Calibration of respiratory inductive plethysmography during quiet and active sleep in lambs

Respiratory inductive plethysmography provides a noninvasive method of measuring breathing patterns. Calibration of respiratory inductive plethysmography requires calculation of gain factors for ribcage and abdomen transducers utilizing 2 breathing patterns with different ribcage and abdomen contributions and tidal volume measured by either spirometry or integrated pneumotachography. The purpose of this study was to determine if respiratory inductive plethysmography can be calibrated to provide accurate measurements during quiet and active sleep in lambs. We used a least squares linear regression calibration technique with breaths selected from quiet sleep and active sleep to calculate gain factors in 6 tracheostomized lambs. Validation of gain factors was performed by comparing tidal volumes obtained simultaneously by respiratory inductive plethysmography and pneumotachography during quiet sleep and active sleep. Tidal volume differences between respiratory inductive plethysmography and pneumotachography on validation runs of 15 consecutive breaths each revealed 90% of validation breaths within +/- 20% during quiet sleep and 82% of validation breaths within +/- 20% during active sleep. These data provide evidence that respiratory inductive plethysmography can be calibrated to allow breathing pattern measurement during sleep.     

Calibration of respiratory inductive plethysmograph during natural breathing

We describe a single-posture method for deriving the proportionality constant (K) between rib cage (RC) and abdominal (AB) amplifiers of the respiratory inductive plethysmograph (RIP). Qualitative diagnostic calibration (QDC) is based on equations of the isovolume maneuver calibration (ISOCAL) and is carried out during a 5-min period of natural breathing without using mouthpiece or mask. In this situation, K approximates the ratio of standard deviations (SD) of the uncalibrated changes of AB-to-RC volume deflections. Validity of calibration was evaluated by 1) analyzing RIP waveforms during an isovolume maneuver and 2) comparing changes of tidal volume (VT) amplitude and functional residual capacity (FRC) level measured by spirometry (SP) with RIP values. Comparisons of VT(RIP) to VT(SP) were also obtained in a variety of postures during natural (uninstructed) preferential RC and AB breathing and with voluntary changes of VT amplitude and FRC level. VT(RIP)-to-VT(SP) comparisons were equal to or closer than published reports for single posture, ISOCAL, multiple- and linear-regression procedures. QDC of RIP in supine posture with comparisons to SP in that posture and others showed better accuracy in horizontal than upright postures.     

Respiratory activity of posterior cricoarytenoid muscle and vocal cords in humans

We examined the respiratory activity of the posterior cricoarytenoid muscle (PCA) simultaneously with the movements of the vocal cords during tidal breathing and panting in four normal seated subjects. A bipolar electrode was constructed to record the surface electromyogram (EMG) of the PCA. The glottis was visualized with a fiberoptic bronchoscope, and the glottic image was recorded simultaneously with tidal volume and a digital time marker on video tape. During quiet breathing the integrated EMG signal (EPCA) showed consistent phasic variations in each subject. The inspiratory onset of EPCA in the four subjects preceded inspiratory flow by 170 +/- 80, 650 +/- 310, 130 +/- 80, and 130 +/- 90 ms (mean +/- SD), respectively. This lead time of the PCA was similar to that between the onset of glottic widening and inspiration in each subject. The proportion of each cycle during which EPCA increased (the duty cycle) was 31 +/- 3% (mean +/- SE), whereas the inspiratory portion of the respiratory cycle constituted 37 +/- 2% (mean +/- SE), respectively. The duty cycle of the PCA remained relatively constant in the same subject on different days. During panting at functional residual capacity, the EPCA increased to 142 +/- 11% of the peak activity recorded during the preceding control breaths. This was accompanied by a sustained increase in the glottic width to 91 +/- 9% of the peak value in the preceding breaths. These results confirm the role of the PCA as a principal abductor of the vocal cords and indicate a temporal relationship between PCA activation and the inspiratory phase of the respiratory cycle during tidal breathing in humans.     

Relative contributions of rib cage and abdomen to breathing in normal subjects.

