Effects of continuous positive- and negative-pressure breathing on the pattern of breathing in man during exercise

Breathing pattern and static lung volumes were studied in 10 subjects at rest and during incremental-load cycle ergometry under three different conditions, viz. with normal pressure in the airways (control) and during continuous positive- and negative-pressure breathing (CPPB, CNPB) of +15 and -15 cmH2O. End-expiratory, end-inspiratory and mid-expiratory volumes were increased by CPPB and decreased by CNPB; these effects were especially pronounced at rest and during mild exercise. Both at rest and during exercise mean inspiratory flow (VT/TI) was exaggerated by CPPB and attenuated by CNPB. At rest these changes were due mainly to concomitant changes in tidal volume (VT) which was increased by CPPB and decreased by CNPB, while inspiratory time duration (TI) was relatively unaffected by pressure breathing. The transition from rest to loadless pedalling induced an increase in VT but no change in TI in the control condition, whereas in the CPPB and CNPB conditions TI decreased and VT remained unaltered. This CPPB- and CNPB-induced change in the volume-time threshold relationship at the onset of pedalling is attributed to increased stretch receptor activity in the extrathoracic portion of the trachea as a result of the increments in transmural pressure. During the course of exercise there was an inverse relationship between the slope of the VT-TI curve and the mid-expiratory volume in that the slope was greater in the control than in the CPPB condition and greatest during CNPB, suggesting that in exercise hyperpnoea the VT-TI relationship is also determined by pulmonary and/or thoracic wall stretch receptors capable of sensing the absolute lung volume.     

The pattern of breathing during hypoxic exercise

Summary Breathing pattern was studied in six subjects in normoxia (F_IO₂=0.21) and hypoxia (F_IO₂=0.12) at rest and during incremental work-rate exercise. Ventilation (V) as well as mean inspiratory flow (V_T/T_I) increased with exercise intensity and were augmented in the hypoxic environment, whereas the ratio between inspiratory (T_I) and total (T_tot) breath durations increased with exercise intensity but was unaffected by hypoxia. The relationship of tidal volume (V_T) and inspiratory time duration (T_I) showed linear, coinciding ranges for the normoxic and hypoxic conditions up to V_T/T_I values of about 2.5 l · s⁻¹. At higher V_T/T_I values T_I continued to decrease, whereas V_T tended to level off, an effect which was more evident in the hypoxic condition. The results suggest that the hypoxic augmentation of exercise hyperpnea is primarily brought about by an enhancement of central inspiratory drive, the timing component being largely unaffected by the hypoxic environment, and that at low to moderate levels of exercise hyperpnea inspiratory off-switch mechanisms are essentially unaffected by moderate hypoxia.     

Cardiodynamic factors affecting hyperpnea during steady-state exercise in man

In order to know the role of cardiodynamic factors for exercise hyperpnea, ventilation and several cardiorespiratory variables were measured simultaneously in human subjects during exercise. Cardiac output (Q) and mixed venous CO2 content (CVCO2) were determined by a rebreathing method. The correlation coefficients (r) for the relationships between minute expiratory ventilation (VE) and each of end-tidal CO2 tension (PETCO2), Q, CVCO2, CO2 flow into the lung (QCO2, the product of Q and CVCO2), oxygen consumption (VO2), and CO2 output (VCO2) were determined during the steady-state exercise up to 90 W. The correlation was highly significant (r = 0.84-0.99, p less than 0.001) in each case except for PETCO2 (r = 0.13, N.S.). The highest correlation was observed in the VE-VCO2 relationship. It was assume that VCO2 released from the pulmonary capillaries into the alveoli is the most likely stimulus leading to exercise hyperpnea. Arterial CO2 oscillation may be regarded as a potential linkage between VCO2 and VE.     

