Effect of diaphragm fatigue on neural respiratory drive

2001 ◽  
Vol 90 (5) ◽  
pp. 1691-1699 ◽  
Author(s):  
Y. M. Luo ◽  
N. Hart ◽  
N. Mustfa ◽  
R. A. Lyall ◽  
M. I. Polkey ◽  
...  
Keyword(s):  
Compound Muscle Action Potential ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Respiratory Drive ◽  
Transdiaphragmatic Pressure ◽  
Muscle Action Potential ◽  
Resistive Loading ◽  
Before And After ◽  
Residual Capacity ◽  
Diaphragm Fatigue

To test the hypothesis that diaphragm fatigue leads to an increase in neural respiratory drive, we measured the esophageal diaphragm electromyogram (EMG) during CO2 rebreathing before and after diaphragm fatigue in six normal subjects. The electrode catheter was positioned on the basis of the amplitude and polarity of the diaphragm compound muscle action potential recorded simultaneously from four pairs of electrodes during bilateral anterior magnetic phrenic nerve stimulation (BAMPS) at functional residual capacity. Two minutes of maximum isocapnic voluntary ventilation (MIVV) were performed in six subjects to induce diaphragm fatigue. A maximal voluntary breathing against an inspiratory resistive loading (IRL) was also performed in four subjects. The reduction of transdiaphragmatic pressure elicited by BAMPS was 22% (range 13–27%) after 2 min of MIVV and was similar, 20% (range 13–26%), after IRL. There was a linear relationship between minute ventilation (V˙e) and the root mean square (RMS) of the EMG during CO2 rebreathing before and after fatigue. The mean slope of the linear regression of RMS on V˙e was similar before and after diaphragm fatigue: 2.80 ± 1.31 vs. 3.29 ± 1.40 for MIVV and 1.51 ± 0.31 vs 1.55 ± 0.31 for IRL, respectively. We conclude that the esophageal diaphragm EMG can be used to assess neural drive and that diaphragm fatigue of the intensity observed in this study does not affect respiratory drive.

Aerobic fitness effects on exercise-induced low-frequency diaphragm fatigue

1996 ◽  
Vol 81 (5) ◽  
pp. 2156-2164 ◽  
Author(s):  
Mark A. Babcock ◽  
David F. Pegelow ◽  
Bruce D. Johnson ◽  
Jerome A. Dempsey
Keyword(s):  
Endurance Exercise ◽  
Aerobic Fitness ◽  
Minute Ventilation ◽  
Low Frequency ◽  
Force Output ◽  
Transdiaphragmatic Pressure ◽  
Fitness Effects ◽  
Residual Capacity ◽  
Exercise Induced ◽  
Diaphragm Fatigue

Babcock, Mark A., David F. Pegelow, Bruce D. Johnson, and Jerome A. Dempsey. Aerobic fitness effects on exercise-induced low-frequency diaphragm fatigue. J. Appl. Physiol. 81(5): 2156–2164, 1996.—We used bilateral phrenic nerve stimulation (BPNS; at 1, 10, and 20 Hz at functional residual capacity) to compare the amount of exercise-induced diaphragm fatigue between two groups of healthy subjects, a high-fit group [maximal O2consumption (V˙o 2 max) = 69.0 ± 1.8 ml ⋅ kg−1 ⋅ min−1, n = 11] and a fit group (V˙o 2 max = 50.4 ± 1.7 ml ⋅ kg−1 ⋅ min−1, n = 13). Both groups exercised at 88–92% V˙o 2 maxfor about the same duration (15.2 ± 1.7 and 17.9 ± 2.6 min for high-fit and fit subjects, respectively, P > 0.05). The supramaximal BPNS test showed a significant reduction ( P< 0.01) in the BPNS transdiaphragmatic pressure (Pdi) immediately after exercise of −23.1 ± 3.1% for the high-fit group and −23.1 ± 3.8% ( P > 0.05) for the fit group. Recovery of the BPNS Pdi took 60 min in both groups. The high-fit group exercised at a higher absolute workload, which resulted in a higher CO2production (+26%), a greater ventilatory demand (+16%) throughout the exercise, and an increased diaphragm force output (+28%) over the initial 60% of the exercise period. Thereafter, diaphragm force output declined, despite a rising minute ventilation, and it was not different between most of the high-fit and fit subjects. In summary, the high-fit subjects showed diaphragm fatigue as a result of heavy endurance exercise but were also partially protected from excessive fatigue, despite high ventilatory requirements, because their hyperventilatory response to endurance exercise was reduced, their diaphragm was utilized less in providing the total ventilatory response, and possibly their diaphragm aerobic capacity was greater.

