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.

AEROBIC FITNESS EFFECTS ON EXERCISE-INDUCED DIAPHRAGM FATIGUE.

1995 ◽  
Vol 27 (Supplement) ◽  
pp. S242
Author(s):  
M. A. Babcock ◽  
D. Pegelow ◽  
J. A. Dempsey
Keyword(s):  
Aerobic Fitness ◽  
Fitness Effects ◽  
Exercise Induced ◽  
Diaphragm Fatigue

Contribution of diaphragmatic power output to exercise-induced diaphragm fatigue

1995 ◽  
Vol 78 (5) ◽  
pp. 1710-1719 ◽  
Author(s):  
M. A. Babcock ◽  
D. F. Pegelow ◽  
S. R. McClaran ◽  
O. E. Suman ◽  
J. A. Dempsey
Keyword(s):  
Endurance Exercise ◽  
Nerve Stimulation ◽  
Extracellular Fluid ◽  
Flow Distribution ◽  
Whole Body ◽  
Transdiaphragmatic Pressure ◽  
First Dorsal Interosseous Muscle ◽  
Normal Humans ◽  
Exercise Induced ◽  
Diaphragm Fatigue

n nine normal humans we compared the effects on diaphragm fatigue of whole body exercise to exhaustion (86–93% of maximal O2 uptake for 13.2 +/- 2.0 min) to voluntary increases in the tidal integral of transdiaphragmatic pressure (integral of Pdi) while at rest at the same magnitude and frequency and for the same duration as those during exercise. After the endurance exercise, we found a consistent and significant fall (-26 +/- 2.9%, range -19.2 to -41.0%) in the Pdi response to supramaximal bilateral phrenic nerve stimulation at all stimulation frequencies (1, 10, and 20 Hz). Integral of Pdi.fB (where fB is breathing frequency) achieved during exercise averaged 509 +/- 81.0 cmH2O/min (range 304.0–957.0 cmH2O/min). At rest, voluntary production of integral of Pdi.fB, which was < 550–600 cmH2O/min (approximately 4 times the resting eupenic integral of Pdi.fB or 60–70% of Pdi capacity), did not result in significant diaphragmatic fatigue, whereas sustained voluntary production of integral of Pdi.fB in excess of these threshold values usually did result in significant fatigue. Thus, with few exceptions (5 of 23 tests) the ventilatory requirements of whole body endurance exercise demanded a level of integral of Pdi.fB that, by itself, was not fatiguing. The rested first dorsal interosseous muscle showed no fatigue in response to supramaximal ulnar nerve stimulation after whole body exercise. We postulate that the effects of locomotor muscle activity, such as competition for blood flow distribution and/or extracellular fluid acidosis, in conjunction with a contracting diaphragm account for most of the exercise-induced diaphragm fatigue.

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.

Respiratory load compensation in chronic airway obstruction

1985 ◽  
Vol 59 (6) ◽  
pp. 1947-1954 ◽  
Author(s):  
M. Lopata ◽  
E. Onal ◽  
G. Cromydas
Keyword(s):  
Airway Obstruction ◽  
Lung Volume ◽  
Average Rate ◽  
Minute Ventilation ◽  
Force Output ◽  
Transdiaphragmatic Pressure ◽  
Load Compensation ◽  
Group A ◽  
Group B ◽  
Chronic Airway

To assess respiratory neuromuscular function and load compensating ability in patients with chronic airway obstruction (CAO), we studied eight stable patients with irreversible airway obstruction during hyperoxic CO2 rebreathing with and without a 17 cmH2O X l-1 X s flow-resistive inspiratory load (IRL). Minute ventilation (VE), transdiaphragmatic pressure (Pdi), and diaphragmatic electromyogram (EMGdi) were monitored. Pdi and EMGdi were obtained via a single gastroesophageal catheter with EMGdi being quantitated as the average rate of rise of inspiratory (moving average) activity. Based on the effects of IRL on the Pdi response to CO2 [delta Pdi/delta arterial CO2 tension (PaCO2)] and the change in Pdi for a given change in EMGdi (delta Pdi/delta EMGdi) during rebreathing, two groups could be clearly identified. Four patients (group A) were able to increase delta Pdi/delta PaCO2 and delta Pdi/delta EMGdi, whereas in the other four (group B) the IRL responses decreased. All group B patients were hyperinflated having significantly greater functional residual capacity (FRC) and residual volume than group A. In addition the IRL induced percent change in delta Pdi/delta PaCO2, and delta VE/delta PaCO2 was negatively correlated with lung volume so that in the hyperinflated group B the higher the FRC the greater was the decrease in Pdi response due to IRL. In both groups the greater the FRC the greater was the decrease in the ventilatory response to loading. Patients with CAO, even with severe airways obstruction, can effect load compensation by increasing diaphragmatic force output, but the presence of increased lung volume with the associated shortened diaphragm prevents such load compensation.

