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To investigate the interindividual differences in respiratory sinus arrhythmia (RSA), recordings of ventilation and electrocardiogram were obtained from 12 healthy subjects for five imposed breathing periods ( TTOT) surrounding each individual's spontaneous breathing period. In addition to the spectral analysis of the R-R interval signal at each breathing period, RSA characteristics were quantified by using a breath-by-breath analysis where a sinusoid was fitted to the changes in instantaneous heart rate in each breath. The amplitude and phase (or delay = phase × TTOT) of this sinusoid were taken as the RSA characteristics for each breath. It was found that for each subject the RSA amplitude- TTOT relationship was linear, whereas the delay- TTOT relationship was parabolic. However, the parameters of these relationships differed between individuals. Linear correlation between the slopes of RSA amplitude versus TTOT regression lines and 1) mean breathing period and 2) mean R-R interval during spontaneous breathing were calculated. Only the correlation coefficient with breathing period was significantly different from zero, indicating that the longer the spontaneous breathing period the lesser the increase in RSA amplitude with increasing breathing period. Similarly, only the correlation coefficient between the curvature of the RSA delay- TTOT parabola and mean breathing period was significantly different from zero; the longer the spontaneous breathing period the larger the curvature of RSA delay. These results suggest that the changes in RSA characteristics induced by changing the breathing period may be explained partly by the spontaneous breathing period of each individual. Furthermore, a transfer function analysis performed on these data suggested interindividual differences in the autonomic modulation of the heart rate.

International audience; Studies of heart rate variability (HRV) have so far produced contradictory evidence to support the common belief that endurance training enhances cardiac parasympathetic tone. This may be related to the fact that most studies failed to specifically isolate the vagally mediated influence of respiration. This study used a cross-sectional comparison of endurance athletes (n=20; ATHL) exhibiting resting bradycardia and age-matched nonathletes (n=12; CRTL) to indirectly assess training effects on amplitude and timing characteristics of respiratory sinus arrhythmia (RSA). Continuous electrocardiogram (ECG) and ventilatory flows were recorded during spontaneous breathing (SP), as well as during breathing at four cycles less than (M4) or more (P4) than SP, to also examine potential repercussions of training on the sensitivity of the cardiac vagal responses to breathing. A fast Fourier transform procedure was used to quantify the standard spectral high-frequency (HF) and low-frequency (LF) components and a respiratory-centered frequency (RCF) component of HRV. RSA was assessed using a breath-by-breath quantification of the amplitude and timing of the maximum change in instantaneous heart rate. Under baseline SP conditions, heart rate was lower in ATHL (62.6+/-6.5 vs. 75.2+/-9 beats/min; p

Mentally imaged but unexecuted physical activity has been reported to induce a cardiorespiratory change. In order to test whether the previous experience of the performed exercise was a prerequisite to observe these changes, ventilation and heart rate were recorded during mental imagination of a rowing race in four groups of volunteers: 12 competitive rowers, 10 non-rower athletes, 12 students (22-30 years old) and 12 senior subjects (50-60 years old). Recordings were performed at rest, during the viewing of a rowing race and during mental imagination of this race. Analysis of variance revealed significant condition effect for all cardiorespiratory variables. All subjects increased their breathing rate (mean increase: 16 breaths.min(-1) in rowers, 8 breaths.min(-1) in athletes, 8 breaths.min(-1) in students, and 6 breaths.min(-1) in seniors), 29 decreased their tidal volume (mean decrease: 100 ml in rowers, 102 ml in athletes, 120 ml in students and 26 ml in seniors), with an increase in the resulting ventilation in 38 subjects (mean increase: 14 l.min(-1) in rowers, 3.6 l.min(-1) in athletes, 2.8 l.min(-1) in students, 2.6 l.min(-1) in seniors). Heart rate was increased in 34 subjects (mean increase: 12 beats.min(-1) in rowers, 5 beats.min(-1) in athletes, 6 beats.min(-1) in students and 5 beats.min(-1) in seniors). The number of subjects who exhibited changes was evenly distributed among the four groups. However, mean values of the changes were higher in rowers than in the three other groups, mainly due to three rowers who exhibited extremely large increases in cardioventilatory variables. Analysis of variance showed no significant group effect for heart rate and breathing rate. These results suggest that rowing experience may not be necessary for changes in heart rate and ventilation to be elicited by mentally imagining a rowing race.

