Influence of Running Stride Frequency in Heart Rate Variability Analysis During Treadmill Exercise Testing

Spectral analysis of heart rate variability (HRV) is a widely accepted approach for assessment of cardiac autonomic function and its relationship to numerous disorders and diseases. As a rule, the non-parametric methods for HRV spectral analysis are tested using the integral pulse frequency modulation (IPFM) model. However, published results with simulated HRV signals show differences requiring further development of the existing methods. With the aim of improving estimation accuracy, an entirely IPFM-based method for HRV analysis is investigated. According to this method, the spectra are computed by finding the least squares solution of two matrix equations that are derived using the IPFM model and involve irregular samples of a signal representing the HRV. The method is validated with various synthesised signals (in all tests, the relative errors of the power estimates at the modulating frequencies are within 3%, and the relative power of the spurious terms is less than 0.8% only) and is furthermore applied to the spectral analysis of R-R interval series obtained from diabetic children. The results, with simulated and real HRV signals, show that the developed method yields very accurate estimations of the spectral region below half the mean heart rate. Moreover, it allows the detection and assessment of certain genuine modulating components beyond the traditional frequency limit of the HRV spectra.

Background: The integrity of the autonomic nervous system (ANS) is essential for keeping physiological processes stable, even under stress. Since there is growing interest in heart rate variability (HRV) analysis for the noninvasive assessment of the ANS in sickle cell anemia (SCA) patients, we studied the behavior of the ANS in the presence of a stressor that simulates daily-life multitasking, the Glittre ADL test (GA-T). Objectives: To evaluate the involvement of the ANS using HRV in adults with SCA during the GA-T and to quantify the strength of the correlation of HRV with lung and muscle functions. Methods: In this cross-sectional study, 16 adults with SCA and 12 healthy controls without sickle cell disease underwent HRV assessment during the GA-T, pulmonary function tests (spirometry, diffusing capacity for carbon monoxide (DLCO), and respiratory muscle testing). Peripheral muscle function [handgrip strength (HGS) and quadriceps strength (QS)] were also measured. Results: Compared to the healthy controls, adults with SCA showed lower HRV, with worse parasympathetic modulation due to reductions in the following indices: the root-mean-square difference of successive normal iRRs (iRR) (RMSSD); the percentage of pairs of consecutive iRRs whose difference is > 50 m (pNN50); the high-frequency component of heart rate variability (HF); and the standard deviation of instantaneous beat-to-beat variability (SD1) (P < 0.001 for all). Compared to healthy controls, individuals with SCA showed greater sympathovagal imbalance (higher ratio between low-frequency and HF components) and lower complexity of the ANS (lower approximate entropy). The GA-T time was correlated with parasympathetic activity indices: RMSSD (rs = -0.650, P < 0.01); pNN50 (rs = -0.932, P < 0.0001), HF (rs = -0.579, P < 0.01), and SD1 (rs = -0.814, P < 0.0001). Correlations between parasympathetic activity indices and DLCO, HGS, and QS measures were also significant. Conclusions: Adults with SCA have low HRV, with low parasympathetic activity, sympathovagal imbalance, and abnormal ANS complexity. In addition, lower HRV is associated with longer GA-T time, greater impairment of pulmonary diffusion, and greater muscle strength dysfunction.