Imposed breathing pattern alters respiratory work during exercise

Previous studies have shown the existence of an ideal respiratory rate (f _R) for a given ventilation at which the respiratory work rate (J·s^–1) is minimum. The purpose of the present study was to measure the effect off _R, tidal volume and breathing pattern on the respiratory work per breath and respiratory work rate during exercise on a cycle ergometer. Three work rates on the cycle ergometer were used and at each work rate the ventilation was kept constant. Two different breathing patterns were applied at each ventilation. Nine male trained cyclists [mean (SD) maximum oxygen consumption, 57 (5.47) ml·kg^–1·min^–1] participated in this study. The results indicated that there was a significant difference in the respiratory work per breath, with different breathing patterns at a given ventilation and for all levels of ventilation. There was no significant difference in the respiratory work rate with different breathing patterns at a given ventilation and for all levels of ventilation. In addition, the respiratory work per breath and respiratory work rate were increased with increasing ventilation. Thus, the data indicated that the manipulation of tidal volume, respiratory rate and breathing pattern had no significant effect on the energy cost of breathing for a given ventilation. The absence of this significant effect on respiratory work rate was observed across a range of ventilation from 24 to 72 l·min^–1. These findings suggest that the breathing pattern is predominantly an expression of the function of the higher respiratory brain center instead of energy economy, at least within this range of ventilation.     

Effects of exercise and CO2 inhalation on the breathing pattern in man

Conflicting opinions exist concerning the breathing pattern in man during resting and stimulated ventilation. Some but not all investigators have reported the existence of an abrupt change, a 'breakpoint', in the relation between mean tidal volume and mean inspiratory time. Different opinions exist as to whether the slope and the intercept for the relation between mean minute ventilation and mean tidal volume are identical regardless of the mode of stimulating the ventilation. We have studied 10 subjects, at rest and during graded stimulation of ventilation by CO2 inhalation and exercise. No breakpoint was observed in the relations between (1) mean tidal volume and mean inspiratory time and (2) mean tidal volume and mean expiratory time, even if a wide range of tidal volumes was achieved in our subjects. Carbon dioxide inhalation (normoxic or hyperoxic) and exercise gave different regression lines for the relation between mean minute ventilation and mean tidal volume in 8 out of 10 subjects with a larger slope during exercise. At exercise inspiratory time decreased with any increase in tidal volume, while during CO2 breathing no consistent change in inspiratory time was seen. Mean inspiratory flow was linearly related to exercise load and apparently also to arterial carbon dioxide pressure. We conclude that CO2 breathing gives a breathing pattern which is different from that obtained with exercise in the majority of normal subjects. Furthermore, we could not confirm the existence of breakpoints in relations describing the breathing pattern of normal man.     

Breathing in man during steady-state exercise on the bicycle at two pedalling frequencies, and during treadmill walking.

1. The breathing pattern, that is the changes in tidal volume (VT), and in inspiratory (TI) and expiratory (TE) durations, has been studied as ventilation increases in exercise. 2. Five healthy subjects were studied in steady-state exercise on a bicycle ergometer, breathing air, at two speeds of pedalling and at six different loads. The pattern was recorded for single breaths. Two of the subjects were also studied while walking on a treadmill with four combinations of speed and gradient. 3. In bicycle exercise, as the CO2 output increased mean VT increased, and mean TI and TE decreased, the absolute decrease in TI being small. The pedalling speed did not affect these relationships. 4. Individual breath durations showed no tendency to group around multiples of the period of rotation of the pedals. 5. In treadmill exercise, no clear influence of stride rate on respiratory rate could be found. The pattern was similar to that found in bicycle exercise. Again no grouping could be found. 6. No evidence of an effect of frequency of limb movement on breathing pattern in submaximal exercise has been found. The selection of breathing pattern seems to be unrelated to the nature of the stimulus but closely geared to the metabolic needs of the body.     

Pulmonary gas exchange and breathing pattern during and after exercise in highly trained athletes