Misunderstanding of the dynamical behavior of the ventilatory system, especially under assisted ventilation, may explain the problems encountered in ventilatory support monitoring. Proportional assist ventilation (PAV) that theoretically gives a breath by breath assistance presents instability with high levels of assistance. We have constructed a mathematical model of interactions between three objects: the central respiratory pattern generator modelled by a modified Van der Pol oscillator, the mechanical respiratory system which is the passive part of the system and a controlled ventilator that follows its own law. The dynamical study of our model shows the existence of two crucial behaviors, i.e. oscillations and damping, depending on only two parameters, namely the time constant of the mechanical respiratory system and a cumulative interaction index. The same result is observed in simulations of spontaneous breathing as well as of PAV. In this last case, increasing assistance leads first to an increase of the tidal volume (VT), a further increase in assistance inducing a decrease in VT, ending in damping of the whole system to an attractive fixed point. We conclude that instabilities observed in PAV may be explained by the different possible dynamical behaviors of the system rather than changes in mechanical characteristics of the respiratory system.

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.

We recorded by pneumotachography the breathing in nine patients with myotonic dystrophy (MD), both seated and supine and with eyes open in both positions. Irregular breathing (coefficient of variation >20% for VT and TTOT) was observed in six of the patients, two of whom showed irregularity in both positions whilst the remaining four had irregular breathing only when supine. In addition, in this latter group, irregularities first appeared in VT and only after a few minutes in TTOT. Whereas in the group exhibiting irregular breathing in both seated and supine positions, irregularities were observed throughout the recording. However, no significant difference in any ventilatory variable was observed as between the two postures. Rib cage (RC) and abdomen (AB) motions were recorded by uncalibrated respiratory inductance plethysmography. Although for MD patients the mean values of the RC/AB ratio lay within the normal range the relative decrease in value as between seated (0.78+/-0.52) and supine (0.31+/-0.13) position was less than in healthy subjects. These observations suggest that MD may cause deficiencies in several mechanisms. Analyses of the respiratory pattern in each patient may provide information leading to the identification of the impaired respiratory mechanisms.

The improvement in motor performance resulting from levodopa administration in patients with Parkinson’s disease (PD) provides the opportunity to investigate ventilatory changes brought about by the disease. The aim of this study has been to investigate these changes in order to specify the mechanisms of the impairment in breathing in PD. Breathing patterns at rest were investigated in 11 patients with idiopathic PD both before (O ff ) and after (O n ) administration of levodopa at a dose improving their motor performance by at least 30%. Airflow (Fleisch head mounted on a mask), rib cage and abdomen movements (inductance plethysmography) were recorded in the O ff condition 1 h after subjects woke up. Subjects then received levodopa and a new set of recordings was obtained 1 h later, in the O n condition. Breath-by-breath processing of recordings was carried out and tidal volume (V t ), inspiratory (T i ) and expiratory (T e ) durations were measured. The main finding was a lengthening of T i resulting in a decrease in ventilation and in V t /T i, and an increase in T i /T tot in the O n compared to the O ff condition. In the O n condition abnormal rib cage–abdomen plots patterns were found in four out of six subjects. A hypothesis on the effect of PD on breathing is proposed on grounds of normal diaphragmatic activity but impaired activity of the other respiratory muscles and more specifically the intercostal muscles.

