Effects of augmented respiratory muscle pressure production on locomotor limb venous return during calf contraction exercise.

We determined effects of augmented inspiratory and expiratory intrathoracic pressure or abdominal pressure (Pab) excursions on within-breath changes in steady-state femoral venous blood flow (Qfv) and net Qfv during tightly controlled (total breath time = 4 s, duty cycle = 0.5) accessory muscle/"rib cage" (DeltaPab <2 cmH2O) or diaphragmatic (DeltaPab >5 cmH2O) breathing. Selectively augmenting inspiratory intrathoracic pressure excursion during rib cage breathing augmented inspiratory facilitation of Qfv from the resting limb (69% and 89% of all flow occurred during nonloaded and loaded inspiration, respectively); however, net Qfv in the steady state was not altered because of slight reductions in femoral venous return during the ensuing expiratory phase of the breath. Selectively augmenting inspiratory esophageal pressure excursion during a predominantly diaphragmatic breath at rest did not alter within-breath changes in Qfv relative to nonloaded conditions (net retrograde flow = -9 +/- 12% and -4 +/- 9% during nonloaded and loaded inspiration, respectively), supporting the notion that the inferior vena cava is completely collapsed by relatively small increases in gastric pressure. Addition of inspiratory + expiratory loading to diaphragmatic breathing at rest resulted in reversal of within-breath changes in Qfv, such that >90% of all anterograde Qfv occurred during inspiration. Inspiratory + expiratory loading also reduced steady-state Qfv during mild- and moderate-intensity calf contractions compared with inspiratory loading alone. We conclude that 1) exaggerated inspiratory pressure excursions may augment within-breath changes in femoral venous return but do not increase net Qfv in the steady state and 2) active expiration during diaphragmatic breathing reduces the steady-state hyperemic response to dynamic exercise by mechanically impeding venous return from the locomotor limb, which may contribute to exercise limitation in health and disease.     

Effect of inspiratory resistive loading on control of ventilation during progressive exercise

Eight healthy volunteers performed gradational tests to exhaustion on a mechanically braked cycle ergometer, with and without the addition of an inspiratory resistive load. Mean slopes for linear ventilatory responses during loaded and unloaded exercise [change in minute ventilation per change in CO2 output (delta VE/delta VCO2)] measured below the anaerobic threshold were 24.1 +/- 1.3 (SE) = l/l of CO2 and 26.2 +/- 1.0 l/l of CO2, respectively (P greater than 0.10). During loaded exercise, decrements in VE, tidal volume, respiratory frequency, arterial O2 saturation, and increases in end-tidal CO2 tension were observed only when work loads exceeded 65% of the unloaded maximum. There was a significant correlation between the resting ventilatory response to hypercapnia delta VE/delta PCO2 and the ventilatory response to VCO2 during exercise (delta VE/delta VCO2; r = 0.88; P less than 0.05). The maximal inspiratory pressure generated during loading correlated with CO2 sensitivity at rest (r = 0.91; P less than 0.05) and with exercise ventilation (delta VE/delta VCO2; r = 0.83; P less than 0.05). Although resistive loading did not alter O2 uptake (VO2) or heart rate (HR) as a function of work load, maximal VO2, HR, and exercise tolerance were decreased to 90% of control values. We conclude that a modest inspiratory resistive load reduces maximum exercise capacity and that CO2 responsiveness may play a role in the control of breathing during exercise when airway resistance is artificially increased.     

Changes in breathing when switching from nares to tracheostomy breathing in awake ponies

