Hypoxic effects on exercise-induced diaphragmatic fatigue in normal healthy humans

We examined the effects of hypoxia on exercise-induced diaphragmatic fatigue. Eleven subjects with a mean maximal O2 uptake of 52.4 +/- 0.7 ml.kg-1.min-1 completed one normoxic (arterial O2 saturation 96-94%) and one hypoxic (inspiratory O2 fraction = 0.15; arterial O2 saturation 83–77%) exercise test at 85% maximal O2 uptake to exhaustion on separate days. Supramaximal bilateral phrenic nerve stimulation (BPNS) was used to determine the pressure generation of the diaphragm pre- and postexercise at 1, 10, and 20 Hz. There was increased flow limitation during hypoxic vs. normoxic exercise. There was a decrease in hypoxic exercise time (normoxic 24.9 +/- 0.7 min vs. hypoxic 15.8 +/- 0.8 min; P < 0.05). After exercise the BPNS transdiaphragmatic pressure (Pdi) was significantly reduced at 1 and 10 Hz after both exercise tests. The BPNS Pdi was recovered to control values by 60 min postnormoxic exercise but was still reduced 90 min posthypoxic exercise. The mean percent fall in the stimulated BPNS Pdi was similar (normoxic -24.8 +/- 4.7%; hypoxic -18.8 +/- 3.0%) after both exercise conditions. Experiencing the same amount of diaphragm fatigue in a shorter time period in hypoxic exercise may have been due to 1) the increased expiratory flow limitation and diaphragmatic muscle work, 2) decreased O2 transport to the diaphragm, and/or 3) increased levels of circulating metabolites.

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Exercise-induced arterial hypoxemia is unaffected by intense physical training: a case report

Applied Physiology Nutrition and Metabolism ◽

10.1139/apnm-2013-0341 ◽

2014 ◽

Vol 39 (2) ◽

pp. 266-269 ◽

Cited By ~ 3

Author(s):

Paolo B. Dominelli ◽

Glen E. Foster ◽

Giulio S. Dominelli ◽

William R. Henderson ◽

Michael S. Koehle ◽

...

Keyword(s):

Oxygen Consumption ◽

Case Report ◽

Aerobic Training ◽

Maximal Exercise ◽

Maximal Oxygen Consumption ◽

Severe Hypoxemia ◽

Exercise Tests ◽

Arterial Hypoxemia ◽

Healthy Humans ◽

Exercise Induced

Exercise-induced arterial hypoxemia (EIAH) occurs in some healthy humans at sea-level, whereby the most aerobically trained individuals develop the most severe hypoxemia. A female competitive runner completed 2 maximal exercise tests. Maximal oxygen consumption increased by 15% between testing days, but the degree of hypoxemia remained similar (PaO2, SaO2; 82 and 80 mm Hg; 93.8% and 92.8%; first and second test, respectively). Our case indicates that EIAH does not necessarily worsen with aerobic training.

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Expiratory flow limitation and intrinsic positive end-expiratory pressure in obesity

Journal of Applied Physiology ◽

10.1152/jappl.1998.85.4.1236 ◽

1998 ◽

Vol 85 (4) ◽

pp. 1236-1243 ◽

Cited By ~ 128

Author(s):

W. Pankow ◽

T. Podszus ◽

T. Gutheil ◽

T. Penzel ◽

J.-H. Peter ◽

...

Keyword(s):