Effect of respiratory muscle weakness on P0.1 induced by partial curarization

1984 ◽  
Vol 57 (4) ◽  
pp. 1150-1157 ◽  
Author(s):  
R. H. Holle ◽  
R. B. Schoene ◽  
E. J. Pavlin
Keyword(s):  
Muscle Weakness ◽  
Respiratory Muscle ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Base Line ◽  
Respiratory Drive ◽  
Respiratory Muscle Weakness ◽  
Residual Capacity ◽  
Mouth Occlusion Pressure ◽  
Line Slope

Mouth occlusion pressure 0.1 s after onset of inspiration (P0.1) reflects central respiratory drive (CRD), but its dependence on respiratory muscle strength is unknown. To clarify this relationship, we produced progressive levels of respiratory muscle weakness by infusion of d-tubocurarine in eight supine spontaneously breathing normal subjects. Hypercapnic ventilatory response (HCVR) was measured before curarization and at mild (mean inspiratory effort 62 +/- 3% of control), moderate (42 +/- 3%), and severe (23 +/- 1%) weakness. At the severe level of weakness 1) supine functional residual capacity was not significantly changed from base line, 2) the percent of base-line slope of delta P0.1/delta PCO2 (122 +/- 27%) was significantly greater (P less than 0.01) than that for change in expired minute ventilation (delta VE)/delta PCO2 (39 +/- 10%), 3) the percent of base-line delta P0.1/delta VE (381 +/- 46%) during HCVR was significantly increased (P less than 0.01), 4) the P0.1 response was significantly increased from base line at two out of three specific levels of PCO2 while the VE was unchanged or significantly decreased, and 5) peak inspiratory resistance did not significantly change. Thus P0.1, unlike VE, did not decrease with even severe respiratory muscle weakness. Indeed, P0.1 increased at two out of three levels of PCO2 under circumstances when higher CRD is expected. One potential explanation for the results is that P0.1 may at least qualitatively reflect CRD up to the level of severe respiratory muscle weakness attained in this study.

scholarly journals Lung elastic recoil during breathing at increased lung volume

1999 ◽  
Vol 87 (4) ◽  
pp. 1491-1495 ◽  
Author(s):  
Joseph R. Rodarte ◽  
Gassan Noredin ◽  
Charles Miller ◽  
Vito Brusasco ◽  
Riccardo Pellegrino ◽  
...  
Keyword(s):  
Stress Relaxation ◽  
Tidal Volume ◽  
Lung Volume ◽  
Normal Subjects ◽  
Dynamic Hyperinflation ◽  
Airway Closure ◽  
Elastic Recoil ◽  
Volume Increase ◽  
Before And After ◽  
Residual Capacity

During dynamic hyperinflation with induced bronchoconstriction, there is a reduction in lung elastic recoil at constant lung volume (R. Pellegrino, O. Wilson, G. Jenouri, and J. R. Rodarte. J. Appl. Physiol. 81: 964–975, 1996). In the present study, lung elastic recoil at control end inspiration was measured in normal subjects in a volume displacement plethysmograph before and after voluntary increases in mean lung volume, which were achieved by one tidal volume increase in functional residual capacity (FRC) with constant tidal volume and by doubling tidal volume with constant FRC. Lung elastic recoil at control end inspiration was significantly decreased by ∼10% within four breaths of increasing FRC. When tidal volume was doubled, the decrease in computed lung recoil at control end inspiration was not significant. Because voluntary increases of lung volume should not produce airway closure, we conclude that stress relaxation was responsible for the decrease in lung recoil.

