Ventilatory response to fatiguing and nonfatiguing resistive loads in awake sheep

1985 ◽  
Vol 59 (3) ◽  
pp. 969-978 ◽  
Author(s):  
N. Sadoul ◽  
A. R. Bazzy ◽  
S. R. Akabas ◽  
G. G. Haddad
Keyword(s):  
Considerable Increase ◽  
Minute Ventilation ◽  
Respiratory Muscles ◽  
Inspiratory Flow ◽  
Transdiaphragmatic Pressure ◽  
Arterial Pco2 ◽  
Residual Capacity ◽  
Alveolar Hypoventilation ◽  
Resistive Loads ◽  
Respiratory Muscle Endurance

To study the changes in ventilation induced by inspiratory flow-resistive (IFR) loads, we applied moderate and severe IFR loads in chronically instrumented and awake sheep. We measured inspired minute ventilation (VI), ventilatory pattern [inspiratory time (TI), expiratory time (TE), respiratory cycle time (TT), tidal volume (VT), mean inspiratory flow (VT/TI), and respiratory duty cycle (TI/TT)], transdiaphragmatic pressure (Pdi), functional residual capacity (FRC), blood gas tensions, and recorded diaphragmatic electromyogram. With both moderate and severe loads, Pdi, TI, and TI/TT increased, TE, TT, VT, VT/TI, and VI decreased, and hypercapnia ensued. FRC did not change significantly with moderate loads but decreased by 30–40% with severe loads. With severe loads, arterial PCO2 (PaCO2) stabilized at approximately 60 Torr within 10–15 min and rose further to levels exceeding 80 Torr when Pdi dropped. This was associated with a lengthening in TE and a decrease in breathing frequency, VI, and TI/TT. We conclude that 1) timing and volume responses to IFR loads are not sufficient to prevent alveolar hypoventilation, 2) with severe loads the considerable increase in Pdi, TI/TT, and PaCO2 may reduce respiratory muscle endurance, and 3) the changes in ventilation associated with neuromuscular fatigue occur after the drop in Pdi. We believe that these ventilatory changes are dictated by the mechanical capability of the respiratory muscles or induced by a decrease in central neural output to these muscles or both.

Metabolic and functional adaptation of the diaphragm to training with resistive loads

1989 ◽  
Vol 66 (2) ◽  
pp. 529-535 ◽  
Author(s):  
S. R. Akabas ◽  
A. R. Bazzy ◽  
S. DiMauro ◽  
G. G. Haddad
Keyword(s):  
Cytochrome Oxidase ◽  
Citrate Synthase ◽  
Minute Ventilation ◽  
Training Session ◽  
Inspiratory Flow ◽  
Functional Adaptation ◽  
Transdiaphragmatic Pressure ◽  
Functional Changes ◽  
Hydroxyacyl Coa Dehydrogenase ◽  
Resistive Loads

To study the metabolic and functional changes that occur during training with inspiratory flow resistive loads, a chronically instrumented unanesthetized sheep preparation was used. Sheep were exposed to resistances ranging from 50 to 100 cmH2O.l–1.s, for 2–4 h/day, 5–6 days/wk, for a total of 3 wk. Load intensity was adjusted to maintain arterial Po2 (PaO2) above 60 Torr and arterial PCO2 (PaCO2) below 45 Torr. Training produced significant (P less than 0.05) increases in citrate synthase, 3-hydroxyacyl-CoA dehydrogenase, and cytochrome oxidase in the costal and crural diaphragm of the trained sheep (n = 9) compared with control sheep (n = 7). Phosphofructokinase did not increase. In the quadriceps, citrate synthase, 3-hydroxyacyl-CoA dehydrogenase, and phosphofructokinase did not change with training but cytochrome oxidase increased significantly (P less than 0.01). Function of the diaphragm was assessed in a subset of five sheep exposed to the same severe load 1 wk before and 2 days after the final training session. After training, sheep had a lower PaCO2 (10–40%), generated a higher transdiaphragmatic pressure (20–40%), and could sustain this level of transdiaphragmatic pressure for 0.5–2 h longer. The respiratory duty cycle was 10–15% lower, whereas minute ventilation and tidal volume were 20–30% higher in the posttraining test. We conclude that 1) training with inspiratory flow resistive loads improves the performance of the respiratory neuromuscular system and 2) the shift in enzyme profile of the diaphragm is at least in part responsible for this improvement.

