Cardiac Vagal Activity Research Articles

P-1352 - Improvement of the link between cardiac vagal influence and delta sleep in sahs by long-term nCPAP treatment

Introduction Numerous cardiovascular events are related to sleep apnea-hypopnea syndrome (SAHS). Several studies reported, in SAHS patients, increased cardiac sympathic influence and altered link between cardiac vagal activity and delta sleep EEG. Nevertheless, short-term nasal CPAP (nCPAP) treatment regulates cardiac sympatho-vagal balance and sleep architecture. Objectives We tested that long-term nCPAP treatment improves the link between cardiac vagal influence and delta sleep EEG across the night. Aims Long-term nCPAP treatment could improve the link between heart rate variability (HRV) and sleep to prevent occurrence of cardiovascular events. Methods Cardiac activity and sleep of 8 middle-aged men suffering from SAHS were recorded before and after at least 6 months of nCPAP treatment. They were matched for sex, age, caffeine, nicotine and alcohol consumption with 14 healthy men. All subjects were free of somatic and psychiatric disorders as well as medication. Sleep architecture, spectral components of HRV and delta power band were calculated across the first three NREM-REM cycles as well as a coherence analysis between cardiac vagal influence and delta sleep EEG. Results AHI was 63.5 ± 22.9 vs 5.5 ± 4.4 events/hour after 47 ± 34 months of nCPAP treatment (mean± standard deviation). Awake, NREM and REM sleep durations were similar between groups as well as spectral HRV components. Coherence analysis revealed decreased gain value for untreated patients in comparison to controls while difference disappeared with nCPAP treatment. Conclusions Long-term nCPAP treatment improves the link between cardiac vagal influence and delta sleep even in the absence of altered HRV.

Modulation of cardiopulmonary depressor reflex in nucleus ambiguus by electroacupuncture: roles of opioids and γ-aminobutyric acid.

Stimulation of cardiopulmonary receptors with phenylbiguanide (PBG) elicits depressor cardiovascular reflex responses, including decreases in blood pressure and heart rate mediated in part by the brain stem parasympathetic cardiac neurons in the nucleus ambiguus (NAmb). The present study examined NAmb neurotransmitter mechanisms underlying the influence of electroacupuncture (EA) on the PBG-induced hypotension and bradycardia. We hypothesized that somatic stimulation during EA modulates PBG responses through opioid and γ-aminobutyric acid (GABA) modulation in the NAmb. Anesthetized and ventilated cats were studied during repeated stimulation with PBG or cardiac vagal afferents while low-frequency EA (2 Hz) was applied at P5-6 acupoints overlying the median nerve for 30 min and NAmb neuronal activity, heart rate, and blood pressure were recorded. Microinjection of kainic acid into the NAmb attenuated the PBG-induced bradycardia from -60 ± 11 to -36 ± 11 beats/min. Likewise, EA reduced the PBG-induced depressor and bradycardia reflex by 52 and 61%, respectively. Cardiac vagal afferent evoked preganglionic cellular activity in the NAmb was reduced by EA for about 60 min. Blockade of opioid or GABA(A) receptors using naloxone and gabazine reversed the EA-related modulation of the evoked cardiac vagal activity by 73 and 53%, respectively. Similarly, naloxone and gabazine reversed EA modulation of the negative chronotropic responses from -11 ± 5 to -23 ± 6 and -13 ± 4 to -24 ± 3 beats/min, respectively. Thus EA at P5-6 decreases PBG evoked hypotension and bradycardia as well as the NAmb PBG-sensitive preganglionic cardiac vagal outflow through opioid and GABA neurotransmitter systems.

Autonomic Nervous System Activation During Social Cognition Tasks in Patients With Schizophrenia and Their Unaffected Relatives

The objective of the study was to determine whether patients with schizophrenia and their unaffected first-degree relatives have abnormal autonomic nervous system (ANS) responses to social cognition tasks. Social cognition impairments are significant in schizophrenia. ANS activity has been shown to be abnormal in schizophrenia patients, and some of the abnormalities seem to be shared by patients' unaffected relatives. Heart rate variability (HRV) was measured at rest and during social cognition tasks, in patients with schizophrenia, their nonpsychotic first-degree relatives, and matched healthy controls (n=19 in each group). Social cognition tasks induced a shortening of the RR interval in unaffected relatives, but not in patients. Social cognition tasks generated decreases in high-frequency (indicating cardiac vagal activity) and low-frequency (reflecting predominantly sympathetic activity) HRV in patients. In relatives, the decrease occurred in the high-frequency component only. Low-frequency HRV was higher in patients during a theory of mind task than a control task. These changes were not observed in the controls. Social cognitive tasks induce a pattern of peripheral autonomic activity different from that seen in generic arousal responses, and this pattern is abnormal in schizophrenia patients. Autonomic abnormalities in unaffected first-degree relatives seem restricted to the parasympathetic division of the ANS.