Summary Highly trained athletes (HT) have been found to show arterial hypoxaemia during strenuous exercise. A lack of compensatory hyperpnoea and/or a limitation of pulmonary diffusion by pulmonary interstitial oedema have been suggested as causes, but the exact role of each is not clear. It is known, however, that interstitial pulmonary oedema may result in rapid shallow breathing (RSB). The purpose of this study was therefore twofold: firstly, to determine the exact role of a lack of compensatory hyperpnoea versus a widened in ideal alveolar minus arterial oxygen partial pressure difference [P _A(i)-aO₂] in the decrease in partial pressure of oxygen in arterial blood (P _aO₂) and, secondly, to detect RSB during recovery in HT. Untrained subjects (UT) and HT performed exhausting incremental exercise. During rest, exercise testing, and recovery, breathing pattern, respiratory gas exchange, and arterial blood gases were measured. The P _A(i)-aO₂ and the difference in tidal volume (V _T) between exercise and recovery for the same level of ventilation, normalized to vital capacity of the subject [V _T(%VC)], were then calculated. A large positive V _T (%VC) was considered to be the sign of RSB. HT showed a marked hypoxaemia (F=11.6, P < 0.0001), higher partial pressure of carbon dioxide in arterial blood (F= 3.51, P < 0.05), and lower ideal partial pressure of oxygen in alveolar gas (P < 0.001). The relationship between P _A(i)-aO₂ and oxygen consumption was the same for the two groups. The widening P _A(i)-aO₂ persisted throughout recovery for both HT and UT. The RSB was observed in HT during recovery. These results would suggest that the lack of compensatory hyperpnoea in HT during submaximal exercise was the major factor in the decrease in P _aO₂. The RSB and the widening P _A(i)-aO₂ during recovery would suggest that interstitial pulmonary oedema was involved during the strenuous exercise in the case of HT. Lastly, the wide P _A(i)-aO₂ observed in UT during recovery would suggest that an increase in extravascular pulmonary water may also have been involved for these subjects, although to a lesser extent.     

Oronasal breathing during exercise

The shift from nasal to oronasal breathing (ONBS) has been observed on 73 subjects with two independent methods. A first group of 63 subjects exercising on a bicycle ergometer at increasing work load (98–196 W) has been observed. On 35 subjects the highest value of ventilation attained with nasal breathing was 40.2±9.41 · min^–1 S.D. Ten subjects breathed through the mouth at all loads, while 5 never opened the mouth. On 13 subjects it was not possible to make reliable measurements. On a second group of 10 subjects utilizing a different techniques which did not need a face mask, the ventilation at which one changes the pattern of breathing was found to be 44.2±13.51·min^–1 S.D. On the same subjects nasal resistance did not show any correlation with ONBS. It is concluded that ONBS is not solely determined by nasal resistance, though an indirect effect due to hypoventilation and hence to changes in alveolar air composition cannot be ruled out. It is likely that ONBS is also influenced by psychological factors.     

Effect of He-O2 breathing on blood gases and ventilation during exercise in normal man

Temporal changes in ventilation (VI) and arterial blood gases after substitution of helium (He) for nitrogen were studied in normal man during constant load exercises of 14 min duration (30 and 90 W). An abrupt switch of helium for air breathing (protocol 1; 5 subjects), or vice-versa (protocol 2; 4 subjects), was made at the 7th min. Whatever the work loads, the effect of He appeared rapidly: higher values of VI (protocol 1) were observed throughout the 7 min period of He-O2 breathing, but were only significant (p less than or equal to 0.05) during the first minute after substitution at 90 W. Reverse pattern was observed in protocol 2. Helium induced alveolar hyperventilation: sustained and significant hypocapnia (p less than or equal to 0.05) was observed during helium breathing. This effect does not seem to be a consequence of pulmonary gas exchange disturbance, in that concomitant Po2 was normal. It is suggested that He could have evoked a reflex which overrode humoral regulation. Significant increase in ventilatory CO2 responses at rest during He-O2 compared to air breathing in seven subjects (p less than or equal to 0.01) seems to confirm this hypothesis.     

Respiratory and circulatory responses to sustained positive-pressure breathing and exercise in man.

To investigate the effects of sustained positive-pressure breathing (PPB) on the adaptation of respiratory and circulatory functions to exercise, 8 healthy volunteers were exposed to PPB of air at 15 and 30 cm H2O in the supine position at rest and while performing leg exercise at 50% of individual maximal working capacity. PPB was both subjectively and objectively better tolerated when combined with exercise than it was at rest. PPB at 30 cm H2O resulted in marked hyperventilation with alkalosis in the resting condition, but did not significantly affect respiratory minute volume, blood gases or acid-base balance during exercise. Cardiac output and left ventricular work were reduced by about one fifth and one third, respectively, both at rest and during exercise. In contrast to the case at normal airway pressure, exercise-induced increase in cardiac output was accompanied by an increment in stroke volume during PPB. Although mean arterial pressure (relative to atmospheric) was elevated by PPB at rest and during exercise, the driving pressure in systemic circuits (arterial minus central venous pressure) was reduced in both conditions. It is concluded that dynamic exercise counteracts deleterious effects of PPB by normalizing respiratory function and by improving cardiac filling by activation of the leg muscle and the abdominal pumps.     