O2 metabolism of the sheep diaphragm during flow resistive loaded breathing

1989 ◽  
Vol 66 (5) ◽  
pp. 2305-2311 ◽  
Author(s):  
A. R. Bazzy ◽  
L. M. Pang ◽  
S. R. Akabas ◽  
G. G. Haddad
Keyword(s):  
Venous Blood ◽  
Inspiratory Flow ◽  
Transdiaphragmatic Pressure ◽  
Arterial Pco2 ◽  
Loaded Breathing ◽  
O2 Diffusion ◽  
Lactate And Pyruvate ◽  
Resistive Loads ◽  
Venous Blood Gas ◽  
Arteriovenous Difference

To determine whether O2 availability limited diaphragmatic performance, we subjected unanesthetized sheep to severe (n = 11) and moderate (n = 3) inspiratory flow resistive loads and studied the phrenic venous effluent. We measured transdiaphragmatic pressure (Pdi), systemic arterial and phrenic venous blood gas tensions, and lactate and pyruvate concentrations. In four sheep with severe loads, we measured O2 saturation (SO2), O2 content, and hemoglobin. We found that with severe loads Pdi increased to 74.7 +/- 6.0 cmH2O by 40 min of loading, remained stable for 20–30 more min, then slowly decreased. In every sheep, arterial PCO2 increased when Pdi decreased. With moderate loads Pdi increased to and maintained levels of 40–55 cmH2O. With both loads, venous PO2, SO2, and O2 content decreased initially and then increased, so that the arteriovenous difference in O2 content decreased as loading continued. Hemoglobin increased slowly in three of four sheep. There were no appreciable changes in arterial or venous lactate and pyruvate during loading or recovery. We conclude that the changes in venous PO2, SO2, and O2 content may be the result of changes in hemoglobin, blood flow to the diaphragm, or limitation of O2 diffusion. Our data do not support the hypothesis that in sheep subjected to inspiratory flow resistive loads O2 availability limits diaphragmatic performance.

Blood flow to respiratory muscles and major organs during inspiratory flow resistive loads

1993 ◽  
Vol 74 (1) ◽  
pp. 428-434 ◽  
Author(s):  
L. M. Pang ◽  
Y. J. Kim ◽  
A. R. Bazzy
Keyword(s):  
Blood Flow ◽  
Muscle Blood Flow ◽  
Respiratory Muscles ◽  
Inspiratory Flow ◽  
The Other ◽  
Transdiaphragmatic Pressure ◽  
Diaphragmatic Fatigue ◽  
Microsphere Method ◽  
Loaded Breathing ◽  
Resistive Loads

To determine whether diaphragmatic fatigue in the intact animal subjected to loaded breathing is associated with a decrease in diaphragmatic blood flow, seven unanesthetized sheep were subjected to severe inspiratory flow resistive (IFR) loads that led to a decrease in transdiaphragmatic pressure (Pdi) and a rise in arterial PCO2 (PaCO2). Blood flow to the diaphragm, other respiratory muscles, limb muscles, and major organs was measured using the radionuclide-labeled microsphere method. With these loads blood flow increased to the diaphragm (621 +/- 242%) and all the other inspiratory and expiratory diaphragm (621 +/- 242%) and all the other inspiratory and expiratory muscles; there was no statistically significant change in blood flow to these muscles at the time when Pdi decreased and PaCO2 rose. Blood flow also increased to the heart (103 +/- 34%), brain (212 +/- 39%), and adrenals (76 +/- 9%), whereas pancreatic flow decreased (-66 +/- 14%). Limb muscle blood flow remained unchanged. We conclude that in unanesthetized sheep subjected to IFR loads 1) we did not demonstrate a decrease in respiratory muscle blood flow associated with diaphragmatic fatigue and ventilatory failure, and 2) there is a redistribution of blood flow among major organs.

