Cardiorespiratory interactions during resistive load breathing

The addition to the respiratory system of a resistive load results in breathing pattern changes and in negative intrathoracic pressure increases. The aim of this study was to use resistive load breathing as a stimulus to the cardiorespiratory interaction and to examine the extent of the changes in heart rate variability (HRV) and respiratory sinus arrhythmia (RSA) in relation to the breathing pattern changes. HRV and RSA were studied in seven healthy subjects where four resistive loads were applied in a random order during the breath and 8-min recording made in each condition. The HRV spectral power components were computed from the R-R interval sequences, and the RSA amplitude and phase were computed from the sinusoid fitting the instantaneous heart rate within each breath. Adding resistive loads resulted in 1) increasing respiratory period, 2) unchanging heart rate, and 3) increasing HRV and changing RSA characteristics. HRV and RSA characteristics are linearly correlated to the respiratory period. These modifications appear to be linked to load-induced changes in the respiratory period in each individual, because HRV and RSA characteristics are similar at a respiratory period obtained either by loading or by imposed frequency breathing. The present results are discussed with regard to the importance of the breathing cycle duration in these cardiorespiratory interactions, suggesting that these interactions may depend on the time necessary for activation and dissipation of neurotransmitters involved in RSA.     

Human sinus arrhythmia: inconsistencies of a teleological hypothesis

Respiratory sinus arrhythmia (RSA) may serve an inherent function in optimizing pulmonary gas exchange efficiency via clustering and scattering of heart beats during the inspiratory and expiratory phases of the respiratory cycle. This study sought to determine whether physiological levels of RSA, enhanced by slow paced breathing, caused more heart beats to cluster in inspiration. In 12 human subjects, we analyzed the histogram distribution of heart beats throughout the respiratory cycle during paced breathing at 12, 9, and 6 breaths/min (br/min). The inspiratory period-to-respiratory period ratio was fixed at approximately 0.5. RSA and its relationship with respiration was characterized in the phase domain by average cubic-spline interpolation of electrocardiographic R wave-to-R wave interval fluctuations throughout all respiratory cycles. Although 6 br/min breathing was associated with a significant increase in RSA amplitude (P < 0.01), we observed no significant increase in the proportion of heart beats in inspiration (P = 0.34). Contrary to assumptions in the literature, we observed no significant clustering of heart beats even with high levels of RSA enhanced by slow breathing. The results of this study do not support the hypothesis that RSA optimizes pulmonary gas exchange efficiency via clustering of heart beats in inspiration.     

Influences of breathing patterns on respiratory sinus arrhythmia in humans during exercise

Persistence of respiratory sinus arrhythmia (RSA) has been described in humans during intense exercise and attributed to an increase in ventilation. However, the direct influence of ventilation on RSA has never been assessed. The dynamic evolution of RSA and its links to ventilation were investigated during exercise in 14 healthy men using an original modeling approach. An evolutive model was estimated from the detrended and high-pass-filtered heart period series. The instantaneous RSA frequency (FRSA, in Hz) and amplitude (ARSA, in ms) were then extracted from all recordings. A(RSA) was calculated with short-time Fourier transform. First, measurements of FRSA and ARSA were performed from data obtained during a graded and maximal exercise test. Influences of different ventilation regimens [changes in tidal volume (VT) and respiratory frequency (FR)] on ARSA were then tested during submaximal [70% peak O2 consumption (VO2peak)] rectangular exercise bouts. Under graded and maximal exercise conditions, ARSA decreased from the beginning of exercise to 61.9 +/- 3.8% VO2peak and then increased up to peak exercise. During the paced breathing protocol, normoventilation (69.4 +/- 8.8 l/min), hyperventilation (81.8 +/- 8.3 l/min), and hypoventilation (56.4 +/- 6.2 l/min) led to significantly (P < 0.01) different ARSA values (3.8 +/- 0.5, 4.6 +/- 0.8, and 2.9 +/- 0.5 ms, respectively). In addition, no statistical difference was found in ARSA when ventilation was kept constant, whatever the FR-VT combinations. Those results indicate that RSA persists for all exercise intensities and increases during the highest intensities. Its persistence and increase are strongly linked to both the frequency and degree of lung inflation, suggesting a mechanical influence of breathing on RSA.     