By use of the method of Konno and Mead and the respiratory magnetometer, the partition of respired gas volumes into rib cage and diaphragm-abdomen components was accomplished in 81 normal subjects including 32 young and middle-aged men, 29 young and middle-aged women, and 20 elderly men. Studied were isovolume maneuvers and the relaxation configuration over the inspiratory capacity range, quiet tidal breathing, increased amplitudes of slow breathing, rapid inspirations and expirations, and both quiet and forceful phonation. No major differences were noted between men and women or between the young and the elderly during any respiratory acts. During quiet breathing most normal subjects are abdominal breathers when supine and thoracic breathers when upright. Rapid respiratory maneuvers were accomplished mostly through rib cage displacement suggesting that rib cage muscles are capable of more rapid action than diaphragm and abdominal muscles. Data from deep breathing and rapid maneuvers supported the view that abdominal and rib cage muscles often act to optimize the mechanical (length-tension) advantage of the diaphragm.     

Inductance plethysmography measurement of CPAP-induced changes in end-expiratory lung volume

The respiratory inductance plethysmograph (RIP) has recently gained popularity in both the research and clinical arenas for measuring tidal volume (VT) and changes in functional residual capacity (delta FRC). It is important however, to define the likelihood that individual RIP measurements of VT and delta FRC would be acceptably accurate (+/- 10%) for clinical and investigational purposes in spontaneously breathing individuals on continuous positive airway pressure (CPAP). Additionally, RIP accuracy has not been compared in these regards after calibration by two commonly employed techniques, the least squares (LSQ) and the quantitative diagnostic calibration (QDC) methods. We compared RIP with pneumotachographic (PTH) measurements of delta FRC and VT during spontaneous mouth breathing on 0-10 cmH2O CPAP. Comparisons were made after RIP calibration with both the LSQ (6 subjects) and QDC (7 subjects) methods. Measurements of delta FRC by RIPLSQ and RIPQDC were highly correlated with PTH measurements (r = 0.94 +/- 0.04 and r = 0.98 +/- 0.01 (SE), respectively). However, only an average of 30% of RIPQDC determinations per subject and 31.4% of RIPLSQ determinations per subject were accurate to +/- 10% of PTH values. An average of 55.2% (QDC) and 68.8% (LSQ) of VT determinations per subject were accurate to +/- 10% of PTH values. We conclude that in normal subjects, over a large number of determinations, RIP values for delta FRC and VT at elevated end-expiratory lung volume correlate well with PTH values. However, regardless of whether QDC or LSQ calibration is used, only about one-third of individual RIP determinations of delta FRC and one-half of two-thirds of VT measurements will be sufficiently accurate for clinical and investigational use.     

Noninvasive ventilatory monitoring with bellows pneumographs in supine subjects

We compared simultaneous measurements of ventilatory movements obtained by a bellows pneumograph (BP) and a respiratory inductive plethysmograph (RIP) vs. integrated volume from a pneumotachograph in seven healthy volunteers during different respiratory patterns. The purpose of this study was to assess if a computer-aided calibration procedure could improve the accuracy of BP, a simple semiquantitative method for noninvasive ventilatory monitoring in supine subjects. Both devices were repeatedly calibrated against a pneumotachograph in the same posture with a computer-aided least-squares method. One calibration maneuver was sufficient to achieve a minimal relative difference in volume measurements between the RIP as well as the BP and the pneumotachograph of less than 1.2 +/- 4.5 (SD) %. The accuracy remained in this range during the subsequent calibrations with time (1 h) and after body movements. However, this difference increased significantly with both devices when the subjects were studied in the lateral decubitus position. The present study indicates that despite theoretical advantages of the RIP, the BP, when properly calibrated, has similar performances in supine subjects for monitoring ventilation; it is simpler and less expensive than the RIP and is devoid of electrical drift and artifacts.     

Activation of the parasternal intercostals during breathing efforts in human subjects

We have tested the possibility that the electromyographic (EMG) activity present in the parasternal intercostal muscles during quiet inspiration was reflexive, rather than agonistic, in nature. Using concentric needle electrodes we measured parasternal EMG activity in four normal subjects during various inspiratory maneuvers. We found that 1) phasic inspiratory activity was invariably present in the parasternal intercostals during quiet breathing, 2) the parasternal EMG activity was generally increased during attempts to perform the tidal breathing maneuver with the diaphragm alone, 3) parasternal EMG activity was markedly decreased or suppressed in the presence of rib cage distortion during diaphragmatic isovolume maneuvers, and 4) that EMG activity could not be voluntarily suppressed during breathing unless the inspired volume was trivial. We conclude that the parasternal EMG activity detected during quiet inspiration in the normal subjects depends on a central involuntary mechanism and is not related to activation of intercostal mechanoreceptors.     