We assessed the consequences of respiratory unloading associated with tracheostomy breathing (TBr). Three normal and three carotid body-denervated (CBD) ponies were prepared with chronic tracheostomies that at rest reduced physiological dead space (VD) from 483 +/- 60 to 255 +/- 30 ml and lung resistance from 1.5 +/- 0.14 to 0.5 +/- 0.07 cmH2O . l-1 . s. At rest and during steady-state mild-to-heavy exercise arterial PCO2 (PaCO2) was approximately 1 Torr higher during nares breathing (NBr) than during TBr. Pulmonary ventilation and tidal volume (VT) were greater and alveolar ventilation was less during NBr than TBr. Breathing frequency (f) did not differ between NBr and TBr at rest, but f during exercise was greater during TBr than during NBr. These responses did not differ between normal and CBD ponies. We also assessed the consequences of increasing external VD (300 ml) and resistance (R, 0.3 cmH2O . l-1 . s) by breathing through a tube. At rest and during mild exercise tube breathing caused PaCO2 to transiently increase 2-3 Torr, but 3-5 min later PaCO2 usually was within 1 Torr of control. Tube breathing did not cause f to change. When external R was increased 1 cmH2O . l-1 . s by breathing through a conventional air collection system, f did not change at rest, but during exercise f was lower than during unencumbered breathing. These responses did not differ between normal, CBD, and hilar nerve-denervated ponies, and they did not differ when external VD or R were added at either the nares or tracheostomy.(ABSTRACT TRUNCATED AT 250 WORDS)     

Movement of the human upper airway during inspiration with and without inspiratory resistive loading

The electromyographic (EMG) activity of human upper airway muscles, particularly the genioglossus, has been widely measured, but the relationship between EMG activity and physical movement of the airway muscles remains unclear. We aimed to measure the motion of the soft tissues surrounding the airway during normal and loaded inspiration on the basis of the hypothesis that this motion would be affected by the addition of resistance to breathing during inspiration. Tagged MR imaging of seven healthy subjects was performed in a 3-T scanner. Tagged 8.6-mm-spaced grids were used, and complementary spatial modulation of magnetization images were acquired beginning ～200 ms before inspiratory airflow. Deformation of tag line intersections was measured. The genioglossus moved anteriorly during normal and loaded inspiration, with less movement during loaded inspiration. The motion of tissues at the anterior border of the upper airway was nonuniform, with larger motions inferiorly. At the level of the soft palate, the lateral dimension of the airway decreased significantly during loaded inspiration (-0.15 ± 0.09 and -0.48 ± 0.09 mm during unloaded and loaded inspiration, respectively, P < 0.05). When resistance to inspiratory flow was added, genioglossus motion and lateral dimensions of the airway at the level of the soft palate decreased. Our results suggest that genioglossus motion begins early to dilate the airway prior to airflow and that inspiratory loading reduces the anterior motion of the genioglossus and increases the collapse of the lateral airway walls at the level of the soft palate.     

Breathlessness during exercise with and without resistive loading

The purpose of this study was to quantify the intensity of breathlessness associated with exercise and respiratory resistive loading, with the specific purpose of isolating the quantitative contributions of inspiratory pressure, length, velocity, and frequency of inspiratory muscle shortening and duty cycle to breathlessness. The intensity of inspiratory pressure was quantified by measurement of estimated esophageal pressure (Pes = pressure at the mouth plus lung pressure), the extent of shortening by tidal volume (VT), and the velocity of shortening by inspiratory flow rate (VI). Six normal subjects underwent five incremental (100 kpm X min-1 X min-1) exercise tests on a cycle ergometer to maximum capacity. The first and last test were unloaded and the intervening tests were performed with external added resistances of 33, 57, and 73 cm H2O X l-1 X s in random order. The resistances were selected to provide a range of pressures, tidal volumes, flow rates, and patterns of breathing. At rest and at the end of each minute during exercise the subjects estimated the intensity of breathlessness (psi) by selecting a number ranging from 0 to 10 (Borg rating scale, 0 indicating no appreciable breathlessness and 10 the maximum tolerable sensation). Breathlessness was significantly and independently related to Pes (P less than 0.0001), VI (P less than 0.0001), frequency of breathing (fb) (P less than 0.01), and duty cycle [ratio of inspiratory duration to total breath duration (TI/TT)] (P less than 0.01): psi = 0.11 Pes + 0.61 VI + 1.99 TI/TT + 0.04 fb - 2.60 (r = 0.83). The results suggest that peak pressure (tension), VI (velocity of inspiratory muscle shortening), TI/TT, and fb contribute independently and collectively to breathlessness. The perception of respiratory muscle effort is ideally suited to subserve this sensation. The neurophysiological mechanism purported is a conscious awareness of the intensity of the outgoing motor command by means of corollary discharge within the central nervous system.     