Effect of inspiratory muscle fatigue on breathing pattern

Our aim was to determine whether inspiratory muscle fatigue changes breathing pattern and whether any changes seen occur before mechanical fatigue develops. Nine normal subjects breathed through a variable inspiratory resistance with a predetermined mouth pressure (Pm) during inspiration and a fixed ratio of inspiratory time to total breath duration. Breathing pattern after resistive breathing (recovery breathing pattern) was compared with breathing pattern at rest and during CO2 rebreathing (control breathing pattern) for each subject. Relative rapid shallow breathing was seen after mechanical fatigue and also in experiments with electromyogram evidence of diaphragmatic fatigue where Pm was maintained at the predetermined level during the period of resistive breathing. In contrast there was no significant difference between recovery and control breathing patterns when neither mechanical nor electromyogram fatigue was seen. It is suggested that breathing pattern after inspiratory muscle fatigue changes in order to minimize respiratory sensation.     

Airway caliber and the work of breathing in humans

Mechanical work rate of breathing was measured in five normal subjects during voluntary eucapnic hyperventilation at rates of approximately 10, 20, 40, 60, and 80 l/min before and after inhalation of 1 mg of ipratropium bromide, an anticholinergic agent. Chest wall recoil pressure was measured over a range of lung volumes in each subject and was used as the reference pressure in the calculation of work rate. There was little change in elastic or resistive work rate at rest when vagal tone was reduced by ipratropium. The mean work at 40, 60, and 80 l/min was 8.9, 17.2, and 34.0 cmH2O.l-1.s before and 5.6, 12.4 and 25.8 cmH2O.l-1.s after ipratropium. This suggests that vagal tone significantly influences the work of breathing at high ventilatory rates, such as occur during strenuous exercise.     

Effects of hypercapnia and hypoxemia on respiratory sinus arrhythmia in conscious humans during spontaneous respiration

Normally, at rest, the amplitude of respiratory sinus arrhythmia (RSA) appears to correlate with cardiac vagal tone. However, recent studies showed that, under stress, RSA dissociates from vagal tone, indicating that separate mechanisms might regulate phasic and tonic vagal activity. This dissociation has been linked to the hypothesis that RSA improves pulmonary gas exchange through preferential distribution of heartbeats in inspiration. We examined the effects of hypercapnia and mild hypoxemia on RSA-vagal dissociation in relation to heartbeat distribution throughout the respiratory cycle in 12 volunteers. We found that hypercapnia, but not hypoxemia, was associated with significant increases in heart rate (HR), tidal volume, and RSA amplitude. The RSA amplitude increase remained statistically significant after adjustment for respiratory rate, tidal volume, and HR. Moreover, the RSA amplitude increase was associated with a paradoxical rise in HR and decrease in low-frequency-to-high-frequency mean amplitude ratio derived from spectral analysis, which is consistent with RSA-vagal dissociation. Although hypercapnia was associated with a significant increase in the percentage of heartbeats during inspiration, this association was largely secondary to increases in the inspiratory period-to-respiratory period ratio, rather than RSA amplitude. Additional model analyses of RSA were consistent with the experimental data. Heartbeat distribution did not change during hypoxemia. These results support the concept of RSA-vagal dissociation during hypercapnia; however, the putative role of RSA in optimizing pulmonary perfusion matching requires further experimental validation.     

Coronary and systemic vascular response to inspiratory resistive breathing.

To evaluate the coronary and systemic cardiovascular response to graded inspiratory resistive breathing, seven dogs were studied 2-4 wk after chronic instrumentation to measure circumflex coronary artery and ascending aortic blood flows as well as aortic and left ventricular (LV) blood pressures. The experiments were performed under chloralose anesthesia (to exclude any confounding emotional effects by dyspnea on cardiovascular variables) and hyperoxic conditions (to prevent chemoreflex activation by hypoxemia). In a randomized fashion, the dogs were subjected to graded inspiratory resistive breathing (spontaneous breathing alone and moderate and severe resistive loading, corresponding to resistances of approximately 0, 40, and 110 cmH2O.s.l-1, respectively). Each run lasted 10 min. Compared with mechanical ventilation with the respiratory muscles at rest, spontaneous breathing alone and moderate and severe inspiratory resistive loading induced pronounced and significant increases in circumflex coronary blood flow (19, 32, and 62%, respectively), which were almost exclusively accounted for by significant decrements in coronary vascular resistance and were paralleled (r = 0.88, P less than 0.0001) by significant increments (18, 31, and 57%) in heart rate transmural-aortic pressure product, an indicator of LV myocardial O2 demand. An increase in myocardial O2 consumption during resistive breathing was confirmed by analysis of coronary sinus blood samples in additional experiments (n = 3). Cardiac output significantly increased (10, 14, and 35%) because of increases in heart rate (15, 24, and 49%), with LV stroke volume and diastolic dimensions remaining unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)     