Diaphragmatic fatigue in man

1977 ◽  
Vol 43 (2) ◽  
pp. 189-197 ◽  
Author(s):  
C. S. Roussos ◽  
P. T. Macklem
Keyword(s):  
Energy Consumption ◽  
Lung Diseases ◽  
Respiratory Muscles ◽  
Transdiaphragmatic Pressure ◽  
Diaphragmatic Fatigue ◽  
Residual Capacity ◽  
The Subject ◽  
Time Required ◽  
The Relationship ◽  
Experimental Runs

The time required (tlim) to produce fatigue of the diaphragm was determined in three normal seated subjects, breathing through a variety of high alinear, inspiratory resistances. During each breath in all experimental runs the subject generated a transdiaphragmatic pressure (Pdi) which was a predetermined fraction of his maximum inspiratory Pdi (Pdimax) at functional residual capacity. The breathing test was performed until the subject was unable to generate this Pdi. The relationship between Pdi/Pdimax and tlim was curvilinear so that when Pdi/Pdimax was small tlim increased markedly for little changes in Pdi/Pdimax. The value of Pdi/Pdimax that could be generated indefinitely (Pdicrit) was around 0.4. Hypoxia appeared to have no influence on Pdicrit, but probably led to a reduction in tlim at Pdi greater than Pdicrit for equal rates of energy consumption. Insofar as the behavior of the diaphragm reflects that of other respiratory muscles it appears that quite high inspiratory loads can be tolerated indefinitely. However, when the energy consumption of the respiratory muscles exceeds a critical level, fatigue should develop. This may be a mechanism of respiratory failure in a variety in a variety of lung diseases.

Chest wall distortion during resistive inspiratory loading

1985 ◽  
Vol 58 (5) ◽  
pp. 1646-1653 ◽  
Author(s):  
E. R. Ringel ◽  
S. H. Loring ◽  
J. Mead ◽  
R. H. Ingram
Keyword(s):  
Chest Wall ◽  
Wall Motion ◽  
Respiratory Muscles ◽  
Underlying Mechanism ◽  
Abdominal Muscles ◽  
Transdiaphragmatic Pressure ◽  
Rib Cage ◽  
Circular Configuration ◽  
Chest Wall Motion ◽  
Resistive Loads

We studied six (1 naive and 5 experienced) subjects breathing with added inspiratory resistive loads while we recorded chest wall motion (anteroposterior rib cage, anteroposterior abdomen, and lateral rib cage) and tidal volumes. In the five experienced subjects, transdiaphragmatic and pleural pressures, and electromyographs of the sternocleidomastoid and abdominal muscles were also measured. Subjects inspired against the resistor spontaneously and then with specific instructions to reach a target pleural or transdiaphragmatic pressure or to maximize selected electromyographic activities. Depending on the instructions, a wide variety of patterns of inspiratory motion resulted. Although the forces leading to a more elliptical or circular configuration of the chest wall can be identified, it is difficult to analyze or predict the configurational results based on insertional and pressure-related contributions of a few individual respiratory muscles. Although overall chest wall respiratory motion cannot be readily inferred from the electromyographic and pressure data we recorded, it is clear that responses to loading can vary substantially within and between individuals. Undoubtedly, the underlying mechanism for the distortional changes with loading are complex and perhaps many are behavioral rather than automatic and/or compensatory.