Intradialytic hypotension, a major source of morbidity during hemodialysis and ultrafiltration, is often accompanied by paradoxical bradycardia. Relatively little is known about the sequential changes in autonomic nervous system activity up to and during the hypotensive episode. Continuous, beat-to-beat measurements of BP and heart rate were made during hemodialysis in patients prone (n = 8) and not prone (n = 11) to develop intradialytic hypotension. Off-line spectral analysis of heart rate variability (HRV) was performed to assess changes in autonomic nervous system activity during dialysis sessions both with and without hypotension. The low frequency (LF) component of HRV is thought to correlate with sympathetic nervous system activity, the high frequency (HF) component with that of the parasympathetic nervous system. In the sessions not complicated by symptomatic hypotension (n = 26), mean arterial BP (MAP) hardly fell, whereas heart rate increased from 77 +/- 2 to 89 +/- 5 bpm (P < 0.05). The LF component of HRV increased from 45.2 +/- 5.0 normalized units (nu) to 59.9 +/- 4.9 nu (P < 0.05), whereas the HF component fell from 54.8 +/- 5.0 to 40.2 +/- 4.4 nu (P < 0.05). These changes agree with compensatory baroreflex-mediated activation of the sympathetic nervous system (and suppressed parasympathetic activity) during ultrafiltration-induced intravascular volume depletion. In the sessions complicated by severe symptomatic hypotension (n = 22), the changes in heart rate and the results of spectral analysis of HRV were similar to those reported above up to the moment of sudden symptomatic (nausea, vomiting, dizziness, cramps) hypotension, whereas MAP had already fallen gradually from 94 +/- 3 to 85 +/- 3 mmHg (P < 0.05). The sudden further reduction in MAP (to 55 +/- 2 mmHg, P < 0.02) was invariably accompanied by bradycardia (heart rate directly before hypotension 90 +/- 2 bpm, during hypotension 69 +/- 3 bpm, P < 0.002). The LF component of HRV fell from 62.8 +/- 4.6 nu directly before to 40.0 +/- 3.7 nu (P < 0.05) during hypotension, whereas the HF component increased from 37.9 +/- 4.7 to 60.3 +/- 3.7 nu (P < 0.05). These findings agree with activation of the cardiodepressor reflex, involving decreased sympathetic and increased parasympathetic nervous system activity, respectively. These findings indicate that activation of the sympatho-inhibitory cardiodepressor reflex (Bezold-Jarisch reflex), which is a physiologic response to a critical reduction in intravascular volume and cardiac filling, is the cause of sudden intradialytic hypotension.

Integral pulse frequency modulation model driven by sympathovagal dynamics: Synthetic vs. real heart rate variability

It has been shown that heart rate variability is decreased in patients with congestive heart failure and that depressed heart rate variability is associated with a propensity to ventricular arrhythmias. Little is known, however, about heart rate variability in patients with both congestive heart failure and ventricular arrhythmias. Spectral heart rate variability was analysed from 24 hour ambulatory electrocardiograms in 15 controls, 15 patients with non-sustained ventricular tachycardia associated with clinically normal hearts (NHVT group), and 40 patients with congestive heart failure (CHF group) secondary to either ischaemic heart disease (n = 15) or idiopathic dilated cardiomyopathy (n = 25). Of the 40 patients with congestive heart failure 15 had no appreciable ventricular arrhythmias (ventricular extrasystoles < 10 beats/h and no salvos) and formed the CHF-VA- group. Another 15 patients with congestive heart failure and non-sustained ventricular tachycardia formed the CHF-NSVT group. Heart rate variability was significantly lower in the CHF group than in controls (mean (SD) total frequency 23 (12) v 43 (13) ms; low frequency 12 (8) v 28 (9) ms; high frequency 8 (5) v 14 (7) ms; p < 0.001). The differences in heart rate variability between controls and the NHVT group, between ischaemic heart disease and dilated cardiomyopathy, and between the CHF-VA- and CHF-NSVT groups were not significant. In the CHF group heart rate variability was significantly related to left ventricular ejection fraction but not associated with ventricular arrhythmias. The frequency of ventricular extrasystoles was significantly related to the high frequency component of heart rate variability (r = 0.54, p < 0.05) in the NHVT group. Stepwise multiple regression analysis showed that in the CHF group, heart rate variability was predominantly related to left ventricular ejection fraction (p < 0.05). There was no significant difference in heart rate variability between survivors (n = 34) and those who died suddenly (n = 6) at one year of follow up in the CHF group. In patients with congestive heart failure, heart rate variability is significantly decreased. The depressed heart rate variability is principally related to the degree of left ventricular impairment and is independent of aetiology and the presence of ventricular arrhythmias. The data suggest that analysis of heart rate variability does not help the identification of patients with congestive heart failure at increased risk of sudden death.