存在睡眠呼吸异常的慢病患者呼吸影响心率变异性的初步分析*

目的: 基于整体整合生理学医学理论提出的呼吸引起循环指标变异的假说,分析研究存在睡眠呼吸异常的慢病患者睡眠期间呼吸和心率变异之间的相关关系。方法: 纳入存在睡眠呼吸异常且呼吸暂停低通气指数（AHI）≥15次/小时的慢病患者11例,签署知情同意书后完成标准化症状限制性极限运动的心肺运动试验（CPET）和睡眠呼吸监测,计算分析病人睡眠期间波浪式呼吸（OB）期与正常平稳呼吸期的呼吸鼻气流、心电图R-R间期心率变异的规律。结果: 存在睡眠呼吸异常的慢病患者CPET峰值摄氧量（Peak VO₂）和无氧阈（AT）为（70.8±13.6）%pred和（71.2±6.1）%pred;CPET有5例存在运动诱发的波浪式呼吸（EIOB）,6例为呼吸不稳定,提示整体功能状态低于正常人。本组慢病患者AHI为每小时（28.8±10.0）次,睡眠呼吸异常总时间占睡眠总时间的比值为（0.38±0.25）;OB周期的平均时间长度为（51.1±14.4）s。本组慢病患者正常平稳呼吸期的呼吸周期数与心率变异周期数的比值（B-n/HRV-B-n）为1.00±0.04,每个呼吸周期节律的心率变异平均幅度（HRV-B-M）为（2.64±1.59） bpm,虽然低于正常人（P<0.05）,但却与无睡眠呼吸异常的慢病患者相似（P>0.05）;HRV-B-M的变异度CV（HRV-B-M的SD/x）为( 0.33±0.11）,期间血氧饱和度（SpO₂）虽略低,但并无明显规律性下降与上升。本组慢病患者的OB期间呼吸周期数与心率变异周期数（OB-B-n/OB-HRV-B-n）比值为（1.22±0.18）,OB期每个呼吸周期节律的心率变异平均幅度（OB-HRV-B-M）为（3.56±1.57）bpm及其变异度（OB-CV =OB-HRV-B-M的SD/x）为（0.59±0.28）,每个OB周期节律的心率变异平均幅度（OB-HRV-OB-M）为（13.75±4.25）bpm,OB期间低通气时SpO₂出现明显的下降,OB期间SpO₂平均变异幅度（OB-SpO₂-OB-M）为（4.79±1.39）%,OB期的OB-B-n/OB-HRV-B-n比值、OB-HRV-OB-M比其正常平稳呼吸期对应指标显著增大（P<0.01）。OB-HRV-B-M虽然与正常平稳呼吸期HRV-B-M相比差异无统计学意义（P>0.05）,但其变异度OB-CV却显著增大（P<0.01）。结论: 睡眠呼吸异常的慢病患者OB期的心率变异幅度大于其正常平稳呼吸期,当呼吸模式发生改变时心率变异也发生明显改变,其平稳呼吸期的呼吸周期数与心率变异周期数的比值与正常人以及无睡眠呼吸异常的慢病患者相同,证实心率变异为呼吸源性;而其OB期间心率变异周期数相对于呼吸周期减少直接源于此时的低通气或者呼吸暂停,心率变异也是呼吸源性。     