Evidence of an altered pattern of breathing during exercise in recipients of heart-lung transplants

Recipients of heart-lung transplants represent an unusual opportunity to study the regulation of ventilation, because the neural pathways between the lungs and the central nervous system are disrupted in these patients. We compared the ventilation response in seven recipients of heart-lung transplants who had normal pulmonary function and seven recipients of heart transplants, all of whom performed incremental bicycle ergometry. The level of ventilation in recipients of heart-lung transplants was similar to that in heart-transplant recipients for equivalent levels of carbon dioxide production. Arterial pH and partial pressure of carbon dioxide at maximal exercise were normal and not significantly different in the two groups, also suggesting that levels of ventilation were appropriate in both groups. However, the rate of the rise in respiratory rate for increasing levels of ventilation was significantly lower in recipients of heart-lung transplants than in heart-transplant recipients, and the initial increase in tidal volume was more rapid in the former group than in the latter. Thus, recipients of heart-lung transplants have an appropriate level of ventilation during exercise as the result of a disproportionate increase in tidal volume at a reduced respiratory rate. We speculate that intrapulmonary receptors are important in regulating the pattern, but not the absolute level, of ventilation during exercise.     

Implications of breath-by-breath oxygen uptake determination on kinetics assessment during exercise

We tested that the breath-by-breath [Formula: see text] determination by an algorithm termed BR did not bias the kinetics parameters. It was compared to two other algorithms using a correction for changes in lung gas stores between two successive breaths (AU, W) and one without correction (NC). Ten healthy male subjects cycled 10min at 15 and 30W below and above ventilatory threshold (VT) after 3min at 0W. The breath-by-breath [Formula: see text] variability was lower with BR than the other methods during the last 3min at each power. [Formula: see text] kinetics was described by a mono-exponential model at power below VT and a bi-exponential model above VT. Differences in parameter were only observed for the primary component between estimates using AU and NC. The between-subject variability in the parameters of the slow component at 15W above VT was lower with AU and BR than W and NC. It was concluded that the BR algorithm could be used to analyse the [Formula: see text] kinetics during exercise.     

Influence of anthropometric characteristics on changes in maximal exercise ventilation and breathing pattern during growth in boys

Summary The aim of this study was to investigate the effect of growth on ventilation and breathing pattern during maximal exercise oxygen consumption (VO_2max and their relationships with anthropometric characteristics. Seventy six untrained schoolboys, aged 10.5–15.5 years, participated in this study. Anthropometric measurements made included body mass, height, armspan, lean body mass, and body surface area. During an incremental exercise test, maximal ventilation (V_Emax), tidal volume (V _Tmax), breathing frequency (f _max), inspiratory and expiratory times (t _Imax and t _Emax), total duration of respiratory cycle (t _TOTmax), mean inspiratory flow (V _T/t _Imax), and inspiration fraction (t _I/t _TOTmax) were measured at VO_2max. A power function was calculated between anthropometric characteristics and ventilatory variables to determine the allometric constants. The results showed firstly, that V_Emax, V _Tmax, t _Imax, t _Emax, t _TOTmax, and V _T/t _Imax increased with age and anthropometric characteristics (P<0.001), f _max decreased (P<0.001), and t _I/t _TOTmax remained constant during growth; secondly that lean body mass explained the greatest percentage of variance of V_Emax (62.1%), V _Tmax (76.8%), and V _T/t _Imax (70.6%), while anthropometric characteristics explained a slight percentage of variance of f _max and timing; and thirdly that V_Emax, V _Tmax, and V _T/t _Imax normalized by lean body mass did not change significantly with age. We concluded that at VO_2max there were marked changes in ventilation and breathing pattern with growth. The changes in V_Emax, V _Tmax, and V _T/t _Imax were strongly related to the changes in lean body mass.     