Influence of lung volume on oxygen cost of resistive breathing

We examined the relationship between the O2 cost of breathing (VO2 resp) and lung volume at constant load, ventilation, work rate, and pressure-time product in five trained normal subjects breathing through an inspiratory resistance at functional residual capacity (FRC) and when lung volume (VL) was increased to 37 +/- 2% (mean +/- SE) of inspiratory capacity (high VL). High VL was maintained using continuous positive airway pressure of 9 +/- 2 cmH2O and with the subjects coached to relax during expiration to minimize respiratory muscle activity. Six paired runs were performed in each subject at constant tidal volume (0.62 +/- 0.2 liters), frequency (23 +/- 1 breaths/min), inspiratory flow rate (0.45 +/- 0.1 l/s), and inspiratory muscle pressure (45 +/- 2% of maximum static pressure at FRC). VO2 resp increased from 109 +/- 15 ml/min at FRC by 41 +/- 11% at high VL (P less than 0.05). Thus the efficiency of breathing at high VL (3.9 +/- 0.2%) was less than that at FRC (5.2 +/- 0.3%, P less than 0.01). The decrease in inspiratory muscle efficiency at high VL may be due to changes in mechanical coupling, in the pattern of recruitment of the respiratory muscles, or in the intrinsic properties of the inspiratory muscles at shorter length. When the work of breathing at high VL was normalized for the decrease in maximum inspiratory muscle pressure with VL, efficiency at high VL (5.2 +/- 0.3%) did not differ from that at FRC (P less than 0.7), suggesting that the fall in efficiency may have been related to the fall in inspiratory muscle strength. During acute hyperinflation the decreased efficiency contributes to the increased O2 cost of breathing and may contribute to the diminished inspiratory muscle endurance.     

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.     

Pressure-time product, work rate, and endurance during resistive breathing in humans

We examined the effect of increasing work rate, without a corresponding increase in the pressure-time product, on energy cost and inspiratory muscle endurance (Tlim) in five normal subjects during inspiratory resistive breathing. Tidal volume, mean inspiratory mouth pressure, duty cycle, and hence the pressure-time product were kept constant, whereas work rate was varied by changing the frequency of breathing. There was a linear decrease in Tlim of -2.1 +/- 0.5 s.J-1.min-1 (r = 0.87 +/- 0.06) with increasing work rate. The data satisfied a model of energy balance during fatiguing runs (Monod and Scherrer. Ergonomics 8: 329-337, 1965) and were consistent with the hypothesis that the rate of energy supply, or respiratory muscle blood flow, is fixed when the pressure-time product is constant. Our results indicate that during inspiratory resistive breathing against fatiguing loads, work rate determines endurance independently of the pressure-time product. On the basis of the model, our results lead to estimates of respiratory muscle blood flow and available energy stores under the conditions of our experiment.     

Respiratory cross-sectional area-flux measurements of the human chest wall

A new device that utilizes the voltages induced in separate coils encircling the rib cage and abdomen by a magnetic field is described for measurement of cross-sectional areas of the human chest wall (rib cage and abdomen) and their variation during breathing. A uniform magnetic field (1.4 X 10(-7) Tesla at 100 kHz) is produced by generating an alternating current at 100 kHz in two square coils, 1.98 m on each side, parallel to the planes of the areas to be measured and placed symmetrically cephalad and caudad to these planes at a mean distance of 0.53 m. We demonstrated that the accuracy of the device on well-defined surfaces (squares, circles, rectangles, ellipses) was within 1% in all cases. Observed errors are due primarily to small inhomogeneities of the magnetic field and variation of the orientation of the coil relative to the field. Using a second magnetic field (80 kHz) perpendicular to the first, we measured the errors due to nonparallel orientation during quiet breathing and inspiratory capacity maneuvers. In 10 normal subjects, orientation effects were less than 2% for the rib cage and less than 0.7% for the abdomen. In five of these subjects, orientation effects at functional residual capacity in lateral and seated postures were generally less than or equal to 5%, but estimated tidal volume during spontaneous breathing was comparable to measurements in the supine posture. In five curarized patients, we assessed the linearity of volume-motion relationships of the rib cage and abdomen, comparing cross-sectional area and circumference measurements. Departures from linearity using cross-sectional areas were only one-third of those using circumferences. In seven normal subjects we compared cross-sectional area measurements with respiratory inductive plethysmography (RIP) and found comparable estimates of lung volume change over a wide range of relative rib cage contributions to tidal volume (-5 to 105%), with slightly higher standard deviations for the RIP (SD = 10% for RIP; SD = 4% for cross-sectional area).     

