scholarly journals The effect of inspiratory muscle fatigue on breathing pattern and ventilatory response to CO2.

1992 ◽  
Vol 455 (1) ◽  
pp. 17-32 ◽  
Author(s):  
M J Mador ◽  
M J Tobin
1993 ◽  
Vol 85 (5) ◽  
pp. 637-642 ◽  
Author(s):  
J. E. Clague ◽  
J. Carter ◽  
M. G. Pearson ◽  
P. M. A. Calverley

1. The physiological basis of inspiratory effort sensation remains uncertain. Previous studies have suggested that pleural pressure, rather than inspiratory muscle fatigue, is the principal determinant of inspiratory effort sensation. However, only a limited range of inspiratory flows and breathing patterns have been examined. We suspected that inspiratory effort sensation was related to the inspiratory muscle tension-time index developed whatever the breathing pattern or load, and that this might explain the additional rise in sensation seen with hypercapnia. 2. To investigate this we measured hypercapnic re-breathing responses in seven normal subjects (six males, age range 21–38 years) with and without an inspiratory resistive load of 10 cm H2O. Pleural and transdiaphragmatic pressures, mouth occlusion pressure and breathing pattern were measured. Diaphragmatic and ribcage tension-time indices were calculated from these data. Inspiratory effort sensation was recorded using a Borg scale at 30s intervals during each rebreathing run. 3. Breathing pattern and inspiratory pressure partitioning were unrelated to changes in inspiratory effort sensation during hypercapnia. Tension-time indices reached pre-fatiguing levels during both free breathing and inspiratory resistive loading. 4. Stepwise multiple regression analysis using pooled mechanical, chemical and breathing pattern variables showed that pleural pressure was more closely related to inspiratory effort sensation than was transdiaphragmatic pressure. When converted to tension-time indices, ribcage tension-time index was the major determinant of inspiratory effort sensation during loaded rebreathing, but partial pressure of CO2 was an important independent variable, whereas during unloaded rebreathing partial pressure of CO2 was the most important determinant of inspiratory effort sensation. 5. These results suggest that the pattern of inspiratory pressure partitioning and inspiratory flow rate have little influence on inspiratory effort sensation during CO2 stimulated breathing. The close association between inspiratory effort sensation and ribcage tension-time index, an index of inspiratory muscle work, suggests that inspiratory effort sensation may forewarn of potential inspiratory muscle fatigue. Changes in PaCO2 have a small independent effect on respiratory perception.


1991 ◽  
Vol 70 (4) ◽  
pp. 1627-1632 ◽  
Author(s):  
M. J. Mador ◽  
F. A. Acevedo

The purpose of this study was to determine whether induction of either inspiratory muscle fatigue (expt 1) or diaphragmatic fatigue (expt 2) would alter the breathing pattern response to large inspiratory resistive loads. In particular, we wondered whether induction of fatigue would result in rapid shallow breathing during inspiratory resistive loading. The breathing pattern during inspiratory resistive loading was measured for 5 min in the absence of fatigue (control) and immediately after induction of either inspiratory muscle fatigue or diaphragmatic fatigue. Data were separately analyzed for the 1st and 5th min of resistive loading to distinguish between immediate and sustained effects. Fatigue was achieved by having the subjects breathe against an inspiratory threshold load while generating a predetermined fraction of either the maximal mouth pressure or maximal transdiaphragmatic pressure until they could no longer reach the target pressure. Compared with control, there were no significant alterations in breathing pattern after induction of fatigue during either the 1st or 5th min of resistive loading, regardless of whether fatigue was induced in the majority of the inspiratory muscles or just in the diaphragm. We conclude that the development of inspiratory muscle fatigue does not alter the breathing pattern response to large inspiratory resistive loads.


1985 ◽  
Vol 59 (4) ◽  
pp. 1152-1158 ◽  
Author(s):  
C. G. Gallagher ◽  
V. I. Hof ◽  
M. Younes

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.


1991 ◽  
Vol 70 (5) ◽  
pp. 2059-2065 ◽  
Author(s):  
M. J. Mador ◽  
F. A. Acevedo

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.


2003 ◽  
Vol 90 (3-4) ◽  
pp. 405-410 ◽  
Author(s):  
Markus Rohrbach ◽  
Claudio Perret ◽  
Bengt Kayser ◽  
Urs Boutellier ◽  
Christina M. Spengler

2001 ◽  
Vol 90 (3) ◽  
pp. 857-864 ◽  
Author(s):  
J. Yu ◽  
Y. Wang ◽  
G. Soukhova ◽  
L. C. Collins ◽  
J. C. Falcone

Recently, a vagally mediated excitatory lung reflex (ELR) causing neural hyperpnea and tachypnea was identified. Because ventilation is regulated through both inspiratory and expiratory processes, we investigated the effects of the ELR on these two processes simultaneously. In anesthetized, open-chest, and artificially ventilated rabbits, we recorded phrenic nerve activity and abdominal muscle activity to assess the breathing pattern when the ELR was evoked by directly injecting hypertonic saline (8.1%, 0.1 ml) into lung parenchyma. Activation of the ELR stimulated inspiratory activity, which was exhibited by increasing amplitude, burst rate, and duty cycle of the phrenic activity (by 22 ± 4, 33 ± 9, and 57 ± 11%, respectively; n = 13; P < 0.001), but suppressed expiratory muscle activity. The expiratory muscle became silent in most cases. On average, the amplitude of expiratory muscle activity decreased by 88 ± 5% ( P < 0.002). The suppression reached the peak at 6.9 ± 1 s and lasted for 200 s (median). Injection of H2O2 into the lung parenchyma produced similar responses. By suppressing expiration, the ELR produces a shift in the workload from expiratory muscle to inspiratory muscle. Therefore, we conclude that the ELR may contribute to inspiratory muscle fatigue, not only by directly increasing the inspiratory activity but also by suppressing expiratory activity.


2004 ◽  
Vol 91 (5-6) ◽  
pp. 656-663 ◽  
Author(s):  
Lee M. Romer ◽  
Matthew W. Bridge ◽  
Alison K. McConnell ◽  
David A. Jones

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