Restrained eating is related to accelerated reaction to high caloric foods and cardiac autonomic dysregulation

Cognitive bias to food-cues and cardiac autonomic dysregulation have both been related to disordered eating behavior in previous research. The present study investigated two possible measures of self-regulatory ability in restrained eaters: resistance to distractor interference and vagal-cardiac control. Young women (N=47) performed a flanker task involving high caloric food-cues or neutral pictures. Vagal-cardiac activity was calculated from baseline heart rate recordings at rest. Restrained eaters did not differ from unrestrained eaters in resistance to distractor interference. However, restrained eaters showed shorter reaction times to high-calorie food-cues as compared to neutral pictures than unrestrained eaters. This attentional bias was further related to low dieting success. Moreover, restrained eating was associated with low parasympathetic activation and sympathovagal imbalance, independent of current body mass. Both attentional bias and cardiac autonomic dysregulation were related to self-reported weight fluctuations. Results are discussed in terms of possible adverse consequences of weight cycling in young women and low self-regulatory ability in restrained eaters.

Central command: control of cardiac sympathetic and vagal efferent nerve activity and the arterial baroreflex during spontaneous motor behaviour in animals

Feedforward control by higher brain centres (termed central command) plays a role in the autonomic regulation of the cardiovascular system during exercise. Over the past 20 years, workers in our laboratory have used the precollicular-premammillary decerebrate animal model to identify the neural circuitry involved in the CNS control of cardiac autonomic outflow and arterial baroreflex function. Contrary to the traditional idea that vagal withdrawal at the onset of exercise causes the increase in heart rate, central command did not decrease cardiac vagal efferent nerve activity but did allow cardiac sympathetic efferent nerve activity to produce cardiac acceleration. In addition, central command-evoked inhibition of the aortic baroreceptor-heart rate reflex blunted the baroreflex-mediated bradycardia elicited by aortic nerve stimulation, further increasing the heart rate at the onset of exercise. Spontaneous motor activity and associated cardiovascular responses disappeared in animals decerebrated at the midcollicular level. These findings indicate that the brain region including the caudal diencephalon and extending to the rostral mesencephalon may play a role in generating central command. Bicuculline microinjected into the midbrain ventral tegmental area of decerebrate rats produced a long-lasting repetitive activation of renal sympathetic nerve activity that was synchronized with the motor nerve discharge. When lidocaine was microinjected into the ventral tegmental area, the spontaneous motor activity and associated cardiovascular responses ceased. From these findings, we conclude that cerebral cortical outputs trigger activation of neural circuits within the caudal brain, including the ventral tegmental area, which causes central command to augment cardiac sympathetic outflow at the onset of exercise in decerebrate animal models.

Medetomidine, an .ALPHA.2-Adrenergic Agonist, Activates Cardiac Vagal Nerve Through Modulation of Baroreflex Control

Although α(2)-adrenergic agonists have been reported to induce a vagal-dominant condition through suppression of sympathetic nerve activity, there is little direct evidence that they directly increase cardiac vagal nerve activity. Using a cardiac microdialysis technique, we investigated the effects of medetomidine, an α(2)-adrenergic agonist, on norepinephrine (NE) and acetylcholine (ACh) release from cardiac nerve endings. A microdialysis probe was implanted into the right atrial wall near the sinoatrial node in anesthetized rabbits and perfused with Ringer's solution containing eserine. Dialysate NE and ACh concentrations were measured using high-performance liquid chromatography. Both 10 and 100µg/kg of intravenous medetomidine significantly decreased mean blood pressure (BP) and the dialysate NE concentration, but only 100µg/kg of medetomidine enhanced ACh release. Combined administration of medetomidine and phenylephrine maintained mean BP at baseline level, and augmented the medetomidine-induced ACh release. When we varied the mean BP using intravenous administration of phenylephrine, treatment with medetomidine significantly steepened the slope of the regression line between mean BP and log ACh concentration. Medetomidine increased ACh release from cardiac vagal nerve endings and augmented baroreflex control of vagal nerve activity.