Ratio of active to passive muscle shortening in the canine diaphragm.

Active and passive shortening of muscle bundles in the canine diaphragm were measured with the objective of testing a consequence of the minimal-work hypothesis: namely, that the ratio of active to passive shortening is the same for all active muscles. Lengths of six muscle bundles in the costal diaphragm and two muscle bundles in the crural diaphragm of each of four bred-for-research beagle dogs were measured by the radiopaque marker technique during the following maneuvers: a passive deflation maneuver from total lung capacity to functional residual capacity, quiet breathing, and forceful inspiratory efforts against an occluded airway at different lung volumes. Shortening per liter increase in lung volume was, on average, 70% greater during quiet breathing than during passive inflation in the prone posture and 40% greater in the supine posture. For the prone posture, the ratio of active to passive shortening was larger in the ventral and midcostal diaphragm than at the dorsal end of the costal diaphragm. For both postures, active shortening during quiet breathing was poorly correlated with passive shortening. However, shortening during forceful inspiratory efforts was highly correlated with passive shortening. The average ratios of active to passive shortening were 1.23 +/- 0.02 and 1.32 +/- 0.03 for the prone and supine postures, respectively. These data, taken together with the data reported in the companion paper (T. A. Wilson, M. Angelillo, A. Legrand, and A. De Troyer, J. Appl. Physiol. 87: 554-560, 1999), support the hypothesis that, during forceful inspiratory efforts, the inspiratory muscles drive the chest wall along the minimal-work trajectory.     

O2 cost of breathing: ventilatory vs. pressure loads.

We compared the O2 cost of breathing (VO2resp) at high levels of ventilation (HV) with that against high inspiratory pressure loads (HP) using an external elastance when end-expiratory volume, work rate (W), and pressure-time product (P) were matched at two levels of ventilation and elastic loading. Each of five normal subjects performed three pairs of loaded runs (one HV and one HP) bracketed by two resting runs. Mean O2 consumption from the pairs of resting runs was subtracted from that of each of the loaded runs to give VO2resp during loaded breathing. Matching for W and P was within 15% in all 15 pairs of runs. During HV runs, ventilation was 398 +/- 24% of corresponding values during HP runs (P < 0.01). Although there was no difference in W (P > 0.05), the VO2resp during HV runs was 237 +/- 33% of that during HP (P < 0.01) and efficiency of HV was 51 +/- 5% of that during HP (P < 0.01). When W was normalized for the decrease in maximum inspiratory pressure with increased mean lung volume, efficiency during HV and HP runs did not differ (P > 0.05). In the second series of experiments, when both HV and HP runs were matched for W but P was allowed to vary, efficiency increased by 1.42 +/- 0.42% (P < 0.05) for each percent decrease in P during HV runs but was unchanged (P > 0.05) during HP runs despite a 193 +/- 10% increase in P.(ABSTRACT TRUNCATED AT 250 WORDS)     

Oxygen cost of inspiratory loading: resistive vs. elastic

We measured the O2 cost of breathing (VO2resp) against external inspiratory elastic (E) and resistive loads (R) when end-expiratory lung volume, tidal volume, breathing frequency, work rate, and pressure-time product were matched in each of six pairs of runs in six subjects. During E, peak inspiratory mouth pressure was 65.7 +/- 1.8% (SD) of the maximum at functional residual capacity. However, during resistive runs, peak inspiratory mouth pressure was 41.1 +/- 2.8% of the maximum at functional residual capacity. In 36 paired runs, where both work rate and pressure-time product were within 10%, VO2resp for E was less than for R (81 and 96 ml/min, respectively; P less than 0.01). During loaded and unloaded breathing with the same tidal volume, we measured the changes in anteroposterior diameter of the lower rib cage in five subjects. In four subjects we also recorded the electromyograms of several fixator and stabilizing muscles. During E and R, the change in anteroposterior diameter of the lower rib cage was -116 +/- 5 and -45 +/- 4% (SE), respectively, of the unloaded value (P less than 0.01), indicating greater deformation during E. Although the peak electromyographic activity was 72 +/- 16% greater during E (P less than 0.01), there was no difference between the loads for area under the electromyogram time curve (P greater than 0.05). However, the time to 50% peak activity was less during R (P less than 0.02). We conclude that, even when work rate and pressure-time product are matched, VO2resp during R is greater than that during E. This difference may be due to preferential recruitment of faster and less efficient muscle fibers.     