Oscillations of heart rate and respiration synchronize during poetry recitation

The objective of this study was to investigate the synchronization between low-frequency breathing patterns and respiratory sinus arrhythmia (RSA) of heart rate during guided recitation of poetry, i.e., recitation of hexameter verse from ancient Greek literature performed in a therapeutic setting. Twenty healthy volunteers performed three different types of exercises with respect to a cross-sectional comparison: 1). recitation of hexameter verse, 2). controlled breathing, and 3). spontaneous breathing. Each exercise was divided into three successive measurements: a 15-min baseline measurement (S1), 20 min of exercise, and a 15-min effect measurement (S2). Breathing patterns and RSA were derived from respiratory traces and electrocardiograms, respectively, which were recorded simultaneously using an ambulatory device. The synchronization was then quantified by the index gamma, which has been adopted from the analysis of weakly coupled chaotic oscillators. During recitation of hexameter verse, gamma was high, indicating prominent cardiorespiratory synchronization. The controlled breathing exercise showed cardiorespiratory synchronization to a lesser extent and all resting periods (S1 and S2) had even fewer cardiorespiratory synchronization. During spontaneous breathing, cardiorespiratory synchronization was minimal and hardly observable. The results were largely determined by the extent of a low-frequency component in the breathing oscillations that emerged from the design of hexameter recitation. In conclusion, recitation of hexameter verse exerts a strong influence on RSA by a prominent low-frequency component in the breathing pattern, generating a strong cardiorespiratory synchronization.     

Respiratory sinus arrhythmia is associated with efficiency of pulmonary gas exchange in healthy humans

Respiratory sinus arrhythmia (RSA) may be associated with improved efficiency of pulmonary gas exchange by matching ventilation to perfusion within each respiratory cycle. Respiration rate, tidal volume, minute ventilation (.VE), exhaled carbon dioxide (.VCO(2)), oxygen consumption (.VO(2)), and heart rate were measured in 10 healthy human volunteers during paced breathing to test the hypothesis that RSA contributes to pulmonary gas exchange efficiency. Cross-spectral analysis of heart rate and respiration was computed to calculate RSA and the coherence and phase between these variables. Pulmonary gas exchange efficiency was measured as the average ventilatory equivalent of CO(2) (.VE/.VCO(2)) and O(2) (.VE/.VO(2)). Across subjects and paced breathing periods, RSA was significantly associated with CO(2) (partial r = -0.53, P = 0.002) and O(2) (partial r = -0.49, P = 0.005) exchange efficiency after controlling for the effects of age, respiration rate, tidal volume, and average heart rate. Phase between heart rate and respiration was significantly associated with CO(2) exchange efficiency (partial r = 0.40, P = 0.03). These results are consistent with previous studies and further support the theory that RSA may improve the efficiency of pulmonary gas exchange.     

Phase-averaged characterization of respiratory sinus arrhythmia pattern

A method for the accurate time-domain characterization of respiratory sinus arrhythmia (RSA) pattern is presented and applied to two groups of healthy subjects to lay the baseline of RSA patterns and to underlay their features: response to standing, stability in successive recordings, and individuality of the shape of RSA pattern. RSA pattern is evaluated by selective averaging of heart rate (HR) changes from multiple respiratory cycles over the respiratory phase and represents the complete modulating function of HR by respiration. The RSA pattern is evaluated with free respiration and even in cases of severe arrhythmia. Estimation error is 6-8% in magnitude, phase resolution is 0.2 rad, and sensitivity margin for respiratory-related HR variability (HRV) components is 1%. RSA magnitude, phase lag, and expiration-to-inspiration time ratio are derived in addition to the entire pattern. In a group of 10 healthy young adults, a phase lag difference of 11.4 +/- 8.5% (mean +/- SD, P < 0.004) was observed between supine and standing postures, possibly ascribed to breathing mechanics. A second group of 15 healthy young adults at supine rest showed stability of the RSA pattern in successive recordings (several weeks apart) as well as individuality among subjects. This may suggest a nonscalar individual long-term index for cardiorespiratory coupling. The method is complementary to the existing statistical and spectral methods. It allows the complete characterization of the primary RSA components and may provide new insight into the effects of vagal activity and changes in clinical conditions.     