Crural diaphragm activation during dynamic contractions at various inspiratory flow rates

1998 ◽  
Vol 85 (2) ◽  
pp. 451-458 ◽  
Author(s):  
Jennifer Beck ◽  
Christer Sinderby ◽  
Lars Lindström ◽  
Alex Grassino
Keyword(s):  
Chest Wall ◽  
Functional Residual Capacity ◽  
Healthy Subjects ◽  
Total Lung Capacity ◽  
Inspiratory Flow ◽  
Transdiaphragmatic Pressure ◽  
Flow Rates ◽  
Lung Capacity ◽  
Dynamic Contractions ◽  
Residual Capacity

The purpose of this study was to evaluate the influence of velocity of shortening on the relationship between diaphragm activation and pressure generation in humans. This was achieved by relating the root mean square (RMS) of the diaphragm electromyogram to the transdiaphragmatic pressure (Pdi) generated during dynamic contractions at different inspiratory flow rates. Five healthy subjects inspired from functional residual capacity to total lung capacity at different flow rates while reproducing identical Pdi and chest wall configuration profiles. To change the inspiratory flow rate, subjects performed the inspirations while breathing across two different inspiratory resistances (10 and 100 cmH2O ⋅ l−1 ⋅ s), at mouth pressure targets of −10, −20, −40, and −60 cmH2O. The diaphragm electromyogram was recorded and analyzed with control of signal contamination and electrode positioning. RMS values obtained for inspirations with identical Pdi and chest wall configuration profiles were compared at the same percentage of inspiratory duration. At inspiratory flows ranging between 0.1 and 1.4 l/s, there was no difference in the RMS for the inspirations from functional residual capacity to total lung capacity when Pdi and chest wall configuration profiles were reproduced ( n = 4). At higher inspiratory flow rates, subjects were not able to reproduce their chest wall displacements and adopted different recruitment patterns. In conclusion, there was no evidence for increased demand of diaphragm activation when healthy subjects breathe with similar chest wall configuration and Pdi profiles, at increasing flow rates up to 1.4 l/s.

Diaphragmatic function in healthy subjects during partial curarization

1980 ◽  
Vol 48 (6) ◽  
pp. 921-926 ◽  
Author(s):  
T. J. Gal ◽  
S. K. Goldberg
Keyword(s):  
Respiratory Muscles ◽  
Upper Airway ◽  
Normal Subjects ◽  
Maximum Effect ◽  
Quiet Breathing ◽  
Transdiaphragmatic Pressure ◽  
Control Value ◽  
Diaphragmatic Function ◽  
Residual Capacity ◽  
Diaphragmatic Weakness

Diaphragmatic function estimated by transdiaphragmatic pressure (Pdi) was studied in eight normal subjects during progressive partial paralysis with d-tubocurarine (dTc). Dynamic Pdi was measured during quiet tidal breathing, maximum deep inspiration, and 12-s maximum voluntary ventilation (MVV). Maximum static transdiaphragmatic pressure (Pdimax) was also measured during maximum static inspiratory efforts at four lung volumes. The maximum effect of dTc at a cumulative dose of 0.2 mg/kg abolished head-lift and handgrip ability. Pdimax at functional residual capacity was decreased to 42% of its control value indicating significant diaphragmatic weakness at this level of curarization. The weakness had no inpact on quiet breathing and a moderate effect on maximum inspiration. In either case Pdi represented an increasing fraction of Pdimax. MVV fell significantly before the Pdi during the maneuver decreased. This decreased MVV in curarized subjects reflects upper airway obstruction caused by pharyngeal muscle weakness and the diminished contribution of the other respiratory muscles that are important at high levels of ventilatory effort but more sensitive to effects of dTc.