Respiratory changes in parasternal intercostal intramuscular pressure

In an attempt to obtain insight in the forces developed by the parasternal intercostal muscles during breathing, changes in parasternal intramuscular pressure (PIP) were measured in 14 supine anesthetized dogs using a microtransducer method. In six animals, during bilateral parasternal stimulation a linear relationship between contractile force exerted on the rib and PIP was demonstrated (r greater than 0.95). In eight animals, during quiet active inspiration, substantial (55 +/- 11.5 cmH2O) PIP was developed. During inspiratory resistive loading and airway occlusion the inspiratory rise in PIP increased in proportion to the inspiratory fall in pleural pressure (r = 0.82). Phrenicotomy and vagotomy resulted in an increase in the inspiratory rise in PIP of 21% and 99%, respectively. During passive deflation, when the parasternal intercostals were passively lengthened, large rises (320 +/- 221 cmH2O) in intramuscular pressure were observed. During passive inflation intramuscular pressure remained constant or even decreased slightly (-8 +/- 25 cmH2O) as expected on the basis of the passive shortening of the muscles. PIP thus invariably increased when tension increased either actively or passively. From PIP it is clear that the parasternals exert significant forces on the ribs during respiratory maneuvers.     

Effects of increase in body temperature on the breathing pattern in premature infants

This study was designed to determine the effects of a mild increase in body temperature within the physiological range (0.8 degrees C) in healthy premature infants. Seven unsedated premature infants (38.4 wk +/- 1.5 postconceptional age) were monitored polygraphically during "morning naps" in an incubator under two different environmental temperatures: (1) normothermia with the incubator temperature set at 25 degrees C and the rectal temperature equal to 36.9 degrees C +/- 0.1; (2) hyperthermia with the incubator temperature set at 35 degrees C and the rectal temperature equal to 37.7 degrees C +/- 0.15. Respiratory frequency and heart rate, respiratory events, i.e., central and obstructive apnea, and periodic breathing with and without apneic oscillations were tabulated. Results for respiratory events were expressed as (1) indices of the total number of respiratory events, and of specific respiratory events per hour of total, quiet and active sleep times; (2) duration of total and specific respiratory events expressed as a percentage of total sleep, quiet and active sleep times. Respiratory frequency and heart rate were significantly increased by hyperthermia (P less than 0.05). Hyperthermia did not significantly modify the indices or the duration of central and obstructive apnea. But the indices and the duration of periodic breathing with and without apneic oscillations were significantly increased by hyperthermia during active sleep (P less than 0.05) but not during quiet sleep. The present study shows that a mild increase in body temperature within the physiological range in premature infants enhances the instability of the breathing pattern during active sleep.     

Respiratory changes in parasternal intercostal length

In an attempt to understand the role of the parasternal intercostals in respiration, we measured the changes in length of these muscles during a variety of static and dynamic respiratory maneuvers. Studies were performed on 39 intercostal spaces from 10 anesthetized dogs, and changes in parasternal intercostal length were assessed with pairs of piezoelectric crystals (sonomicrometry). During static maneuvers (passive inflation-deflation, isovolume maneuvers, changes in body position), the parasternal intercostals shortened whenever the rib cage inflated, and they lengthened whenever the rib cage contracted. The changes in parasternal intercostal length, however, were much smaller than the changes in diaphragmatic length, averaging 9.2% of the resting length during inflation from residual volume to total lung capacity and 1.3% during tilting from supine to upright. During quiet breathing the parasternal intercostals always shortened during inspiration and lengthened during expiration. In the intact animals the inspiratory parasternal shortening was close to that seen for the same increase in lung volume during passive inflation and averaged 3.5%. After bilateral phrenicotomy, however, the parasternal intercostal shortening during inspiration markedly increased, whereas tidal volume diminished. These results indicate that 1) the parasternal intercostals in the dog are real agonists (as opposed to fixators) and actively contribute to expand the rib cage and the lung during quiet inspiration, 2) the relationship between lung volume and parasternal length is not unique but depends on the relative contribution of the various inspiratory muscles to tidal volume, and 3) the physiological range of operating length of the parasternal intercostals is considerably smaller than that of the diaphragm.(ABSTRACT TRUNCATED AT 250 WORDS)     

Does rib cage-abdominal paradox signify respiratory muscle fatigue?