Effect of ozone on breathing in dogs: vagal and nonvagal mechanisms

We exposed two awake dogs with a chronic tracheostomy and the cervical vagus nerves exteriorized in skin loops to 1.0 ppm of ozone (O3) for 2 h at intervals of 4 wk. We measured ventilatory variables before and after O3 exposure during rest and exercise before and after vagal block. We compared the effects of vagal blockade, exercise, and O3 on the primary determinants of breathing pattern (VT/TI, VT/TE, TI, and TE) in each of three conditions: base line (steady state), during hypercapnia, and after inhalation of 1% histamine. Under base-line conditions, O3 increased respiratory rate and decreased tidal volume (VT) by shortening time of expiration (TE) and time of inspiration (TI) without affecting VT/TI, an indicator of the neural drive to breathing. During progressive hypercapnia, O3 shortened TE and TI by effects both on tonic (nonvolume-related) and on phasic (volume-related) vagal inputs, and only the latter were prevented completely by cooling of the vagus nerves. Histamine-induced tachypnea was increased by O3 and was totally blocked by cooling the vagus nerves. We conclude that O3 shortens the timing of respiration without increasing ventilatory drive, shortens TI and TE through vagal and nonvagal pathways, increases tonic nonvagal and phasic vagal inputs, and stimulates more than one vagal fiber type.     

Ventilatory failure during loaded breathing: the role of central neural drive

Minute ventilation (VE), arterial blood gases, diaphragmatic electromyogram (EMG) activity, centroid frequency (Fc) and peak inspiratory airway pressures (Paw) were measured in five unanesthetized tracheostomized infant monkeys during various intensities of inspiratory resistive loaded breathing (IRL) until either 1) ventilatory failure occurred (failed trial) or 2) normocapnia was sustained for 1 h (successful trial). During successful trials VE and arterial PCO2 (PaCO2) were sustained at base-line levels, and an increase in peak integrated diaphragmatic EMG activity and peak inspiratory Paw occurred. In contrast, during ventilatory failure runs, VE decreased and PaCO2 rose compared with their respective base-line values. The fall in VE occurred secondary to a significant decline in breathing frequency. Tidal volume was sustained at base-line levels during all trials (both successful and failed groups). Inspiratory Paw's and peak moving time average EMG were sustained at elevated levels during ventilatory failure runs, suggesting that the respiratory muscles did not fail as pressure generators. Furthermore, the EMG Fc did not change from base line during either successful or failed trials. These data suggest that peripheral muscle fatigue did not occur, although in the absence of a more direct test of muscle performance, i.e., a force-frequency curve, we cannot rule out the possibility that a component of peripheral failure contributed to our results. Ventilatory failure during severe IRL in the infant monkey was most clearly associated with an alteration in the respiratory center timing mechanism, i.e., such failure was a function of a decline in respiratory frequency.     

Hemodynamic effects of resistive breathing

To examine the acute hemodynamic effects induced by large swings in intrathoracic pressure such as may be generated by obstructive lung disease, airway obstruction was simulated by means of two different fixed external alinear resistances and the results were compared with those for unobstructed breathing (C). Eight normal subjects breathed through external resistances during inspiration (I), expiration (E), or both (IE) at rest (Re) and exercise (Ex). The resistances were chosen to induce similar mouth pressure (Pm) swings at Re and Ex. Pleural pressures (Ppl) were found to correlate closely with Pm. During IE resistive breathing mean swings in Pm were -31 and +19 cmH2O at Re and -38 and +22 cmH2O at Ex, with a corresponding decrease in minute ventilation (-30 and -18%) and an increase in end-tidal PCO2 (+5.6 and +4.2 Torr); these were associated with an increase in heart rate (delta HR = 4 and 6 beats/min) and systolic systemic arterial pressure (delta Psas = 10 and 14 Torr at Re and Ex, respectively). O2 consumption and cardiac output did not change. The myocardial O2 consumption, estimated from the product HR X (Psas--Ppl), increased by 17 and 20% at Re and Ex, respectively. Changes in mechanics, gas exchange, and hemodynamics were less pronounced during I or E resistive loading. It is concluded that breathing through a tight external resistance during IE at Re and Ex increases the metabolic load on the myocardium.     