Mechanisms of pulsus paradoxus in airway obstruction

To assess the mechanisms of pulsus paradoxus (i.e., inspiratory decline of greater than or equal to 10 Torr in systolic pressure) in airway obstruction, we studied 12 patients with chronic airflow obstruction before and during breathing through an external resistance that provided loads during both inspiration and expiration. Esophageal pressure (Ppl) and brachial artery pressure, relative to either atmospheric (Pa) or esophageal pressure (Patm), were measured simultaneously during normal and loaded breathing. It was assumed that changes in intrathoracic systemic arterial transmural pressure were adequately represented by Patm. During control, no significant difference between systolic fluctuation (delta Pa) and pleural swings (delta Ppl) was found. Concurrently, inspiratory and expiratory Patm were nearly identical. By contrast, under maximally loaded conditions, higher magnitudes of delta Ppl than delta Pa were found and consequently Patm rose with inspiration. In this connection, the plot of delta Pa against delta Ppl showed that the slopes for delta Ppl less than or equal to 15 Torr (1.2 Torr delta Pa/delta Ppl) and delta Ppl greater than 15 Torr (0.4 Torr delta Pa/delta Ppl) were significantly different. Under all experimental conditions we found during inspiration a rise in diastolic Patm that is consistent with an increase in left ventricular afterload.(ABSTRACT TRUNCATED AT 250 WORDS)     

Within-breath electromyographic changes during loaded breathing in adult sheep

To investigate the changes in diaphragm electromyogram (EMG) during the course of severe loaded breathing, we subjected five conscious adult sheep to inspiratory flow resistive breathing (resistance greater than 150 cmH2O X l-1 X s) for up to 2-3 h and studied the total EMG power per breath (iEMG) and the EMG power per unit time after dividing the duration of EMG activity within each breath into three equal parts (iEMG1, iEMG2, and iEMG3). Both total breath iEMG and transdiaphragmatic pressure (Pdi) increased, remained at a high level for a certain period of time, and then started to fall. A change in the pattern of iEMG within a breath was observed during loaded breathing. The increase in total-breath iEMG was associated mostly with an increase in iEMG3, or the last part of the EMG power within each inspiration. Similarly, the decrease in total breath iEMG was primarily due to a decrease in iEMG3. We conclude that, in sheep subjected to severe IFR loads for prolonged periods the marked increase in total-breath iEMG at the beginning of loaded breathing and the marked decrease in this iEMG at the time of decrease in Pdi are largely due to changes in iEMG that occur during the latter third of each breath. We speculate that during loaded breathing the recruitment pattern of diaphragmatic muscle fibers changes during the course of an inspiratory effort.     

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)     

Respiratory volume-time relationships during resistive loading in the cat.

The first-breath (neural) effects of graded resistive loads added separately during inspiration and expiration was studied in seven anesthetized cats before and after bilateral vagotomy. Additions of airflow resistance during inspiration reduced the volume inspired (VI) and increased inspiratory duration (TI). The duration of the ensuing unloaded expiration (TE) was unchanged. Vagotomy eliminated the TI modulation with inspiratory loads. Tracheal occlusion at the onset of inspiration yielded TI values similar to the fixed values observed following vagotomy. Resistive loads added during expiration produced similar results. Expired volume (VE) decreased and (TE) increased approaching the values obtained after vagotomy. Unlike the inspiratory resistive loads, loading during expiration results in an upward shift in the functional residual capacity (FRC). The FRC shift produces a time lag between the onset of diaphragmatic (EMG) activity and the initiation of airflow of the next (unloaded) inspiration. These studies suggest separate volume-time relationships for the inspiratory and expiratory phases of the breathing cycle. Both relationships are dependent upon vagally mediated volume feedback.     