Studies suggesting that abnormal motion of the rib cage (RC) and abdomen (Ab) may indicate respiratory muscle fatigue have not separated the influence of respiratory load from that of fatigue in its pathogenesis. We hypothesized that abnormalities on RC-Ab motion are primarily related to increased load rather than fatigue. We tested this hypothesis in subjects breathing against resistive loads while maintaining 30 and 60% of maximum mouth pressure (Pmmax). RC-Ab asynchrony and paradox and the degree of variation in compartmental contribution to tidal volume were measured by inductive plethysmography and quantitated by the Konno-Mead method of analysis. Comparing measurements of base line and 30 and 60% of Pmmax indicated that the degree of asynchrony, paradox, and variation in compartmental contribution were significantly related to the level of the load; significant abnormalities were observed at even 30% of Pmmax, a target pressure that can be sustained indefinitely. In another group of subjects, fatigue was induced by sustaining 60% of Pmmax to the limits of tolerance. Indexes of abnormal RC-Ab motion increased from base line during the 1st min of loaded breathing but displayed no progression from the beginning to the end of the fatigue run. Immediately on discontinuation of the load, the indexes returned to levels similar to base line despite persistence of the fatigue state. These results in healthy subjects breathing against severe resistances indicate that RC-Ab asynchrony and paradox and variation in compartmental contribution to tidal volume are predominantly due to increases in respiratory load rather than muscle fatigue.     

Effects of inspiratory elastic load on respiratory control in hypercapnia and exercise

Five healthy young men underwent two separate steady-state incremental exercise runs within the aerobic range on a treadmill with alternating periods of breathing with no load (NL) and with a discontinuous inspiratory elastic load (IEL) of approximately 10 cmH2O/l. End-tidal PCO2 was maintained constant throughout each run at the eucapnic or a constant hypercapnic level by adding 0-5% CO2 to the inspired O2. Hypercapnia caused a steepening, as well as upward shift, relative to the corresponding eucapnic ventilation-CO2 output (VE-VCO2) relationship in NL and IEL. Compared with NL, the VE-VCO2 slope was depressed by IEL, more so in hypercapnic [-28.7 +/- 7.2 (SE) %] than in eucapnic exercise (-16.0 +/- 2.8%). The steady-state hypercapnic ventilatory response at rest was also markedly depressed (-32.1 +/- 11.2%). Occlusion pressure response was augmented in response to IEL during eucapnic exercise (88.7 +/- 13.3%) but not during CO2 inhalation at rest or during exercise. Breathing pattern characteristics were similar regardless of the type of stimulus input and the level of inspiratory load. Results are consistent with the notion that the control of VE and breathing pattern may both be influenced by a balance between the prevailing chemical drive and a propensity of the controller to reduce respiratory effort.     

Effect of respiratory muscle fatigue on subsequent exercise performance.

The purpose of this study was to determine whether induction of inspiratory muscle fatigue might impair subsequent exercise performance. Ten healthy subjects cycled to volitional exhaustion at 90% of their maximal capacity. Oxygen consumption, breathing pattern, and a visual analogue scale for respiratory effort were measured. Exercise was performed on three separate occasions, once immediately after induction of fatigue, whereas the other two episodes served as controls. Fatigue was achieved by having the subjects breathe against an inspiratory threshold load while generating 80% of their predetermined maximal mouth pressure until they could no longer reach the target pressure. After induction of fatigue, exercise time was reduced compared with control, 238 +/- 69 vs. 311 +/- 96 (SD) s (P less than 0.001). During the last minute of exercise, oxygen consumption and heart rate were lower after induction of fatigue than during control, 2,234 +/- 472 vs. 2,533 +/- 548 ml/min (P less than 0.002) and 167 +/- 15 vs. 177 +/- 12 beats/min (P less than 0.002). At exercise isotime, minutes ventilation and the visual analogue scale for respiratory effort were larger after induction of fatigue than during control. In addition, at exercise isotime, relative tachypnea was observed after induction of fatigue. We conclude that induction of inspiratory muscle fatigue can impair subsequent performance of high-intensity exercise and alter the pattern of breathing during such exercise.