Supine Position ◽

Lateral Position ◽

Normal Weight ◽

Upright Position ◽

Flow Limitation ◽

Positive End Expiratory Pressure ◽

Expiratory Flow Limitation ◽

Transdiaphragmatic Pressure ◽

Expiratory Flow ◽

The Right

Breathing at very low lung volumes might be affected by decreased expiratory airflow and air trapping. Our purpose was to detect expiratory flow limitation (EFL) and, as a consequence, intrinsic positive end-expiratory pressure (PEEPi) in grossly obese subjects (OS). Eight OS with a mean body mass index (BMI) of 44 ± 5 kg/m2 and six age-matched normal-weight control subjects (CS) were studied in different body positions. Negative expiratory pressure (NEP) was used to determine EFL. In contrast to CS, EFL was found in two of eight OS in the upright position and in seven of eight OS in the supine position. Dynamic PEEPi and mean transdiaphragmatic pressure (mean Pdi) were measured in all six CS and in six of eight OS. In OS, PEEPi increased from 0.14 ± 0.06 (SD) kPa in the upright position to 0.41 ± 0.11 kPa in the supine position ( P < 0.05) and decreased to 0.20 ± 0.08 kPa in the right lateral position ( P < 0.05, compared with supine), whereas, in CS, PEEPi was significantly smaller (<0.05 kPa) in each position. In OS, mean Pdi in each position was significantly larger compared with CS. Mean Pdi increased from 1.02 ± 0.32 kPa in the upright position to 1.26 ± 0.17 kPa in the supine position (not significant) and decreased to 1.06 ± 0.26 kPa in the right lateral position ( P < 0.05, compared with supine), whereas there were no significant changes in CS. We conclude that in OS 1) tidal breathing can be affected by EFL and PEEPi; 2) EFL and PEEPi are promoted by the supine posture; and 3) the increased diaphragmatic load in the supine position is, in part, related to PEEPi.

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Epidemiology Of Exercise-Induced Hypoxemia In Athletes And The Role Of Expiratory Flow Limitation

10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5195 ◽

2011 ◽

Author(s):

Sat Sharma ◽

Gerard Coneys ◽

Peter Lu ◽

Cris Labossiere

Keyword(s):

Flow Limitation ◽

Expiratory Flow Limitation ◽

Expiratory Flow ◽

Exercise Induced

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Respiratory effort sensation during exercise with induced expiratory-flow limitation in healthy humans

Journal of Applied Physiology ◽

10.1152/jappl.1997.83.3.936 ◽

1997 ◽

Vol 83 (3) ◽

pp. 936-947 ◽

Cited By ~ 39

Author(s):

Bengt Kayser ◽

Pawel Sliwinski ◽

Sheng Yan ◽

Mirek Tobiasz ◽

Peter T. Macklem

Keyword(s):

Healthy Subjects ◽

Flow Limitation ◽

Respiratory Effort ◽

Expiratory Flow Limitation ◽

Healthy Humans ◽

Inspiratory Muscles ◽

Expiratory Muscles ◽

Expiratory Flow ◽

End Tidal ◽

Pressure Changes

Kayser, Bengt, Pawel Sliwinski, Sheng Yan, Mirek Tobiasz, and Peter T. Macklem. Respiratory effort sensation during exercise with induced expiratory-flow limitation in healthy humans. J. Appl. Physiol. 83(3): 936–947, 1997.—Nine healthy subjects (age 31 ± 4 yr) exercised with and without expiratory-flow limitation (maximal flow ∼1 l/s). We monitored flow, end-tidal [Formula: see text], esophageal (Pes) and gastric pressures, changes in end-expiratory lung volume, and perception (sensation) of difficulty in breathing. Subjects cycled at increasing intensity (+25 W/30 s) until symptom limitation. During the flow-limited run, exercise performance was limited in all subjects by maximum sensation. Sensation was equally determined by inspiratory and expiratory pressure changes. In both runs, 90% of the variance in sensation could be explained by the Pes swings (difference between peak inspiratory and peak expiratory Pes). End-tidal[Formula: see text] did not explain any variance in sensation in the control run and added only 3% to the explained variance in the flow-limited run. We conclude that in healthy subjects, during normal as well as expiratory flow-limited exercise, the pleural pressure generation of the expiratory muscles is equally related to the perception of difficulty in breathing as that of the inspiratory muscles.

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Diaphragmatic fatigue in normoxia and hyperoxia

Journal of Applied Physiology ◽

10.1152/jappl.1985.58.3.738 ◽

1985 ◽

Vol 58 (3) ◽

pp. 738-742 ◽

Cited By ~ 15

Author(s):

R. L. Pardy ◽

P. T. Bye

Keyword(s):