Effect of elastic loading on ventilatory pattern during progressive exercise

Ventilatory responses to progressive exercise, with and without an inspiratory elastic load (14.0 cmH2O/l), were measured in eight healthy subjects. Mean values for unloaded ventilatory responses were 24.41 +/- 1.35 (SE) l/l CO2 and 22.17 +/- 1.07 l/l O2 and for loaded responses were 24.15 +/- 1.93 l/l CO2 and 20.41 +/- 1.66 l/l O2 (P greater than 0.10, loaded vs. unloaded). At levels of exercise up to 80% of maximum O2 consumption (VO2max), minute ventilation (VE) during inspiratory elastic loading was associated with smaller tidal volume (mean change = 0.74 +/- 0.06 ml; P less than 0.05) and higher breathing frequency (mean increase = 10.2 +/- 0.98 breaths/min; P less than 0.05). At levels of exercise greater than 80% of VO2max and at exhaustion, VE was decreased significantly by the elastic load (P less than 0.05). Increases in respiratory rate at these levels of exercise were inadequate to maintain VE at control levels. The reduction in VE at exhaustion was accompanied by significant decreases in O2 consumption and CO2 production. The changes in ventilatory pattern during extrinsic elastic loading support the notion that, in patients with fibrotic lung disease, mechanical factors may play a role in determining ventilatory pattern.     

Relationships between forced vital capacity and subjective responses to added resistive load to inspiration

1. 1. This study was conducted to investigate the effects of forced vital capacity on breathing pattern and subjective responses to inspiratory resistance.

2. 2. The subjects were divided into two groups according to their %FVC [large (L) and small (S) group; five subjects in each].

3. 3. Added inspiratory resistances were 0.6 (control), 1.5 (R1), 2.5 (R2), 3.1 (R3) cmH₂O · 1⁻¹ · s.

4. 4. Breathing pattern was analyzed by personal computer during rest and exercise with bicycle ergometer.

5. 5. The degree of sensation of breathing difficulty was expressed in SNS reported in our previous study.

6. 6. SNS in S group increased with resistance while no tendency was observed in L group. SNS in S group was significantly greater than that in L group at R3 condition.

7. 7. The breathing pattern of S group was characterized in smaller tidal volume and faster respiratory frequency compared to those of L group with no resistive load.

8. 8. However, outstanding changes in breathing pattern were observed in S group with longer inspiratory time and lower mean inspiratory flow rate when resistive loads were added, which led to increased tidal volume and decreased respiratory frequency.

Effects of expiratory loading on respiration in humans

We examined the effects of expiratory resistive loads of 10 and 18 cmH2O.l-1.s in healthy subjects on ventilation and occlusion pressure responses to CO2, respiratory muscle electromyogram, pattern of breathing, and thoracoabdominal movements. In addition, we compared ventilation and occlusion pressure responses to CO2 breathing elicited by breathing through an inspiratory resistive load of 10 cmH2O.l-1.s to those produced by an expiratory load of similar magnitude. Both inspiratory and expiratory loads decreased ventilatory responses to CO2 and increased the tidal volume achieved at any given level of ventilation. Depression of ventilatory responses to Co2 was greater with the larger than with the smaller expiratory load, but the decrease was in proportion to the difference in the severity of the loads. Occlusion pressure responses were increased significantly by the inspiratory resistive load but not by the smaller expiratory load. However, occlusion pressure responses to CO2 were significantly larger with the greater expiratory load than control. Increase in occlusion pressure observed could not be explained by changes in functional residual capacity or chemical drive. The larger expiratory load also produced significant increases in electrical activity measured during both inspiration and expiration. These results suggest that sufficiently severe impediments to breathing, even when they are exclusively expiratory, can enhance inspiratory muscle activity in conscious humans.     