We read with great interest the arguments presented by Coote & White (2015) in favour of the traditional view that exercise training decreases resting heart rate by an increase in the tonic discharge of the vagal nerves. However, we are not persuaded. Coote & White (2015) quote Maciel et al. (1985); however, Maciel et al. (1985) showed that the intrinsic heart rate of trained athletes remains lower after full vagal nerve block. Although Ordway et al. (1982) reported that there was no training-induced bradycardia in six cardiac-denervated dogs, there is evidence to the contrary: Kavanagh et al. (1988) reported that in eight highly compliant cardiac transplant patients (with no evidence of cardiac reinnervation) there was. Coote & White (2015) state that the high frequency (HF) component of heart rate variability (HRV) is a robust surrogate for vagal tone and the increase in the HF component in athletes is evidence of increased vagal tone. However, we have argued that HRV cannot be used in any simple way to measure autonomic nerve activity (Monfredi et al. 2014). Our arguments are based on those of Zaza & Lombardi (2001), who showed that the HF component (like other measures of HRV) is highly sensitive to the heart rate. For example, on training Al-Ani et al. (1996) observed a 12 beats min–1 decrease in the resting heart rate (69 decreased to 57 beats min–1) and a 1.5-fold increase in the HF component, whereas Zaza & Lombardi (2001) calculated that a 10 beats min–1 decrease (70 to 60 beats min–1) will cause a 3-fold increase simply because of the decrease in heart rate alone. Coote & White (2015) mention the sensitivity of the baroreceptor–heart rate reflex; this is a commonly used index of autonomic balance, but this too relies on HRV and is therefore flawed (Zaza & Lombardi (2001). The data from Danson & Paterson (2003) quoted by Coote & White (2015) showing a training-induced upregulation of NOS-1 in intracardiac cholinergic ganglia are fascinating; the data indicate an improvement in vagal neurotransmission but this does not prove it is responsible for the training-induced bradycardia. For example, our own data demonstrate a training-induced reduction in the sinus node of mRNA for the M2 receptor and Kir3.1, Kir3.4, HCN4, Cav1.2 and Cav1.3 channels (responsible for the ACh-sensitive currents IK,ACh, If and ICa,L) (D'Souza et al. 2014); these changes potentially reduce the sensitivity of the sinus node to vagal tone. Overall, given that direct recording of cardiac vagal activity is currently unfeasible, the available evidence tips the balance in favour of electrophysiological remodelling of the sinus node to explain the resting bradycardia in athletes. A challenge for neuroscientists is to measure vagal activity to the sinus node directly and not rely on questionable surrogates. Readers are invited to give their views on this and the accompanying CrossTalk articles in this issue by submitting a brief (250 word) comment. Comments may be submitted up to 6 weeks after publication of the article, at which point the discussion will close and the CrossTalk authors will be invited to submit a ‘Last Word’. Please email your comment to jphysiol@physoc.org. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article. None declared.

Background: Total spinal anesthesia (TSA) after injections of local anesthetics into the intrathecal space during epidural anesthesia is not rare. TSA anesthetizes cranial nerves and peripheral nerves, causes specific circulatory disturbances related to autonomic imbalance. Spectral analysis of heart rate variability (HRV) and blood pressure variability (BPV) provide a dynamic assessment of sympathetic and parasympathetic tone. Cross-spectral analysis has been used to emphasize this dynamic baroreflex control of HR as a frequency-dependent phenomenon and allows an assessment of baroreflex function. To examine the effects of TSA on the autonomic nervous system, we used spectral and cross-spectral analytic methods. Methods: We investigated 14 rats before and after TSA. Power spectral densities of blood pressure (BP) and heart rate (HR) were estimated by fast Fourier transform. To evaluate the effect of TSA on baroreflex function, the cross spectral gain, phase, and coherence between beat-to-beat BP and HR signals were calculated by using transfer function analysis. Results: With the onset of TSA, BP and HR significantly decreased. TSA significantly decreased the low frequency (LF) and high frequency (HF) components of HRV and BPV. Baroreflex sensitivity (BRS) obtained from transfer function gain between these variables was significantly decreased. Conclusions: TSA reduces the LF and HF components of HRV and BPV. These suggest that TSA in rats decreases both parasympathetic and sympathetic drive. Moreover, the decrease in BRS suggests impairment of cardiac baroreflex buffering function during TSA.