In order to determine changes in breathing patterns brought about by resistive loading, ventilation was recorded in 11 healthy subjects with four linear resistances (3.57, 5.75, 8.76 and 13.13 cmH 2 O L −1 sec) added in a random order throughout the entire breath. At steady state, a breath-by-breath analysis of airflow was used to quantify the pattern of breathing in terms of respiratory variables: T i , T e , Tt, V t , V t /T i , T i /Tt, and by taking T i , T e , V t all together (TRIAD) and also the shape of the entire airflow profile quantified by harmonic analysis (ASTER). Group analysis using ANOVA showed significant changes in all variables. There were increasing changes with increasing loads in all variables, the smallest changes being in T i /Tt. Within to between-individual comparisons between two loads showed that only T i /Tt and the ASTER were more similar within than between-individuals for all comparisons. It was concluded that at steady state mechanisms of load compensation come into play inducing changes in the pattern of breathing proportional to the loads while maintaining some of the individual characteristics.

Objective To assess the accuracy of respiratory inductive plethysmography (RIP) waveforms to those obtained with whole body plethysmograph (BP) as this device gives a plethysmographic signal and a pneumotachograph (PNT). Design Randomized controlled trial. Setting Physiologic laboratory in a university hospital. Participants Eleven subjects from the laboratory staff. Interventions This study was achieved during four consecutive periods in subjects breathing spontaneously and through different added resistive loads. Using the least square method calibration, two RIP waveforms, VRIP.BP(t) and VRIP.PNT(t), were simultaneously calculated with coefficients obtained from BP and from PNT volume waveforms, respectively VBP(t) and VPNT(t). For each recording, to compare volume waveforms, we calculated their differences in term of distances, DRIP-BP and DRIP-PNT, between the normalized RIP volume signal (respectively, V _ RIP.BP[t] and V _ RIP.PNT[t]) and its normalized reference (respectively, V _ BP[t] and V _ PNT[t]). We also calculated the distance DPNT-BP between the two normalized references V _ BP(t) and V _ PNT(t). Results No significant effect of load or time on the distance occurred. Including all the recordings, the mean distance DRIP-BP (3.4±1.1%) appears significantly lower than both the mean distance DRIP-PNT (4.5±1.3%; p Conclusion The RIP seems reasonably accurate for analysis of respiratory waveform while subjects subsequently breathe against resistive loads.

Fourteen subjects learned to adjust their breath pattern to two target breaths displayed on a video screen, by using visual feedback, during two sessions 24 h apart. These two targets were respectively the smallest and the largest breaths of a ten-breath sample previously recorded from each subject's resting spontaneous breathing. Performances were significantly better for the large than for the small target breath. This cannot be directly inferred from current knowledge related to the control of movement time and amplitude, but rather it may be inferred from the periodic character of breathing, to the higher mental load during the small breath task, or to the presumably different frequencies of target breaths in the whole span of spontaneous breathing. In the second session, performance on the two targets levelled out as a result of learning.

the characteristic pattern of breathing for an individual when awake at rest may be due to forebrain influences upon breathing. To examine this hypothesis we have studied the breathing pattern in 18 healthy subjects during relaxed wakefulness (W) and during Stage 4 sleep (S4), when forebrain influences upon breathing are absent or minimal. Inspiratory and expiratory times, respiratory frequency, tidal volume, and ventilation were quantified noninvasively by respiratory inductance plethysmography. The stability of respiratory variables between W and S4 sleep was tested within individuals. The results show that (i) individuals breathe differently from each other when awake and when in S4 sleep; the range between individuals during sleep being as large as it is when awake; (ii) differences in breathing pattern between two S4 periods within an individual are relatively small; (iii) the characteristic breathing pattern of an individual when awake tends to be maintained in S4 sleep. This persistence of a respiratory ‘personality’ into S4 sleep probably indicates that there are individual differences in respiratory rhythm generation in the absence of any forebrain influences upon breathing.