Breathing Pattern ◽

Minute Ventilation ◽

Random Order ◽

Similar Degree ◽

Endurance Time ◽

Transdiaphragmatic Pressure ◽

Perceived Effort ◽

Diaphragmatic Fatigue ◽

End Tidal ◽

Arterial O2 Saturation

Diaphragmatic fatigue was induced in six normal young men inspiring against a variable alinear resistance. Breathing pattern was rigidly controlled (tidal volume 0.75 liter, 12 breaths . min-1). Fatigue was defined as an inability to continue to generate a target transdiaphragmatic pressure (Pdi = 0.65 - 0.84 Pdimax). Diaphragmatic electromyogram (EMG, esophageal electrode) and perceived effort (PE, open-ended scale) were recorded. Subjects were tested on an identical resistance inspiring air or 100% O2 in random order on different days. They were unaware of the gas mixture inspired. Mean endurance time (tlim) +/- SE for air was 4.1 +/- 1.4 min and for O2 was 8.6 +/- 2.7 min (P less than 0.005). The increased tlim in O2 was associated with a delay in onset of EMG changes heralding diaphragmatic fatigue and a decrease in PE at any time during the study compared with the level of PE in air. Arterial O2 saturation (ear oximeter) remained at the resting level of 99.0 +/- 0.2% in O2 and decreased from the resting level of 97.2 +/- 0.2% by 2.8 +/- 0.7% (P less than 0.01) in air. The end-tidal CO2 fraction increased to a similar degree in air and O2 studies. We conclude that when breathing pattern, minute ventilation, and Pdi are held constant during inspiratory resistive loading, breathing O2 delays the onset of diaphragm fatigue and decreases PE.

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Exercise-induced diaphragmatic fatigue in healthy humans.

The Journal of Physiology ◽

10.1113/jphysiol.1993.sp019477 ◽

1993 ◽

Vol 460 (1) ◽

pp. 385-405 ◽

Cited By ~ 268

Author(s):

B D Johnson ◽

M A Babcock ◽

O E Suman ◽

J A Dempsey

Keyword(s):

Healthy Humans ◽

Diaphragmatic Fatigue ◽

Exercise Induced

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

Journal of Applied Physiology ◽

10.1152/japplphysiol.01341.2009 ◽

2010 ◽

Vol 109 (1) ◽

pp. 35-46 ◽

Cited By ~ 59

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.

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No effect of arm-crank exercise on diaphragmatic fatigue or ventilatory constraint in Paralympic athletes with cervical spinal cord injury

Journal of Applied Physiology ◽

10.1152/japplphysiol.00227.2010 ◽

2010 ◽

Vol 109 (2) ◽

pp. 358-366 ◽

Cited By ~ 22

Author(s):

Bryan J. Taylor ◽

Christopher R. West ◽

Lee M. Romer

Keyword(s):

Spinal Cord ◽

Spinal Cord Injury ◽

Cervical Spinal Cord ◽

Work Of Breathing ◽

Cervical Spinal Cord Injury ◽

Flow Volume ◽

Transdiaphragmatic Pressure ◽

Cord Injury ◽

Diaphragmatic Fatigue ◽

Exercise Induced

Cervical spinal cord injury (CSCI) results in a decrease in the capacity of the lungs and chest wall for pressure, volume, and airflow generation. We asked whether such impairments might increase the potential for exercise-induced diaphragmatic fatigue and mechanical ventilatory constraint in this population. Seven Paralympic wheelchair rugby players (mean ± SD peak oxygen uptake = 16.9 ± 4.9 ml·kg−1·min−1) with traumatic CSCI (C5–C7) performed arm-crank exercise to the limit of tolerance at 90% of their predetermined peak work rate. Diaphragm function was assessed before and 15 and 30 min after exercise by measuring the twitch transdiaphragmatic pressure (Pdi,tw) response to bilateral anterolateral magnetic stimulation of the phrenic nerves. Ventilatory constraint was assessed by measuring the tidal flow volume responses to exercise in relation to the maximal flow volume envelope. Pdi,tw was not different from baseline at any time after exercise (unpotentiated Pdi,tw = 19.3 ± 5.6 cmH2O at baseline, 19.8 ± 5.0 cmH2O at 15 min after exercise, and 19.4 ± 5.7 cmH2O at 30 min after exercise; P = 0.16). During exercise, there was a sudden, sustained rise in operating lung volumes and an eightfold increase in the work of breathing. However, only two subjects showed expiratory flow limitation, and there was substantial capacity to increase both flow and volume (<50% of maximal breathing reserve). In conclusion, highly trained athletes with CSCI do not develop exercise-induced diaphragmatic fatigue and rarely reach mechanical ventilatory constraint.

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