Steady-state response of quadriplegic subjects to inspiratory resistive load

Normal subjects preserve tidal volume (VT) in the face of added inspiratory resistance by increasing maximal amplitude and duration of the rising phase of respiratory driving pressure (DP) and by changing the shape of this phase to one that is more concave to the time axis. To explore the possible role of chest wall afferents in mediating these responses, we determined averaged DP in eight quadriplegic subjects during steady-state unloaded breathing and while breathing through an inspiratory resistance (8.5 cmH2O X 1(-1) X s). As with normal subjects, quadriplegics preserved VT (loaded VT = 106% control) by utilizing all three mechanisms. However, prolongation of the inspiratory duration derived from the DP waveform (+22% vs. +42%) and shape response were significantly less in the quadriplegic subjects. Shape response was completely absent in subjects with C4 lesions. The results provide strong evidence that respiratory muscle spindles are responsible for shape response and that changes in afferent feedback from the chest wall play an important role in mediating inspiratory prolongation.     

Background ventilatory stimulus as a determinant of load compensation

Compensation for inspiratory flow-resistive loading was compared during progressive hypercapnia and incremental exercise to determine the effect of changing the background ventilatory stimulus and to assess the influence of the interindividual variability of the unloaded CO2 response on evaluation of load compensation in normal subjects. During progressive hypercapnia, ventilatory response was incompletely defended with loading (mean unloaded delta VE/delta PCO2 = 3.02 +/- 2.29, loaded = 1.60 +/- 0.67 1.min-1.Torr-1 CO2, where VE is minute ventilation and PCO2 is CO2 partial pressure; P less than 0.01). Furthermore the degree of defense of ventilation with loading was inversely correlated with the magnitude of the unloaded CO2 response. During exercise, loading produced no depression in ventilatory response (mean delta VE/delta VCO2 unloaded = 20.5 +/- 1.9, loaded = 19.2 +/- 2.5 l.min-1.l-1.min-1 CO2 where VCO is CO2 production; P = NS), and no relationship was demonstrated between degree of defense of the exercise ventilatory response and the unloaded CO2 response. Differences in load compensation during CO2 rebreathing and exercise suggest the presence of independent ventilatory control mechanisms in these states. The type of background ventilatory stimulus should therefore be considered in load compensation assessment.     

Respiration during exercise in conscious laryngectomized humans

We compared respiratory patterning at rest and during steady cycle exercise at work rates of 30, 60, and 90 W in 7 male chronically laryngectomized subjects and 13 normal controls. Breathing was measured with a pneumotachograph and end-tidal PCO2 by mass spectrometer. Inspired air was humidified and enriched to 35% O2. Peak flow, volume, and times for the inspiratory and expiratory half cycles, time for expiratory flow, minute ventilation, and mean inspiratory flow were computer averaged over at least 40 breaths at rest and during the last 2 min of 5-min periods at each work rate. During the transition from rest to exercise and with increasing work rate in both groups, there was an increase in respiratory rate and depth with selective and progressive shortening of expiratory time; these responses were not significantly different between the two groups, but there was a suggestion that respiratory "drive" as quantitated by mean inspiratory flow may limit in the laryngectomized subjects at high work rates. Time for expiratory flow increased on transition from rest to exercise and then decreased in both groups as the work rate increased; it was shorter in the laryngectomy than control group at all levels. In the laryngectomized subjects there was significantly more breath-by-breath scatter in some variables at rest, but there was no difference during exercise. It is concluded that chronic removal of the larynx and upper airways in mildly hyperoxic conscious humans has only subtle and, therefore, functionally insignificant effects on breathing during moderate exercise. Evidence is provided that the upper airways can modulate expiratory flow but not expiratory time during exercise.     

Significance of airway resistance for the pattern of breathing and lung volumes in exercising humans

The effects of increased airway resistance on lung volumes and pattern of breathing were studied in eight subjects performing leg exercise on a cycle ergometer. Airway resistance was changed 1) by increasing the density (D) of the respired gas by a factor of 4.2 and changing the inspired gas from O2 at 1.3 bar to air at 6 bar and 2) by increasing airway flow rates by exposing the subjects to incremental work loads of 0-200 W. Increased gas D caused a slower and deeper respiration at rest and during exercise and, at work loads greater than 120 W, depressed the responses of ventilation and mean inspiratory flow. Raised airway resistance induced by increases in D and/or airway flow rates altered respiratory timing by increasing the ratio of inspiratory time (TI) to total breath duration. Furthermore, analyses of the relationships between tidal volume and TI and between end-inspiratory volume and TI revealed elevation of Hering-Breuer inspiratory volume thresholds. We propose that this elevation, and hence exercise-induced increases of tidal volume, can largely be explained by previous observations that the threshold of the inspiratory off-switch mechanisms depends on central inspiratory activity (cf. C. von Euler, J. Appl. Physiol. 55: 1647-1659, 1983), which in turn increases with airway resistance (Acta Physiol. Scand. 120: 557-565, 1984).     