Effect of acute hypoxia on respiration and brain stem blood flow in the piglet

1991 ◽  
Vol 70 (1) ◽  
pp. 251-259 ◽  
Author(s):  
R. A. Darnall ◽  
G. Green ◽  
L. Pinto ◽  
N. Hart
Keyword(s):  
Blood Flow ◽  
Brain Stem ◽  
Minute Ventilation ◽  
Acute Hypoxia ◽  
Extracellular Fluid ◽  
Respiratory Drive ◽  
Peripheral Chemoreceptor ◽  
Before And After ◽  
Spontaneously Breathing ◽  
Local Brain

Changes in local brain stem perfusion that alter extracellular fluid Pco2 and/or [H+] near central chemoreceptors may contribute to the decrease in respiration observed during hypoxia after peripheral chemoreceptor denervation and to the delayed decrease observed during hypoxia in the newborn. In this study, we measured the changes in respiration and brain stem blood flow (BBF) during 2–4 min of hypoxic hypoxia in both intact and denervated piglets and calculated the changes in brain stem Pco2 and [H+] that would be expected to occur as a result of the changes in BBF. All animals were anesthetized, spontaneously breathing, and between 2 and 7 days of age. Respiratory and other variables were measured before and during hypoxia in all animals, and BBF (microspheres) was measured in a subgroup of intact and denervated animals at 0, 30, and 260 s and at 0 and 80 s, respectively. During hypoxia, minute ventilation increased and then decreased (biphasic response) in the intact animals but decreased only in the denervated animals. BBF increased in a near linear fashion, and calculated brain stem extracellular fluid Pco2 and [H+] decreased over the first 80 s both before and after denervation. We speculate that a rapid increase in BBF during acute hypoxia decreases brain stem extracellular fluid Pco2 and [H+], which, in turn, negatively modulate the increase in respiratory drive produced by peripheral chemoreceptor input to the central respiratory generator.

Augmentation of CO2 drives by chlormadinone acetate, a synthetic progesterone

1984 ◽  
Vol 56 (6) ◽  
pp. 1627-1632 ◽  
Author(s):  
H. Kimura ◽  
F. Hayashi ◽  
A. Yoshida ◽  
S. Watanabe ◽  
I. Hashizume ◽  
...  
Keyword(s):  
Minute Ventilation ◽  
Inspiratory Flow ◽  
Pressure Response ◽  
Respiratory Drive ◽  
Occlusion Pressure ◽  
Physiological Basis ◽  
Load Compensation ◽  
Chlormadinone Acetate ◽  
Arterial Blood ◽  
Resistive Loading

We studied 10 male subjects who were administered chlormadinone acetate (CMA), a potent synthetic progesterone, to clarify the physiological basis of its respiratory effects. Arterial blood gas tension, resting ventilation, and respiratory drive assessed by ventilatory and occlusion pressure response to CO2 with and without inspiratory flow-resistive loading were measured before and 4 wk after CMA administration. In all subjects, arterial PCO2 decreased significantly by 5.7 +/- 0.6 (SE) Torr with an increase in minute ventilation by 1.8 +/- 0.6 l X min-1, whereas no significant changes were seen in O2 uptake. During unloaded conditions, both slopes of occlusion pressure and ventilatory response to CO2 increased, being statistically significant in the former but showing nonsignificant trends in the latter. Furthermore, inspiratory flow-resistive loading (16 cmH2O X l(-1) X s) increased both slopes more markedly after CMA. The magnitudes of load compensation, assessed by the ratio of loaded to unloaded slope of the occlusion pressure response curve, were increased significantly. We concluded CMA is a potent respiratory stimulant that increases the CO2 chemosensitivity and neuromechanical drives in the load-compensation mechanism.

Effect of digitalis on the diaphragm in anesthetized dogs

1987 ◽  
Vol 63 (1) ◽  
pp. 277-284 ◽  
Author(s):  
Y. Kikuchi ◽  
W. Hida ◽  
C. Shindoh ◽  
T. Chonan ◽  
H. Miki ◽  
...  
Keyword(s):  
Nerve Stimulation ◽  
Phrenic Nerve ◽  
Stimulus Frequency ◽  
Dependent Manner ◽  
Phrenic Nerve Stimulation ◽  
Transdiaphragmatic Pressure ◽  
Mechanically Ventilated ◽  
Before And After ◽  
Residual Capacity ◽  
Anesthetized Dogs