Differential effects of metoprolol and atenolol to neuropeptide Y blockade in coronary artery disease

Objective. To explore possible differential effects between metoprolol and atenolol in patients with coronary artery disease. Design. The study was randomized, double blind, two-way crossover with the Y1 antagonist AR-H040922 given as IV infusion for 2 h or placebo. Most patients were treated with metoprolol or atenolol. In a post hoc analysis we compared the hemodynamic response to exercise of the Y1 antagonist in patients on metoprolol (n = 16) and atenolol (n = 5), and assessed respiratory sinus arrhythmia (RSA), an indirect measurement of cardiac vagal activation, in the placebo phase in patients on metoprolol (n = 26) and on atenolol (n = 24). Results. 1) The Y1 antagonist reduced the systolic blood pressure rise during and after exercise during atenolol, but not during metoprolol, while heart rate and maximal load were similar with the two beta-blockers and not affected by the Y1 antagonist. 2) At equal heart- and respiration-rate 7–8 min after exercise the RSA was significantly lower in atenolol than in metoprolol patients, while no difference was seen at rest before exercise. Conclusion. These findings from this hypothesis generating study indicate that peripheral effects of NPY contribute less to cardiovascular stress reactions in patients on metoprolol than in those on atenolol.

Effects of short-term food deprivation on interoceptive awareness, feelings and autonomic cardiac activity

The perception of internal bodily signals (interoception) plays a relevant role for emotion processing and feelings. This study investigated changes of interoceptive awareness and cardiac autonomic activity induced by short-term food deprivation and its relationship to hunger and affective experience. 20 healthy women were exposed to 24h of food deprivation in a controlled setting. Interoceptive awareness was assessed by using a heartbeat tracking task. Felt hunger, cardiac autonomic activity, mood and subjective appraisal of interoceptive sensations were assessed before and after fasting. Results show that short-term fasting intensifies interoceptive awareness, not restricted to food cues, via changes of autonomic cardiac and/or cardiodynamic activity. The increase of interoceptive awareness was positively related to felt hunger. Additionally, the results demonstrate the role of cardiac vagal activity as a potential index of emotion related self-regulation, for hunger, mood and the affective appraisal of interoceptive signals during acute fasting.

Brain frontal cortical activation is related to cardiac vagal activity in the depressive elderly: A pilot study

Brain frontal cortical activation is related to cardiac vagal activity in the depressive elderly: A pilot study

Very low frequency oscillations in the power spectra of heart rate variability during dry supine immersion and exposure to non-hypoxic hypobaria

The origin of very low frequency (VLF) oscillations in the power spectra of heart rate variability (HRV) is controversial with possible mechanisms involving thermoregulation and/or renin-angiotensin-aldosterone system. Recently, a major contribution from vagal influences has been suggested. The present study investigated the behaviour of VLF (0.004–0.040 Hz) components of HRV power spectra in a group of healthy male volunteers during their exposure to (1) dry, supine, immersion in thermo-neutral water for 6 h (n = 7) and (2) non-hypoxic hypobaria (breathing 40–60% oxygen at 15 000′ simulated in a decompression chamber) for 5 h (n = 15). The two manoeuvres are established to increase vagal outflow. During both the manoeuvres, all the frequency domain indices of HRV exhibited a significant increase. Increase in HRV was much more than that in the R-R interval. At 6 h of immersion, the R-R interval increased by ∼15% but the total power increased ∼fourfold. Similarly, at 5 h of exposure to hypobaria, total power increased ∼twofold with a very modest increase in an R-R of ∼9%. Increase in spectral power was appreciable even after normalization with mean R-R2. Increase in VLF during immersion was more than reported during enalaprilat blockade of angiotensin convertase enzyme. Plasma renin activity did not vary during hypobaria. There was a significant increase in pNN50, an established marker of cardiac vagal activity. Centre frequencies of the spectra and slope (β) of the relation between log(PSD) and log(frequency) did not change. Results were supportive of the notion that the parasympathetic system is pre-potent to influence slower (than respiratory) frequency components in HRV spectrum. Additionally, such an effect was without a change in the time constant of effector responses or pacemaker frequencies of VLF and LF periodicities and HRV was not a simple linear surrogate for cardiac vagal effects. An invariance of spectral exponent (β) ruled out contamination of VLF and LF spectra from fractal power as an alternate explanation.