Ventilatory adjustments during sustained resistive unloading in exercising humans

Effect of He-O2-breathing (79.1%:20.9%) compared to air-breathing on inspiratory ventilation (VI) and its different components [tidal volume (VT), the duration of the phases of each respiratory cycle (tI, tTOT)] as well as on inspiratory mouth occlusion pressure (P0.1) were studied in six normal men at rest and during 72 constant-load exercises (90 W) over a much longer period than in previous studies. Results showed that, irrespective of the order of administration of the two gases (7 min air----7 min He-O2 or vice versa): at rest, P0.1 decreased during He-O2 inhalation but no changes in VI and breathing pattern were detectable; during exercise, sustained He-induced hyperventilation was observed without any change in the absolute value of P0.1; increase in P0.1 between the resting period and exercise (delta P0.1) was significantly higher during He-O2-breathing than during air breathing; this He-induced hyperventilation was associated with a sustained increase in VT/tI, but with constant tI/tTOT. Helium-breathing during exercise cannot be a simple situation of resistance unloading, as has been suggested. We conclude that He-O2-breathing, after the initial compensation period, induces reflex changes in ventilatory control with an increase in inspiratory neural drive. Moreover, it appears that exercise P0.1 is not a legitimate index of inspiratory neural drive whenever rest P0.1 changes according to the nature of the inhaled gas mixture.     

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.     

Estimation of respiratory impedance and source pressure using a Thévenin equivalent circuit model

The objective of this paper is to present a new technique which can provide both active respiration source pressure and lung impedance in a single noninvasive test. The method is based upon a Thévenin equivalent circuit model of respiratory mechanics. Using this model, the equivalent source pressure and source impedance can be computed from the measured changes of respiratory pressures and flows in two consecutive cycles before and after addition of purely resistive loads to the mouth. In maximal breathing the source parameters were reproducible in six normal human subjects. The total respiratory resistance during maximal breathing had an average value of 3.46 cmH2O l-1 s-1, and the total dynamic compliance had an average value of 0.078 l cmH2O-1. The airway resistances measured using a plethysmographic method were within the range of 45-65% of the estimated total respiratory resistances. These two resistances were related with a correlation coefficient of 0.98. An average value of the magnitudes of the fundamental components of the source pressure was 6.73 cmH2O during maximal breathing and 2.09 cmH2O during spontaneous breathing.     

Nasal and oral airway pressure-flow relationships.

We examined the inspiratory and expiratory pressure-flow relationships of both the oral and nasal airways before and after exercise in normal upright subjects. With the use of a partitioned facemask, nasal resistance was measured using posterior rhinomanometry, and oral resistance was measured by recording transoral pressure during oral breathing. Both the nasal and oral pressure-flow relationships for inspiration and expiration were curvilinear and were well described by a power function of the form delta P = aVb (where P is pressure, V is flow, a and b are constants) (r2 = 0.96 +/- 0.01). The exponent b describes the curvilinearity of the pressure-flow curve and can be used to infer the flow regimen. At rest, the inspiratory nasal and oral curves suggested a similar degree of turbulence (b = 1.77 +/- 0.06 and 1.83 +/- 0.04, respectively). However, inspiratory flow regimens were inferred to be more turbulent than those during expiration both before and after exercise. After exercise, decreases in inspiratory nasal resistance at low flows were associated with a change in flow regimen from fully turbulent to orifice flow over the entire flow range. Thus the application of a power function to nasal and oral pressure-flow data permits representation of the whole relationship and allows insight into the nature of the flow regimens.