EGs), epicardium monophasic action potential (MAPs) and light output signals to analyze myocardial electrical activity. EGs and MAP showed that ChR2 expression in the heart can be flexibly controlled by blue light across different illumination sites with corresponding triggered ectopic rhythm. Illumination intensity, pulse duration, and impulse frequency were associated with the light capture rate. Continuous illumination with the threshold intensity on the left ventricle had little influence on sinus rhythm and ventricular electrophysiology. Our results support that flexible control of the cardiac rhythm with optogenetics provides an innovative approach to cardiac research and therapy.

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Background: Heart rate variability (HRV) analysis is a clinical tool frequently used to characterize cardiac autonomic status. The aim of this study was to establish normative values for short-term HRV parameters by considering their main determinants in school-aged children. Methods: Five-minute electrocardiograms were taken from 312 non-athlete children (153 boys) at age of 6 to 13 years for computation of conventional time- and frequency-domain HRV parameters. Heart rate (HR), respiratory rate, age, body mass index, and sex were considered as their potential determinants. Multiple regression analysis revealed that HR was the principal predictor of all standard HRV indices. To develop their universal normative limits, standard HRV parameters were corrected for prevailing HR. Results: The HRV correction for HR yielded the parameters which became independent on both sex and HR, and only poorly dependent on age (with small effect size). Normal ranges were calculated for both time- and frequency-domain indices (the latter computed with either fast Fourier transform and autoregressive method). To facilitate recalculation of standard HRV parameters into corrected ones, a calculator was created and attached as a Supplementary Material that can be downloaded and used for both research and clinical purposes. Conclusion: This study provides HRV normative values for school-aged children which have been developed independently of their major determinants. The calculator accessible in the Supplementary Material can considerably simplify determination if HRV parameters accommodate within normal limits.

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In most clinical cases, left ventricular hypertrophy (LVH) occurs over time from persistent cardiac stress. At the molecular level, this results in both transient and long-term changes to metabolic, sarcomeric, ion handling, and stress signaling pathways. Although this is initially an adaptive change, the mechanisms underlying LVH eventually lead to maladaptive changes including fibrosis, decreased cardiac function, and failure. Understanding the regulators of long-term changes, which are largely driven by transcriptional remodeling, is a crucial step in identifying novel therapeutic targets for preventing the downstream negative effects of LVH and treatments that could reverse or prevent it. The development of effective therapeutics, however, will require a critical understanding of what to target, how to modify important pathways, and how to identify the stage of pathology in which a specific treatment should be used.

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