Sympatho-vagal interaction in the recovery phase of exercise

Reciprocal autonomic regulation occurs during incremental exercise. We hypothesized that sympatho-vagal interplay may become altered after exercise because of the differences in recovery patterns of autonomic arms. The cardiac vagal activity was assessed by measurement of beat-to-beat R-R interval oscillations using a Poincaré plot method (SD1), and muscle sympathetic nervous activity (MSNA) was measured from peroneus nerve by a microneurography technique during and after exercise in 16 healthy subjects. Autonomic regulation was compared between the rest and after exercise (3·5 ± 1·0 min after exercise) at equal heart rates (HR). SD1 was at the equal level at the recovery phase (40 ± 21 ms) compared to the resting condition (38 ± 16 ms, P = ns) at comparable HR (57 ± 10 for both). MSNA was higher at the recovery phase (40 ± 19 burst per 100 heartbeats) than at rest (25 ± 13 burst per 100 heartbeats, P<0·0001). The difference of MSNA activity between rest and late recovery phase had a strong positive correlation with the difference in SD1 (r = 0·78, P<0·001) at equal HRs. Subjects who have a higher sympathetic activity in the recovery phase of exercise have a more augmented cardiac vagal activity resulting in an accentuated sympatho-vagal outflow. The altered autonomic interaction observed here may partly explain the clustering of various cardiovascular events to the recovery phase of exercise.

Delta Entropy of Heart Rate Variability Along with Deepening Anesthesia

Conventional time and frequency domain measures of heart rate variability (HRV) are strongly influenced by anesthetic drugs, and are therefore not able to detect subtle changes in HRV, even during light anesthesia. Approximate entropy of R-R intervals is an HRV measure that has a tendency to decrease during anesthesia, but it is severely compromised by low-frequency variations of the signal. However, the negative effect of the low-frequency variations can be eliminated by differentiating the R-R interval tachogram before analysis. We designed this study to investigate characteristics of a novel HRV measure, named δ entropy (dEn), during deepening anesthesia. Eight healthy subjects were anesthetized with sevoflurane and 8 with propofol in a stepwise manner using 3 escalating concentrations (2%, 3%, and 4% end-tidal concentration and 7.4 ± 1.7, 12.3 ± 2.6, and 18.3 ± 5.0 μg/mL plasma concentration, respectively) at 30-minute intervals. A third group of 8 subjects received a supramaximal IV dose of glycopyrrolate without anesthesia to examine the effect of cardiac vagal activity on dEn. We computed dEn at baseline, during each step of anesthesia and during the anticholinergic blockade. The dEn decreased along with deepening levels of sevoflurane and propofol anesthesia up to 33% (95% confidence interval [CI] 21%-44%) and 38% (95% CI 28%-48%), respectively. At each anesthesia level, dEn differed significantly (P < 0.05) from that measured at the preceding level, similarly in both the sevoflurane and propofol groups. Parasympathetic blockade by glycopyrrolate was found to decrease dEn by 17% (95% CI 6%-28%). The dEn is a novel HRV measure able to detect subtle sympathetic- and parasympathetic-mediated alterations in HRV both during deepening levels of sevoflurane and propofol anesthesia and during exceedingly deep anesthesia.

Acupuncture to Danzhong but not to Zhongting increases the cardiac vagal component of heart rate variability

There is currently no convincing evidence that acupuncture has any specific effects on autonomic nervous function as assessed by heart rate variability (HRV). We examined whether the stimulation of neighboring acupunctural points, Danzhong (CV17) and Zhongting (CV16) on the anterior median line of the thorax, induced different effects on HRV. In 14 healthy males, epifascial acupunctural stimulation (single instantaneous needle stimulation on the fascial surface without producing De-Qi sensation) was performed at CV17 and CV16 on different days in a clinical study utilizing a cross-over design. We found that the stimulation of CV17, but not of CV16, decreased the heart rate ( P = 0.01, repeated measures ANOVA) and increased the power of the high-frequency component of the HRV, an index of cardiac vagal activity ( P = 0.01). The low-frequency to high-frequency ratio, an index of sympathetic activity showed no significant changes for either point. Our observations could not be explained as either nonspecific or psychological/placebo effects of needle stimulation. This study provides strong evidence for the presence of a specific acupunctural point that causes the modulation of cardiac autonomic function.