We examined the effect of digitalis on diaphragmatic contractility and fatigability in 19 anesthetized mechanically ventilated dogs. The diaphragmatic force was assessed from transdiaphragmatic pressure (Pdi) developed at functional residual capacity against an occluded airway during cervical phrenic nerve stimulation. In a first group of five dogs, Pdi-stimulus frequency relationships were compared before and after administration of ouabain in doses of 0.01, 0.02, and 0.04 mg/kg. In a second group, diaphragmatic fatigue was produced by bilateral phrenic nerve stimulation at 30 Hz. Ten seconds of stimulation and 15 s of mechanical ventilation were repeated for 30 min. The rates of decrease in Pdi were compared between two groups, one of 0.05 mg/kg deslanoside-treated dogs (n = 7) and one of nontreated dogs (n = 7). After ouabain administration Pdi was significantly greater at each frequency in a dose-dependent manner. On the other hand, the rate of decrease in Pdi in the deslanoside group was significantly smaller than that in the nontreated group, whereas deslanoside did not greatly change the Pdi-frequency curves in fresh diaphragm. We conclude that ouabain improves contractility of the fresh diaphragm and that deslanoside has a protective effect against fatigability.

Assessment of transdiaphragmatic pressure in humans

1985 ◽  
Vol 58 (5) ◽  
pp. 1469-1476 ◽  
Author(s):  
D. Laporta ◽  
A. Grassino
Keyword(s):  
Pulmonary Disease ◽  
Visual Feedback ◽  
Random Order ◽  
Normal Subjects ◽  
Chronic Obstructive ◽  
Disease Group ◽  
Obstructive Pulmonary Disease ◽  
Transdiaphragmatic Pressure ◽  
Residual Capacity ◽  
Group 1

Maximal force developed by the diaphragm at functional residual capacity is a useful index to establish muscle weakness; however, great disparity in its reproducibility can be observed among reports in the literature. We evaluated five maneuvers to measure maximal transdiaphragmatic pressure (Pdimax) in order to establish best reproducibility and value. Thirty-five naive subjects, including 10 normal subjects (group 1), 12 patients with chronic obstructive pulmonary disease (group 2), and 13 patients with restrictive pulmonary disease (group 3), were studied. Each subject performed five separate maneuvers in random order that were repeated until reproducible values were obtained. The maneuvers were Mueller with (A) and without mouthpiece (B), abdominal expulsive effort with open glottis (C), two-step (maneuver C combined with Mueller effort) (D), and feedback [two-step with visual feedback of pleural (Ppl) and abdominal (Pab) pressure] (E). The greatest reproducible Pdimax values were obtained with maneuver E (P less than 0.01) (group 1: 180 +/- 14 cmH2O). The second best maneuvers were A, B, and D (group 1: 154 +/- 25 cmH2O). Maneuver C produced the lowest values. For all maneuvers, group 1 produced higher values than groups 2 and 3 (P less than 0.001), which were similar. The Ppl to Pdi ratio was 0.6 in maneuvers A and B, 0.4 in D and E, and 0.2 in C. We conclude that visual feedback of Ppl and Pab helped the subjects to elicit maximal diaphragmatic effort in a reproducible fashion. It is likely that the great variability of values in Pdimax previously reported are the result of inadequate techniques.

Effects of fenoterol on inspiratory effort sensation and fatigue during inspiratory threshold loading

1996 ◽  
Vol 80 (3) ◽  
pp. 727-733 ◽  
Author(s):  
J. Suzuki ◽  
S. Suzuki ◽  
T. Okubo
Keyword(s):  
Low Frequency ◽  
Normal Subjects ◽  
Motor Command ◽  
Inspiratory Effort ◽  
Double Blind ◽  
Endurance Time ◽  
Transdiaphragmatic Pressure ◽  
Mouth Pressure ◽  
Residual Capacity ◽  
Low Frequency Power