Respiratory Sinus Arrhythmia Versus Neck/Trapezius EMG and Incentive Inspirometry Biofeedback for Asthma: A Pilot Study

This pilot study compared biofeedback to increase respiratory sinus arrhythmia (RSA) with EMG and incentive inspirometry biofeedback in asthmatic adults. A three-group design (Waiting List Control n = 5, RSA biofeedback n = 6, and EMG biofeedback n = 6) was used. Six sessions of training were given in each of the biofeedback groups. In each of three testing sessions, five min. of respiratory resistance and EKG were obtained before and after a 20-min biofeedback session. Additional five-min epochs of data were collected at the beginning and end of the biofeedback period (or, in the control group, self-relaxation). Decreases in respiratory impedance occurred only in the RSA biofeedback group. Traub-Hering-Mayer (THM) waves (.03-.12 Hz) in heart period increased significantly in amplitude during RSA biofeedback. Subjects did not report significantly more relaxation during EMG or RSA biofeedback than during the control condition. However, decreases in pulmonary impedance, across groups, were associated with increases in relaxation. The results are consistent with Vaschillo's theory that RSA biofeedback exercises homeostatic autonomic reflex mechanisms through increasing the amplitude of cardiac oscillations. However, deep breathing during RSA biofeedback is a possible alternate explanation.     

O2 cost of inspiratory and expiratory resistive breathing in humans

In six normal male subjects we compared the O2 cost of resistive breathing (VO2 resp) between equivalent external inspiratory (IRL) and expiratory loads (ERL) studied separately. Each subject performed four pairs of runs matched for tidal volume, breathing frequency, flow rates, lung volume, pressure-time product, and work rate. Basal O2 uptake, measured before and after pairs of loaded runs, was subtracted from that measured during resistive breathing to obtain VO2 resp. For an equivalent load, the VO2 resp during ERL (184 +/- 17 ml O2/min) was nearly twice that obtained during IRL (97 +/- 9 ml O2/min). This twofold difference in efficiency between inspiratory and expiratory resistive breathing may reflect the relatively lower mechanical advantage of the expiratory muscles in overcoming respiratory loads. Variable recruitment of expiratory muscles may explain the large variation of results obtained in studies of respiratory muscle efficiency in normal subjects.     

Effect of mechanical loading on breathing patterns in women

First-breath ventilatory responses to graded inspiratory elastic and resistive loads were obtained from 80 women unfamiliar with respiratory experimentation. For each load 1) responses from different subjects ranged from a weak tidal volume defense coupled with an increased breathing frequency to a strong tidal volume defense coupled with a decreased frequency; 2) strong tidal volume defenders employed longer inspirations than did weak tidal volume defenders; and 3) individual respiratory frequency responses were mediated by changes in inspiratory and/or expiratory timing. Thus the group response was qualitatively the same as that reported for 80 men. Quantitatively, however, mean inspiratory airflow responses of women exceeded those of men by an amount attributable to women's higher intrinsic respiratory elastance. Tidal volume responses, on the other hand, did not differ significantly, suggesting that men and women produce different neural adjustments to loads. In support of this hypothesis, analysis of respiratory timing responses revealed that 1) men actively prolonged inspiration more than women during resistive loading; and 2) women actively shortened inspiration more than men during elastic loading. These findings indicate that the load-compensating behavior exhibited by men and women is similar but not identical.     

Effects of N2O narcosis on breathing and effort sensations during exercise and inspiratory resistive loading