Vagus Nerve Stimulation in Heart Failure

Despite significant progress in heart failure (HF) therapeutics in the past quarter century, HF remains a major cause of illness and death. And the disease prevalence is rising with the rapidly aging of the population. Thus, new treatments are needed to halt and reverse the devastating consequences of HF. Autonomic imbalance, characterized by sympathetic activation and vagal withdrawal, is involved in the development and progression of HF. Previous clinical studies indicate that diminished cardiac vagal activity and increased heart rate predict a high mortality rate in patients with HF. Experimental and clinical studies support the use of pharmacologic agents that inhibit sympathetic activity as effective lomg-term therapy for patients with HF. In contrast, modulation of vagal activity as potential therapy for HF has received only limited attention over the years. In 2004, we have reported the effects of VNS on HF in rats. Rats developed HF after myocardial infarction and were randomized to VNS and sham stimulated groups. A significant improvement of left ventricular function and survival rate from 50% to 86% compared to sham stimulated animals was observed after 140 days. In this presentation, we will review the results of recent experimental studies that support for the possibility of VNS as a long-term therapy for HF. We will also discuss present challenges and future directions of VNS therapy for HF.

Acute Effect of Whole-Body Periodic Acceleration on Heart Rate Variability and Brachial Flow-Mediated Vasodilatation

Whole-body periodic acceleration (WBPA) is reported to up-regulate endothelial nitric oxide (NO) synthase (eNOS) in animal studies and to improve brachial artery endothelial function (BAEF) measured by brachial artery flow-mediated vasodilatation (FMD) in humans. These findings were obtained by repeated application of WBPA. However, single acute effect of WBPA on BAEF in humans is not fully understood. In addition, the effect of WBPA on cardiac autonomic function assessed by heart rate variability (HRV) has not been studied. Thus, we performed 45 min WBPA in 14 healthy volunteers aged 30±10 years old and measured BAEF and HRV before and after WBPA. HRV indices were measured by Holter ECG as LF, HF Mean RR, SDNN, SD index, rMSSD and pNN50. WBPA increased FMD (from 6.4±3.4 to 7.5±3.0%, P<0.01) and increased Mean RR, HF, rMSSD and pNN50. Conclusions: These results suggest that single application of WBPA acutely and effectively improves BAEF and increases cardiac vagal activity. WBPA could ameliorate ischemic arrhythmias in humans.

CARDIOVASCULAR TOLERANCE AND AUTONOMIC NERVOUS RESPONSES IN UNSEDATED UPPER GASTROINTESTINAL SMALL‐CALIBER ENDOSCOPY: A COMPARISON BETWEEN TRANSNASAL AND PERORAL PROCEDURES WITH NEWLY DEVELOPED MOUTHPIECE

Transnasal esophagogastroduodenoscopy (EGD) with small-caliber endoscopy appears to be less stressful to the cardiovascular system and has good patient tolerance. ENDO LEADER, a newly developed mouthpiece for peroral EGD with small-caliber endoscopy, is expected to reduce patient stress. We compared the patient acceptance, cardiovascular tolerance and autonomic nervous responses between transnasal EGD and peroral EGD with ENDO LEADER. A total of 130 patients (transnasal group, 77; peroral group, 53) were enrolled. Pulse rate (P), blood pressure (BP), and peripheral blood oxygen saturation (SpO(2) ) were monitored. Acceptance of EGD was also assessed. Autonomic nervous responses were evaluated through analysis of heart rate variability using amplitude of the high-frequency component (HF) and low-frequency-to-high-frequency power ratio (LF/HF) as indices of cardiac vagal activity and sympathetic activity, respectively. Analysis of patient acceptance showed no differences between the two groups, except with regard to nasal pain. Increases in BP and P between before and during EGD examination were significantly higher in the peroral group. Although throat pain and overall tolerance scores were significantly correlated with ΔBP and ΔP, no correlations with nasal pain score were noted. Heart rate variability analysis revealed that heart rate increased significantly in the peroral group, but there were no differences in ΔHF or ΔLF/HF between the two groups. Patient acceptance was not significantly different between the transnasal and peroral with ENDO LEADER groups; however, transnasal EGD appears to be less stressful to the sympathetic nervous system, leading to smaller elevations in BP, P and heart rate.