We studied the effects of a single dose of fenoterol on the relationship between inspiratory effort sensation (IES) and inspiratory muscle fatigue induced by inspiratory threshold loading in healthy subjects. The magnitude of the threshold was 60% of maximal static inspiratory mouth pressure (PI,mmax) at functional residual capacity, and the duty cycle was 0.5. Subjects continued the threshold loaded breathing until the target mouth pressure could no longer be maintained (endurance time). The intensity of the IES was scored with a modified Borg scale. Either fenoterol (5 mg) or a placebo was given orally 2 h before loading in a randomized double-blind crossover protocol. The endurance time with fenoterol (34.4 +/- 8.6 min) was longer than that with the placebo (22.2 +/- 7.1 min; P < 0.05). The ratio of high- to low-frequency power of the diaphragmatic electromyogram (EMGdi) decreased during loading; the decrease was less with fenoterol (P < 0.05). The EMGdi also decreased with loading; the decrease was greater on fenoterol treatment (P < 0.01). The PI,mmax and maximal transdiaphragmatic pressure (Pdi) were similarly decreased after loading on either treatment. The intensity of the IES rose with time during loading in both groups but was lower with fenoterol than with the placebo (P < 0.05). The ratio of Pdi to integrated activity of the EMGdi increased with fenoterol (P < 0.05). Fenoterol treatment increased both superimposed Pdi twitch and Pdi twitch of relaxed diaphragm and decreased the value of (1-superimposed Pdi twitch/Pdi twitch of relaxed diaphragm). Thus we conclude that in normal subjects fenoterol reduces diaphragmatic fatigue and decreases the motor command to the diaphragm, resulting in a decrease in IES during inspiratory threshold loading and a prolongation of endurance.

Effects of separate rib cage and abdominal restriction on exercise performance in normal humans

1985 ◽  
Vol 58 (6) ◽  
pp. 2020-2026 ◽  
Author(s):  
S. N. Hussain ◽  
B. Rabinovitch ◽  
P. T. Macklem ◽  
R. L. Pardy
Keyword(s):  
Minute Ventilation ◽  
Normal Subjects ◽  
Cycle Ergometer ◽  
Abdominal Muscle ◽  
Work Rate ◽  
Abdominal Pressure ◽  
Transdiaphragmatic Pressure ◽  
Rib Cage ◽  
Constant Work Rate ◽  
And Control

We assessed the effects of selective restriction of movements of the rib cage (Res,rc) and abdomen (Res,ab) on ventilatory pattern, transdiaphragmatic pressure (Pdi), and electrical activity of the diaphragm (Edi) in five normal subjects exercising at a constant work rate (80% of maximum power output) on a cycle ergometer till exhaustion. Restriction of movements was achieved by an inelastic corset applied tightly around the rib cage or abdomen. Edi was recorded by an esophageal electrode, rectified, and then integrated, and peak values during inspiration were measured. Each subject exercised at the same work rate on 3 days: with Res,rc, with Res,ab, and without restriction (control). Res,rc but not Res,ab reduced exercise time (tlim). Up to tlim, minute ventilation (VE) was similar in all three conditions. At any level of VE, however, Res,rc decreased tidal volume and inspiratory and expiratory time, whereas Res,ab had no effect on the pattern of breathing. Res,ab was associated with higher inspiratory Pdi swings at any level of VE, whereas peak Edi was similar to control. Inspiratory Pdi swings were the same with Res,rc as control, but the peak Edi for a given Pdi was greater with Res,rc (P less than 0.05). During Res,rc the abdominal pressure swings in expiration were greater than with Res,ab and control. We conclude that Res,rc altered the pattern of breathing in normal subjects in high-intensity exercise, decreased diaphragmatic contractility, increased abdominal muscle recruitment in expiration, and reduced tlim. On the other hand, Res,ab had no effect on breathing pattern or tlim but was associated with increased diaphragmatic contractility.

Effect of body posture on lung volumes

1961 ◽  
Vol 16 (1) ◽  
pp. 27-29 ◽  
Author(s):  
Francisco Moreno ◽  
Harold A. Lyons
Keyword(s):  
Tidal Volume ◽  
Prone Position ◽  
Supine Position ◽  
Total Lung Capacity ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Body Posture ◽  
Mean Values ◽  
Lung Capacity ◽  
Residual Capacity

The changes produced by body posture on total lung capacity and its subdivisions have been reported for all positions except the prone position. Twenty normal subjects, twelve males and eight females, had determinations of total lung capacity in the three body positions, sitting, supine and prone. Tidal volume, minute ventilation and O2 consumption were also measured. The changes found on assumption of the supine position from the sitting position were similar to those previously reported. For the prone position, a smaller inspiratory capacity and a larger expiratory reserve volume were found. The mean values were changed, respectively, –8% and +37%. Associated with these changes was a significant increase of the functional residual capacity by 636 ml. Ventilation did not change significantly from that found during sitting, unlike the findings associated with the supine position, in which position the tidal volume was decreased. Respiratory frequency remained the same for all positions. Submitted on April 5, 1960

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