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.

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.

Electromyogram pattern of diaphragmatic fatigue

1979 ◽  
Vol 46 (1) ◽  
pp. 1-7 ◽  
Author(s):  
D. Gross ◽  
A. Grassino ◽  
W. R. Ross ◽  
P. T. Macklem
Keyword(s):  
High Frequency ◽  
Low Frequency ◽  
Normal Subjects ◽  
Progressive Increase ◽  
Transdiaphragmatic Pressure ◽  
Diaphragmatic Fatigue ◽  
Inspiratory Resistance ◽  
Residual Capacity ◽  
Emg Power Spectrum ◽  
Pressure Generator

We studied the effect of breathing at various levels of transdiaphragmatic pressure (Pdi) on the EMG power spectrum of the diaphragm. The diaphragmatic EMG was measured simultaneously with a bipolar esophageal electrode (EE) and surface electrode (SE) placed on the ventral portion of the sixth and seventh intercostal spaces in five normal subjects breathing at functional residual capacity (FRC) against an inspiratory resistance. During each fatigue run the subjects generated a Pdi, with each inspiration, that was 25, 50, or 75% of maximum Pdi (Pdimax) for a period up to 15 min. During runs at 50 and 75% of the Pdimax, which are known to produce fatigue, we found for both EE and SE a progressive increase in the amplitude of the low-frequency (L = 20-46.7 Hz) and a decrease in the high-frequency (H = 150-350 Hz) component of the EMG. These changes were not seen at 25% of Pdimax. The diaphragmatic H/L ratio was independent of Pdi when the diaphragm was not fatigued. H/L fell while the diaphragm performed fatiguing work and this was more rapid at higher Pdi's. It was thus concluded that frequency spectrum analysis of the EMG can detect diaphragmatic fatigue reliably, prior to the time when the diaphragm fails as a pressure generator.

scholarly journals Sex differences in exercise-induced diaphragmatic fatigue in endurance-trained athletes

2010 ◽  
Vol 109 (1) ◽  
pp. 35-46 ◽  
Author(s):  
Jordan A. Guenette ◽  
Lee M. Romer ◽  
Jordan S. Querido ◽  
Romeo Chua ◽  
Neil D. Eves ◽  
...  
Keyword(s):  
Sex Differences ◽  
Aerobic Capacity ◽  
Female Athletes ◽  
Maximal Aerobic Capacity ◽  
Transdiaphragmatic Pressure ◽  
Pressure Time ◽  
Diaphragmatic Fatigue ◽  
Exercise Induced ◽  
Pressure Time Product ◽  
Diaphragm Fatigue

There is evidence that female athletes may be more susceptible to exercise-induced arterial hypoxemia and expiratory flow limitation and have greater increases in operational lung volumes during exercise relative to men. These pulmonary limitations may ultimately lead to greater levels of diaphragmatic fatigue in women. Accordingly, the purpose of this study was to determine whether there are sex differences in the prevalence and severity of exercise-induced diaphragmatic fatigue in 38 healthy endurance-trained men ( n = 19; maximal aerobic capacity = 64.0 ± 1.9 ml·kg−1·min−1) and women ( n = 19; maximal aerobic capacity = 57.1 ± 1.5 ml·kg−1·min−1). Transdiaphragmatic pressure (Pdi) was calculated as the difference between gastric and esophageal pressures. Inspiratory pressure-time products of the diaphragm and esophagus were calculated as the product of breathing frequency and the Pdi and esophageal pressure time integrals, respectively. Cervical magnetic stimulation was used to measure potentiated Pdi twitches (Pdi,tw) before and 10, 30, and 60 min after a constant-load cycling test performed at 90% of peak work rate until exhaustion. Diaphragm fatigue was considered present if there was a ≥15% reduction in Pdi,tw after exercise. Diaphragm fatigue occurred in 11 of 19 men (58%) and 8 of 19 women (42%). The percent drop in Pdi,tw at 10, 30, and 60 min after exercise in men ( n = 11) was 30.6 ± 2.3, 20.7 ± 3.2, and 13.3 ± 4.5%, respectively, whereas results in women ( n = 8) were 21.0 ± 2.1, 11.6 ± 2.9, and 9.7 ± 4.2%, respectively, with sex differences occurring at 10 and 30 min ( P < 0.05). Men continued to have a reduced contribution of the diaphragm to total inspiratory force output (pressure-time product of the diaphragm/pressure-time product of the esophagus) during exercise, whereas diaphragmatic contribution in women changed very little over time. The findings from this study point to a female diaphragm that is more resistant to fatigue relative to their male counterparts.