Reduced cardiac vagal activity in obese children and adolescents

Obese children present with various cardiovascular risk factors affecting their future health. In adults, cardiac autonomic function is a major risk factor, predicting cardiovascular morbidity and mortality. We hypothesized that obese children and adolescents had a lower cardiac vagal activity than lean subjects. We measured cardiac spontaneous baroreflex sensitivity (BRS), reflecting the dynamic regulation of cardiac vagal function, in large groups of obese and lean young individuals. Cardiac BRS, using the sequence approach, was assessed in 120 obese (59 girls), 43 overweight (23 girls) and 148 lean subjects (78 girls). Obese subjects showed a decreased BRS compared to both overweight and lean subjects [16±7 versus 21±9 (P<0·01) and 22±10 ms per mmHg (P<0·0001), respectively]. The differences remained after correcting for age, gender and pubertal status. Children with obesity had low vagal activity at rest, and there was no gender difference.

Metoprolol, but not atenolol, reduces stress induced neuropeptide Y release in pigs

Objectives. To explore if β-adrenergic receptors in the brain are involved in acute and delayed cardiovascular responses to a brief emotional stress, by comparing the effects of the β1-blockers metoprolol (lipophilic) and atenolol (hydrophilic). Design. Male dominant pigs, singleliving, freely moving, with telemetric recordings of intra-arterial pressure and ECG and assay of plasma levels of the adrenergic cotransmittor neuropeptide Y (NPY), were confronted with four alien pigs for three minutes at weekly intervals. Weeks 1 and 4 were controls, in weeks 2 and 3 randomized crossover treatment with metoprolol or atenolol were given. Results. The confrontation caused instant and transient tachycardia and more prolonged effects in terms of increased plasma NPY levels, increased arterial pressure and reduced cardiac vagal activation. The two β-blockers inhibited the tachycardia equally, but only metoprolol reduced the prolonged effects. Conclusions. Emotionally induced sympathetic activation involves peripheral release of NPY causing a prolonged increase of arterial pressure and a reduction of cardiac vagal activity. These effects are prevented by central nervous β-adrenoceptor blockade.

Increased Total Heart Rate Variability and Enhanced Cardiac Vagal Autonomic Activity in Healthy Humans with Sinus Bradycardia

Sinus bradycardia can be defined as a sinus rhythm with a resting heart rate of 60 beats per minute or less. While it is assumed that increased autonomic parasympathetic activity is associated with sinus bradycardia, such an association has yet to be proven. The aims of this study were to compute a number of heart rate variability (HRV) parameters in healthy individuals with sinus bradycardia and determine whether there was a significant vagal component to sinus bradycardia. Forty-three healthy adults with normal sinus rhythm and 25 healthy adults with sinus bradycardia had an electrocardiogram recorded for 20 minutes, from which HRV indices were calculated. Results showed significant increases in SDNN (standard deviation of NN intervals) (P< 0.05), RMSDD (square root of the mean squared differences of successive NN intervals) (P< 0.05), and DFA32 (detrended fluctuation analysis) (P< 0.05) in bradycardic subjects compared with subjects with normal sinus rhythm. There were no significant differences in sympathetic frequency domain indices between the two groups. In conclusion, there were significant increases in total heart variability and increased parasympathetic drive in subjects with bradycardia. Clinically, bradycardia is likely to be cardioprotective in aging populations based upon these HRV findings.

Efficient and cost‐effective estimation of the influence of respiratory variables on respiratory sinus arrhythmia

Researchers are interested in respiratory sinus arrhythmia (RSA) as an index of cardiac vagal activity. Yet, debate exists about how to account for respiratory influences on quantitative indices of RSA. T. Ritz, M. Thons, and B. Dahme (2001) developed a within-individual correction procedure by which the effects of respiration on RSA may be estimated using regression models. We replicated their procedure substituting a spectral high-frequency measure of RSA for a time-domain statistic and a respiratory belt's relative measure of tidal volume for the direct assessment provided by a pneumotachograph. The standardized slopes from the respiratory belt and pneumotachography-derived regression equations (estimated across a 6-min paced breathing protocol) were positively correlated (r=0.93, p<.001); correlations were similar across 2- and 4-min time courses parsed from the 6-min protocol. Our results offer methodological alternatives to the research community.