The ventilatory system as many biological systems is a complex dynamical one involving many controls and regulations. More over, in a reconstructed phase space respiratory data present a structure similar to a strange attractor (cf. Figure 1). In this way, considering the respiratory system as a deterministic chaotic one seems to be a good hypothesis to understand breathing and its variability. This hypothesis remains controversial. Donaldson (1992) shows that respiratory trajectories of resting human are not random but chaotic using the Largest Lyapunov Exponent (LLE). Unfortunately, Hughson et al. (1995) said that previous suggestion of Donaldson (1992) that human respiratory pattern was chaotic appears from the outcome of surrogate data analysis in their study to have been premature. Similarly, Fortrat et al. (1997), in human resting breathing could not conclude that ventilation derive from a deterministic chaotic system. On the contrary, Sammon et al. (1991, 1993a, 1993b) show that irregular inspiratory-expiratory phase switching and central respiratory pattern generator (CRPG) output in rats are consistent with low-dimensional chaos. Small et al. (1999) bring evidence that respiratory variability in infants during quiet sleep is deterministic and not random. Starting from the hypothesis that controlling the presence of chaos by changing a parameter of a system brings further evidence of the chaotic nature of the system we tried to modify, experimentally and on simulations, the chaotic dimension of the ventilatory system by changing the resistive load in resting breathing human.

The use of respiratory inductance plethysmography (RIP) for measurement of breathing is appealing not only because of its noninvasive nature but also because it provides rib cage and abdomen cross sectional area changes.

In adult awake human subjects at rest, there exists a diversity in the breathing pattern not only in terms of tidal volume and inspiratory and expiratory duration and derived variables (TTOT, VT/TI and TI/TTOT) but also in the airflow profile. Besides this diversity, in every recording of ventilation at rest in steady-state condition breath-to-breath fluctuations are observed in ventilatory variables. This variability is non random and may be explained either by a central neural mechanism or by instability in the chemical feedback loops. Beyond this variability, each individual appears to select one particular pattern among the infinite number of possible combination of ventilatory variables and airflow profile. This one particular pattern appears to be a relatively stable characteristic of an adult individual being reproducible in several conditions and above all, after a long period of time. Consequences of this individuality of breathing pattern are discussed with regard to the selection of control subjects for a study and also per se: are there physiological situations where differences may be observed solely because of the differences in the pattern of breathing?

The purpose of this study was to assess the effects of a particular breathing pattern training (BPT) on forced expiratory volume during the first second (FEV1) and forced vital capacity (FVC) in patients with chronic obstructive pulmonary disease (COPD). The subjects adjusted each breath to a target breath displayed on a video screen, by using visual feedback. This target was chosen in an individual sample recorded at rest. We used a randomized, controlled group design. Twenty patients with stable COPD, FEV1 less than 1.5 liters, undergoing a traditional rehabilitation program were randomly assigned to the BPT group or to the control group. Each BPT subject underwent 30-35 training sessions spread out over four weeks, in addition to the traditional program. FEV1 and FVC were performed before and after this program. ANOVAs showed that FEV1 and FVC significantly improved in BPT subjects, with a mean percent increase of 22% and 19%, respectively. Corresponding changes in controls were not significant. This study showed short-term increases in FEV1 and FVC in COPD patients practicing BPT in addition to respiratory rehabilitation, in comparison with controls. Further studies should incorporate outcome data to clarify the mechanisms and the duration of this effect.