Respiratory muscle function during CO2 rebreathing with inspiratory flow-resistive loading

1983 ◽  
Vol 54 (2) ◽  
pp. 475-482 ◽  
Author(s):  
M. Lopata ◽  
E. Onal ◽  
A. S. Ginzburg
Keyword(s):  
Respiratory Muscle ◽  
Inspiratory Flow ◽  
Passive Component ◽  
Transdiaphragmatic Pressure ◽  
Co2 Partial Pressure ◽  
Load Compensation ◽  
Co2 Rebreathing ◽  
Gastric Pressure ◽  
Resistive Loads ◽  
Muscle Groups

We investigated the respiratory muscle contribution to inspiratory load compensation by measuring diaphragmatic and intercostal electromyograms (EMGdi and EMGic), transdiaphragmatic pressure (Pdi), and thoracoabdominal motion during CO2 rebreathing with and without 15 cmH2O X l-1 X s inspiratory flow resistance (IRL) in normal sitting volunteers. During IRL compared with control, Pdi measured during airflow and during airway occlusion increased for a given change in CO2 partial pressure and EMGdi, and there was a greater decrease in abdominal (AB) end expiratory anteroposterior dimensions with increased expiratory gastric pressure (Pga), this leading to an inspiratory decline in Pga with outward AB movement, indicating a passive component to the descent of the abdomen-diaphragm. The response of EMGic to IRL was similar to that of EMGdi, though rib cage (RC)-Pga plots did infer intercostal muscle contribution. We conclude that during CO2 rebreathing with IRL there is improved diaphragmatic neuromuscular coupling, the prolongation of inspiration promoting a force-velocity advantage, and increased AB action serving to optimize diaphragm length and configuration, as well as to provide its own passive inspiratory action. Intercostal action provides increased assistance also. Therefore, compensation for inspiratory resistive loads results from the combined and integrated effort of all respiratory muscle groups.

Effects of hyperinflation and CPAP on work of breathing and respiratory failure in dogs

1994 ◽  
Vol 77 (2) ◽  
pp. 819-827 ◽  
Author(s):  
E. Shade ◽  
Y. Kawagoe ◽  
R. G. Brower ◽  
S. Permutt ◽  
H. E. Fessler
Keyword(s):  
Respiratory Failure ◽  
Airway Resistance ◽  
Minute Ventilation ◽  
Work Of Breathing ◽  
Respiratory Muscles ◽  
Arterial Pco2 ◽  
Hemodynamic Compromise ◽  
Mechanical Analogue ◽  
Characteristic Features ◽  
Inspiratory Work

Increased end-expiratory lung volume (EELV) and airway resistance are both characteristic features of obstructive lung disease. Increased EELV alone loads the respiratory muscles and may cause respiratory failure, changes that could be reversed by continuous positive airway pressure (CPAP). To study the effects of elevated EELV on respiration without increased airway resistance, we used a mechanical analogue of airway closure to increase EELV in six spontaneously breathing anesthetized dogs. Hyperinflation of 0.84 +/- 0.11 liter for 30 min decreased minute ventilation from 4.8 +/- 0.37 to 3.5 +/- 0.21 l/min and increased arterial PCO2 from 40.3 +/- 1.5 to 73.2 +/- 8.1 Torr (both P < 0.01). Inspiratory work per breath increased 3-fold, work per liter increased 3.7-fold, and work per minute increased 2.8-fold (all P < 0.01). CPAP at 15 cmH2O restored minute ventilation to 4.3 +/- 0.3 l/min and reduced arterial PCO2 to 54 +/- 6.6 Torr (NS vs. baseline). All measurements of inspiratory work were also restored to baseline, but cardiac output was reduced (baseline 3.09 +/- 0.36, hyperinflation 2.71 +/- 0.36, hyperinflation + CPAP 1.94 +/- 0.29 l/min; P < 0.05, baseline vs. hyperinflation + CPAP). We conclude that increases in EELV mimic important features of airway obstruction, increase inspiratory work, and can cause respiratory failure independent of increased airway resistance. This respiratory failure is reversed by CPAP at the potential expense of hemodynamic compromise.

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.

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