Fothergill, D. M., and N. A. Carlson. Effects ofN₂O narcosis on breathing andeffort sensations during exercise and inspiratory resistive loading.J. Appl. Physiol. 81(4):1562-1571, 1996.The influence of nitrous oxide(N₂O) narcosis on the responses toexercise and inspiratory resistive loading was studied in thirteen maleUS Navy divers. Each diver performed an incremental bicycle exercisetest at 1 ATA to volitional exhaustion while breathing a 23%N₂O gas mixture and a nonnarcoticgas of the same PO₂, density, andviscosity. The same gas mixtures were used during four subsequent30-min steady-state submaximal exercise trials in which the subjectsbreathed the mixtures both with and without an inspiratory resistance(5.5 vs. 1.1 cmH₂O ^· s ^· l¹at 1 l/s). Throughout each test, subjective ratings of respiratory effort (RE), leg exertion, and narcosis were obtained with acategory-ratio scale. The level of narcosis was rated between slightand moderate for the N₂O mixturebut showed great individual variation. Perceived leg exertion and thetime to exhaustion were not significantly different with the twobreathing mixtures. Heart rate was unaffected by the gas mixture andinspiratory resistance at rest and during steady-state exercise but wassignificantly lower with the N₂O mixture during incremental exercise (P < 0.05). Despite significant increases in inspiratory occlusionpressure (13%; P < 0.05),esophageal pressure (12%; P < 0.001), expired minute ventilation (4%;P < 0.01), and the work rate ofbreathing (15%; P < 0.001) when the subjects breathed the N₂O mixture,RE during both steady-state and incremental exercise was 25% lowerwith the narcotic gas than with the nonnarcotic mixture(P < 0.05). We conclude that the narcotic-mediated changes in ventilation, heart rate, and RE induced by23% N₂O are not of sufficientmagnitude to influence exercise tolerance at surface pressure.Furthermore, the load-compensating respiratory reflexes responsible formaintaining ventilation during resistive breathing are not depressed byN₂O narcosis.

     

Incoherent oscillations of respiratory sinus arrhythmia during acute mental stress in humans

Respiratory sinus arrhythmia (RSA) has been widely used as a measure of the cardiac vagal control in response to stress. However, RSA seems not to be a generalized indicator because of its dependency on respiratory parameter and individual variations of RSA amplitude (A(RSA)). We hypothesized that phase-lag variations between RSA and respiration may serve as a normalized index of the degree of mental stress. Twenty healthy volunteers performed mental arithmetic task (ART) after 5 min of resting control followed by 5 min of recovery. Breathing pattern, beat-to-beat R-R intervals, and blood pressure (BP) were determined using inductance plethysmography, electrocardiography, and a Finapres device, respectively. The analytic signals of breathing and RSA were obtained by Hilbert transform and the degree of phase synchronization (λ) was quantified. With the use of spectral analysis, heart rate variability (HRV) was estimated for the low-frequency (LF) and high-frequency (HF) bands. A steady-state 3-min resting period (REST), the first 3 min (ART1), and the last 3 min (ART2) of the ART period (ranged from 6- to 19 min) and the last 3 min of the recovery period (RCV) were analyzed separately. Heart rate, systolic BP, and breathing frequency (f(R)) increased and λ, A(RSA), and HF power decreased from REST to ART (P < 0.01). The λ was correlated with normalized A(RSA) and the HF power. The decrease in λ could not be explained solely by the increase in f(R). We conclude that mental stress exerts an influence on RSA oscillations, inducing incoherent phase lag with respect to breathing, in addition to a decrease in RSA.     

Respiratory sinus arrhythmia, cardiac vagal control, and daily activity

Ambulatory respiratory sinus arrhythmia (RSA) or high-frequency heart rate (HR) variability is frequently employed as an index of cardiac parasympathetic control and related to risk or severity of cardiovascular disease. However, laboratory studies indicate variations in physical activity and respiratory parameters of rate and tidal volume may confound estimation of vagal activity. Because little is known about these relations outside the laboratory, we examined ambulatory relations among RSA, respiration, physical activity, and HR during waking hours by employing a multichannel monitoring system. Forty healthy young-to-middle aged adults underwent daytime monitoring that included continuous registration of the ECG, respiration (inductance plethysmography), and accelerometry motion activity. Within-individual regression analyses were performed to examine minute-to-minute relations between RSA and respiration, HR, and indexes of physical activity (minute ventilation and motion). HR changes were assumed to be strongly related to within-individual variations of vagal tone. RSA adjusted for respiratory parameters and unadjusted RSA were compared for strength of prediction of other measures. Unadjusted RSA was related to respiratory parameters (R = 0.80) and moderately predicted minute-to-minute HR and activity variances (means = 56%, HR; 48%, minute ventilation; and 37%, motion). Adjusted RSA predicted significantly more HR and activity variance (means = 75%, 76%, and 57%, respectively) with narrower confidence intervals. We conclude that ambulatory RSA magnitude is associated with respiratory variations and physical activity. Adjustment for respiratory parameters substantially improves relations between RSA and significantly vagally mediated HR and physical activity. Concurrent monitoring of respiration and physical activity may enhance HR variability accuracy to predict autonomic control.