scholarly journals Exercise-induced diaphragm fatigue in a Paralympic champion rower with spinal cord injury

2018 ◽  
Vol 124 (3) ◽  
pp. 805-811 ◽  
Author(s):  
Nicholas B. Tiller ◽  
Thomas R. Aggar ◽  
Christopher R. West ◽  
Lee M. Romer
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Pulmonary Ventilation ◽  
Time Trial ◽  
Upper Body ◽  
Upper Body Exercise ◽  
Transdiaphragmatic Pressure ◽  
Cord Injury ◽  
Exercise Induced ◽  
Diaphragm Fatigue

The aim of this case report was to determine whether maximal upper body exercise was sufficient to induce diaphragm fatigue in a Paralympic champion adaptive rower with low-lesion spinal cord injury (SCI). An elite arms-only oarsman (age: 28 yr; stature: 1.89 m; and mass: 90.4 kg) with motor-complete SCI (T12) performed a 1,000-m time trial on an adapted rowing ergometer. Exercise measurements comprised pulmonary ventilation and gas exchange, diaphragm EMG-derived indexes of neural respiratory drive, and intrathoracic pressure-derived indexes of respiratory mechanics. Diaphragm fatigue was assessed by measuring pre- to postexercise changes in the twitch transdiaphragmatic pressure (Pdi,tw) response to anterolateral magnetic stimulation of the phrenic nerves. The time trial (248 ± 25 W, 3.9 min) elicited a peak O2 uptake of 3.46 l/min and a peak pulmonary ventilation of 150 l/min (57% MVV). Breath-to-stroke ratio was 1:1 during the initial 400 m and 2:1 thereafter. The ratio of inspiratory transdiaphragmatic pressure to diaphragm EMG (neuromuscular efficiency) fell from rest to 600 m (16.0 vs. 3.0). Potentiated Pdi,tw was substantially reduced (−33%) at 15–20 min postexercise, with only partial recovery (−12%) at 30–35 min. This is the first report of exercise-induced diaphragm fatigue in SCI. The decrease in diaphragm neuromuscular efficiency during exercise suggests that the fatigue was partly due to factors independent of ventilation (e.g., posture and locomotion). NEW & NOTEWORTHY This case report provides the first objective evidence of exercise-induced diaphragm fatigue in spinal cord injury (SCI) and, for that matter, in any population undertaking upper body exercise. Our data support the notion that high levels of exercise hyperpnea and factors other than ventilation (e.g., posture and locomotion) are responsible for the fatigue noted after upper body exercise. The findings extend our understanding of the limits of physiological function in SCI.

Effects of loaded breathing and hypoxia on diaphragm metabolism as measured by 31P-NMR spectroscopy

2000 ◽  
Vol 88 (3) ◽  
pp. 933-938 ◽  
Author(s):  
Peter J. Radell ◽  
Scott M. Eleff ◽  
David G. Nichols
Keyword(s):  
Nuclear Magnetic Resonance ◽  
Respiratory Failure ◽  
Magnetic Resonance ◽  
Aerobic Metabolism ◽  
Resonance Spectroscopy ◽  
Force Output ◽  
Transdiaphragmatic Pressure ◽  
Loaded Breathing ◽  
Diaphragm Fatigue ◽  
Nuclear Magnetic

Diaphragm fatigue may contribute to respiratory failure.31P-nuclear magnetic resonance spectroscopy is a useful tool to assess energetic changes within the diaphragm during fatigue, as indicated by Pi accumulation and phosphocreatine (PCr) depletion. We hypothesized that loaded breathing during hypoxia would lead to diaphragm fatigue and inadequate aerobic metabolism. Seven piglets were anesthetized by using halothane inhalation. Diaphragmatic contractility was assessed by transdiaphragmatic pressure (Pdi) at end expiration with the airway occluded. A nuclear magnetic resonance surface coil placed under the right hemidiaphragm measured Pi and PCr during four conditions: control, inspiratory resistive breathing (IRB), IRB with hypoxia, and recovery (IRB without hypoxia). IRB alone resulted in hypercarbia (32 ± 7 to 61 ± 21 Torr) and respiratory acidosis but no change in diaphragm force output or aerobic metabolism. Combined IRB and hypoxia resulted in decreased force output (Pdi decreased by 40%; from 30 ± 17 to 19 ± 11 mmHg) and evidence of metabolic stress (ratio of Pi to PCr increased by 290%; from 0.19 ± 0.09 to 0.74 ± 0.27). We conclude that diaphragm fatigue associated with inadequate aerobic oxidative metabolism occurs in the setting of loaded breathing and hypoxia. Conversely, aerobic metabolism and force output of the diaphragm remain unchanged from control during loaded normoxic or hyperoxic breathing despite the onset of respiratory failure.

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