1. To assess whether voluntary control of breathing is impaired in patients with chronic obstructive pulmonary disease, a group of such patients performed a tracking task, requiring volitional control of respiratory muscles. 2. Eight patients (mean age 60 years; mean ratio of forced expiratory volume in 1 s to forced vital capacity = 31%) took part in the study. Five of the seven patients in whom blood gas measurements were made were mildly hypoxaemic (Pao2 = 53–71 mmHg), and one of these was hypercapnic (Paco2 = 55 mmHg). Each subject performed a compensatory ventilatory tracking task using a tracking system which comprised a fixed target displayed on a monitor screen and a cursor moving in a line bisecting the target. The position of the cursor was perturbed by a forcing function and patients were required to keep the cursor on the target by breathing in and out of a spirometer. 3. To allow for any non-specific deficiency in motor control, patients performed a similar manual tracking task, using their dominant arm to move a joystick. As a control group, 11 healthy subjects (mean age 58 years; mean ratio of forced expiratory volume in 1 s to forced vital capacity = 77%) underwent an identical experimental protocol. 4. Motor control performances were measured in terms of the error between the target position and the subject's positioning of the cursor. Indices of performance were the root mean square of the error and the averages of the zero errors (i.e. end expiration/arm movement towards the trunk) and the peak errors (i.e. end inspiration/arm movement from the trunk). 5. For manual tracking, patients with chronic obstructive pulmonary disease, were not significantly different from control subjects in terms of mean root mean square (69.3 versus 60.9), mean zero error (93.8 versus 72.2) or mean peak error (99.5 versus 82.7). For ventilatory tracking, mean root mean square was significantly higher in patients (83.4 versus 65.9). This was due to a significantly higher mean zero error (101.4 versus 66.1); mean peak error was not significantly different (68.3 versus 82.1). Comparison of flows achieved during ventilatory tracking with those possible during a maximal forced expiratory manoeuvre in the patients suggested that poor expiratory control in this group could be explained by their degree of airflow limitation rather than a deficiency in motor control per se. 6. These results provide no evidence that patients with chronic obstructive pulmonary disease have any impairment in their voluntary motor control of breathing.

Sixteen healthy adult subjects underwent two studies separated by 4-5 years to test whether their resting pattern of breathing was reproducible over time. From breath-by-breath analysis of airflow, measured with a pneumotachometer, the pattern of breathing was quantified in terms of individual respiratory variables; inspiratory time (TI), expiratory time (TE), total breath duration (TTOT), tidal volume (VT), VT/TI, TI/TTOT, and by taking TI, TE and VT all together (TRIAD). Also, the shape of the entire airflow profile was quantified by harmonic analysis (ASTER). A statistical analysis was designed to compare differences between the 1st and the 2nd recording within individuals with those differences observed between random pairs of recordings from the two studies in the same 16 individuals. It was found that all variables were significantly more similar within-individuals than between-individuals; this is best demonstrated when considering the ASTER and/or the TRIAD. It was concluded that the individuality of breathing pattern is maintained over a long period despite changes in smoking habit, weight, mild respiratory diseases, and other changes which occurred between the two studies in our subjects.

The existence of a characteristic pattern of breathing for each individual, when awake at rest, has previously been demonstrated1,2. In an endeavour to measure an individual’s breathing pattern when awake at rest it is desirable, but difficult, to minimise forebrain influences upon breathing3. No matter how careful one is in controlling the experimental conditions, one can never be certain that such forebrain influences are absent and it is possible that they account for an individual’s particular breathing pattern when at rest i.e. when respiratory ‘drive’ is minimal.

In awake man, voluntary and involuntary forebrain influences can interact with and can override the automatic control of breathing. These ‘behavioural’ influences diminish as the metabolic demands increase (Asmussen, 1977; Morgan & Cameron, 1985) having therefore their greatest potential effect upon breathing during relaxed wakefulness. A probable example of a behavioural influence was documented by Asmussen (1977) who showed that subjects increase their ventilation significantly when they merely open their eyes to read. We have recently repeated Asmussen’s experiment but with noninvasive techniques and an improved experimental design (Shea et al, 1987). We found that breathing is stimulated in a small (approx 6%) but consistent manner by opening the eyes to read and that it is also stimulated when the eyes are opened without reading. Similar changes in breathing were found when auditory stimulation was added to the baseline condition with eyes closed. Breathing was stimulated more when the auditory or visual stimuli had ‘meaning’ ie. reading or listening to a story.