Purpose: Heart rate variability (HRV) has been used for decades as a tool for measuring systemic health through the autonomic nervous system (ANS). The purpose of this paper was to examine the literature on HRV and to investigate its use in the long COVID (LC) population. Summary of Key Points: Measurement devices vary significantly in their validity and reliability when compared with the gold standard of electrocardiogram (ECG). Wrist and hand devices typically demonstrate diminished validity for capturing HRV signal, while chest strap devices often exhibit high reliability and validity. Lack of transparency in third-party software used to clean and analyze HRV data makes assessment for accuracy problematic. This is of particular concern when single beat miscalculations can result in significantly dissimilar output. The conditions under which HRV data are collected, such as natural or paced breathing, activity intensity, and patient position, can dramatically affect HRV readings. While some individual HRV metrics have consistently been shown to reflect certain components of the ANS, such as high-frequency power as a measure of parasympathetic function, the meaning of other metrics is less clear. Recommendations for Clinical Practice: Heart rate variability can be an extraordinarily valuable tool to measure systemic function. However, it is recommended that clinicians be judicious in the interpretation of HRV, considering inconsistencies in presentation. This is particularly true in LC, where individual HRV varies greatly. In all populations, clinicians should consider using valid devices to assess trends in HRV values over time, along with consideration of unique physical conditions.

This paper introduces an efficient algorithm to reconstruct heart rate signal based on an integral pulse frequency modulation (IPFM) model. The heart rate signal was reconstructed by the summation of a set of sinc functions with different weights, whose value could be determined from the IPFM process. Simulation study demonstrated that the signal reconstructed by the proposed method would preserve high frequency component with less distortion than the popular derivative of cubic spline interpolation (DCSI) method. When applied to the spectral analysis of heart rate variability (HRV) of simulated heart rate signal, the proposed method achieved smaller bias than the DCSI method. Therefore, the proposed method would be beneficial for the reconstruction of heart rate signal and the relevant spectral analysis of HRV in the future.

Cardiovascular reflexes during anesthesia induction and tracheal intubation in elderly patients: The influence of thoracic epidural anesthesia

Many patients with severe obstructive sleep apnea (OSA) do not complain of excessive daytime sleepiness (EDS), possibly due to increased sympathetic nervous activity (SNA) and accompanying heightened alertness. We hypothesized that in patients with OSA, those without subjective EDS (Epworth Sleepiness Scale, ESS score < 11) would have higher very low frequency (VLF) heart rate variability (HRV) during sleep, reflecting greater sympathetic heart rate modulation than patients with an ESS score ≥ 11. Patients with severe OSA (AHI ≥ 30: 26 with and 65 without heart failure) were divided into those with and without EDS. Heart rate (HR) signals were acquired in stage 2 sleep during periods of recurrent apneas and hypopneas and submitted to coarse graining spectral analysis, which extracts harmonic, neurally mediated contributions to HRV from total spectral power. Because the apnea-hyperpnea cycle entrains muscle SNA at VLF (0 to 0.04 Hz), VLF power was our principal between-group comparison. Subjects without EDS had higher harmonic VLF power (944 ± 839 vs 447 ± 461 msec(2), p = 0.003) than those with EDS, irrespective of the presence or absence of heart failure (1218 ± 944 vs 426 ± 299 msec(2), p = 0.043, and 1029 ± 873 vs 503 ± 533 msec(2), p = 0.003, respectively). ESS scores correlated inversely with VLF power in all (r = -0.294, p = 0.005) and in heart failure subjects (r = -0.468, p = 0.016). Patients with severe OSA but without EDS have higher VLF-HRV than those with EDS. This finding suggests that patients with severe OSA but without EDS have greater sympathetic modulation of HRV than those with EDS that may reflect elevated adrenergically mediated alertness. Taranto Montemurro L; Floras JS; Picton P; Kasai T; Alshaer H; Gabriel JM; Bradley TD. Relationship of heart rate variability to sleepiness in patients with obstructive sleep apnea with and without heart failure.