Respiratory and circulatory responses to sustained positive-pressure breathing and exercise in man

To investigate the effects of sustained positive-pressure breathing (PPB) on the adaptation of respiratory and circulatory functions to exercise, 8 healthy volunteers were exposed to PPB of air at 15 and 30 cm H₂O in the supine position at rest and while performing leg exercise at 50% of individual maximal working capacity. PPB was both subjectively and objectively better tolerated when combined with exercise than it was at rest. PPB at 30 cm H_aO resulted in marked hyperventilation with alkalosis in the resting condition, but did not significantly affect respiratory minute volume, blood gases or acid-base balance during exercise. Cardiac output and left ventricular work were reduced by about one fifth and one third, respectively, both at rest and during exercise. In contrast to the case at normal airway pressure, exercise-induced increase in cardiac output was accompanied by an increment in stroke volume during PPB. Although mean arterial pressure (relative to atmospheric) was elevated by PPB at rest and during exercise, the driving pressure in systemic circuits (arterial minus central venous pressure) was reduced in both conditions. It is concluded that dynamic exercise counteracts deleterious effects of PPB by normalizing respiratory function and by improving cardiac filling by activation of the leg muscle and the abdominal pumps.     

Dynamic control of breathing during exercise and hypercapnia

The dynamic influences of end-tidal CO₂ and exercise on ventilation are compared when CO₂ and exercise are imposed separately and when they are imposed simultaneously. Five human subjects are studied. The subjects performed three trials: random work rate forcing, random CO₂ inhalation and their simultaneous loading. The work rate was varied between 20 and 80 W as a pseudorandom binary sequence. The concentration of inspired CO₂ was varied randomly between 0 and 7 per cent, adjusted so that it produced approximately the same amount of ventilatory fluctuations as the random work load. The relative contribution of each variable was analysed using multivariate autoregressive analysis at frequencies ranging from 0·1 to 1 cycle min⁻¹. The results show that the dynamics of the response to CO₂ inhalation, exercise and their combination are nonlinear and that the combination of CO₂ inhalation and exercise magnifies the nonlinear behaviour. Ventilation is largely unaffected by either work rate or end-tidal CO₂ at 1 cycle min⁻¹. During simultaneous CO₂ and work rate forcing, ventilation tends to follow the change in the end-tidal CO₂.     

Airway anaesthesia and breathing pattern during exercise in normal subjects and in eucapnic patients with chronic airflow obstruction

In order to deprive vagal upper and large airway receptors, an aerosol of 4% lidocaine (240 mg) was delivered to eight normal subjects and to eight eucapnic patients with chronic obstructive pulmonary disease (COPD). After this procedure, gag reflex (mechanical irritation of the larynx) and cough reflex tested by an aerosol of 10% citric acid were absent in all subjects. The anaesthesia was tolerated well by all the subjects and did not influence baseline pulmonary function tests. Moreover, during exercise, before and after lidocaine, no significant difference in O2 intake (VO2) or in blood gases (measured in patients only) could be observed. After lidocaine administration, no significant changes were seen in any of the respiratory variables studied in normal subjects or in COPD patients compared to the basal conditions. This could indicate that vagal upper and large airway receptors do not play an important role for the breathing pattern and ventilatory drive during exercise either in normal subjects or eucapnic patients with COPD.     

Ventilatory response and pattern of breathing during hypercapnia

In an attempt to narrow the definition of normal ventilatory response to hypercapnia (SVE), we studied 105 healthy Caucasians, aged from 18 to 80 years and living at sea level. The mean and SD of SVE were 2.18 +/- 0.77 1 X min-1 X mmHg-1 in males and 1.70 +/- 0.74 in females, narrower than the ranges previously reported. The 95% tolerance limits were 0.491-3.735 and 0.241-2.963 respectively. SVE was correlated with height, body surface area, static and dynamic lung volumes (p less than 0.01), age and weight (p less than 0.05). A prediction formula for SVE was derived on the basis of FEV1, which of the above parameters best correlated with SVE. The separate measurement of the tidal volume and frequency changes (SVT, Sf and SVT/Sf) showed that the SVT and SVT/Sf were significantly higher in males than in females even after adjustment for lung volume (p less than 0.01 and p less than 0.02 respectively), suggesting a different pattern of response to hypercapnia between the sexes.