Physiology of brain death is characterized by major disturbances of autonomic nervous system (ANS) activity which can lead to graft dysfunction. These findings exhibit the importance of early diagnosis of brain death to improve transplantation outcome. The aim of this prospective study was to assess whether heart rate variability (HRV) analysis, a noninvasive method to investigate ANS activity in comatose patients, could achieve this goal. A total of 14 brain-injured patients were included in the study as soon as they exhibited the clinical signs of imminent brain death. The electrocardiogram was then recorded from two leads with a Holter digital monitor. The clinical diagnosis of brain death was considered after an autonomic storm had occurred. HRV was assessed from 6 h before to 6 h after brain death in both time domain and spectral analysis, estimating either global ANS activity (index of variability, total power), parasympathetic activity (percentage of delta of R-R interval >50 ms, root mean square for successive interval differences, LnHF) or sympathetic activity (LnLF). Hourly averages of these variables were compared by using one-way analysis of variance. To assess whether HRV could per se diagnose brain death, receiver operating characteristic curves were generated for total power, root mean square for successive interval differences, and LnHF. We observed, for 6 h before brain death, a progressive extinction of the influence of the ANS on cardiovascular regulation. There was no activity in the two components of the ANS as soon as brain death occurred. HRV analysis appeared to be a very sensitive but a less specific method of diagnosing brain death. A total of 14 brain-injured patients with the clinical criteria of imminent brain death were enrolled for electrocardiogram recording and heart rate variability analysis (a noninvasive method to investigate autonomic nervous system activity). For 6 h before brain death, we observed a progressive extinction of autonomic nervous system activity which was not present as soon as brain death was clinically evoked.

Age-adjusted normal confidence intervals for heart rate variability in healthy subjects during head-up tilt

Heart rate variability (HRV) analysis, which is providing information about the autonomic nervous system with noninvasive method, performed with using digitized electrocardiogram records. In this study, whether HRV analysis can be done from heart sounds (which are recorded with electronic stethoscopes) has been investigated. For this purpose, an algorithm has been developed for detecting the consecutive heart time period from simultaneously recorded heart sounds and ECG. Some standard HRV parameters are calculated and compared from the HRV derived from ECG and heart sound signals. The experimental results show that, both HRV parameters derived from the heart sounds while the resting position and the ECG are very close. In conclusion, they can be used in HRV analysis.

The aim of this study was to investigate the usefulness of heart rate variability (HRV) and urinary catecholamines (CA) as objective indices of heat stress effect. We examined physiological responses, subjective symptoms, HRV and urinary CA to evaluate the effect of heat exposure on the autonomic nervous system. Six healthy male students volunteered for this study. They were exposed on different days to either a thermoneutral condition at wet bulb globe temperature (WBGT) 21 degrees C, or a heated condition at WBGT 35 degrees C for 30 min, while seated on a chair. In the thermoneutral condition, differences of all parameters between the values before and after 30 min exposure were not statistically significant. In the heated condition, heart rate, body temperature and scores for subjective symptoms (feverishness, sweating, mood, and face flushing) significantly increased after 30 min exposure (p<0.05). Also, the high frequency component (HF%) of HRV significantly decreased and the low frequency/high frequency (LF/HF) ratio of HRV significantly increased after 30 min exposure to the heated condition (p<0.05). There were no significant differences between the amounts of urinary CA before and after the 30 min exposures; however, the norepinephrine amount after 30 min exposure to the heated condition was significantly greater than that of the thermoneutral condition (p<0.05). The heat exposure (WBGT 35 degrees C) induced activation of the sympathetic nervous system and a withdrawal of the parasympathetic nervous system. These findings coincide with observed changes of heart rate, body temperature and subjective symptoms. It is suggested that HRV (HF% and LF/HF ratio) and urinary norepinephrine may be useful objective indices of heat stress; HRV seems to be more sensitive to heat stress than urinary CA.