Contribution of diaphragmatic power output to 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.

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

Journal of Applied Physiology ◽

10.1152/jappl.1996.81.5.2156 ◽

1996 ◽

Vol 81 (5) ◽

pp. 2156-2164 ◽

Cited By ~ 54

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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Intracellular and extracellular acid-base status and H+ exchange with the environment after exhaustive exercise in the rainbow trout

Journal of Experimental Biology ◽

10.1242/jeb.123.1.93 ◽

1986 ◽

Vol 123 (1) ◽

pp. 93-121 ◽

Cited By ~ 3

Author(s):

C. L. Milligan ◽

C. M. Wood

Keyword(s):

Rainbow Trout ◽

Venous Blood ◽

Extracellular Fluid ◽

Exhaustive Exercise ◽

Whole Body ◽

Acid Base ◽

Acid Load ◽

Acid Base Status ◽

Lactate Levels ◽

Exercise Induced

Exhaustive exercise induced a severe short-lived (0–1 h) respiratory, and longer-lived (0–4 h) metabolic, acidosis in the extracellular fluid of the rainbow trout. Blood ‘lactate’ load exceeded blood ‘metabolic acid’ load from 1–12 h after exercise. Over-compensation occurred, so that by 8–12 h, metabolic alkalosis prevailed, but by 24 h, resting acid-base status had been restored. Acid-base changes were similar, and lactate levels identical, in arterial and venous blood. However, at rest venous RBC pHi was significantly higher than arterial (7.42 versus 7.31). After exercise, arterial RBC pHi remained constant, whereas venous RBC pHi fell significantly (to 7.18) but was fully restored by 1 h. Resting mean whole-body pHi, measured by DMO distribution, averaged approx. 7.25 at a pHe of approx. 7.82 and fell after exercise to a low of 6.78 at a pHe of approx. 7.30. Whole-body pHi was slower to recover than pHe, requiring up to 12 h, with no subsequent alkalosis. Whole-body ECFV decreased by about 70 ml kg-1 due to a fluid shift into the ICF. Net H+ excretion to the water increased 1 h after exercise accompanied by an elevation in ammonia efflux. At 8–12 h, H+ excretion was reduced to resting levels and at 12–24 h, a net H+ uptake occurred. Lactate excretion amounted to approx. 1% of the net H+ excretion and only approx. 2% of the whole blood load. Only a small amount of the anaerobically produced H+ in the ICF appeared in the ECF and subsequently in the water. By 24 h, all the H+ excreted had been taken back up, thus correcting the extracellular alkalosis. The bulk of the H+ load remained intracellular, to be cleared by aerobic metabolism.

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Transcutaneous electrical nerve stimulation reduces exercise-induced perceived pain and improves endurance exercise performance

European Journal of Applied Physiology ◽

10.1007/s00421-016-3532-6 ◽

2017 ◽

Vol 117 (3) ◽

pp. 483-492 ◽

Cited By ~ 13

Author(s):

Ali H. Y. Astokorki ◽

Alexis R. Mauger

Keyword(s):

Endurance Exercise ◽

Nerve Stimulation ◽

Exercise Performance ◽

Transcutaneous Electrical Nerve Stimulation ◽

Electrical Nerve Stimulation ◽

Perceived Pain ◽

Exercise Induced

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Nicotinamide Riboside supplementation does not alter whole-body or skeletal muscle metabolic responses to a single bout of endurance exercise

10.1101/2020.06.23.143446 ◽

2020 ◽

Author(s):

Ben Stocks ◽

Stephen P. Ashcroft ◽

Sophie Joanisse ◽

Yasir S. Elhassan ◽

Gareth G. Lavery ◽

...

Keyword(s):

Skeletal Muscle ◽

Mrna Expression ◽

Endurance Exercise ◽

Vastus Lateralis ◽

Whole Body ◽

Endurance Capacity ◽

Similar Response ◽

Transcriptional Responses ◽

Nicotinamide Riboside ◽

Exercise Induced

AbstractOral supplementation of the NAD+ precursor Nicotinamide Riboside (NR) has been reported to increase Sirtuin (SIRT) signalling, mitochondrial biogenesis and endurance capacity in rodent skeletal muscle. However, whether NR supplementation can elicit a similar response in human skeletal muscle is unclear. This study aimed to assess the effect of 7-day NR supplementation on exercise-induced transduction and transcriptional responses in skeletal muscle of young, healthy, recreationally active human volunteers. In a double-blinded, randomised, counter-balanced, crossover design, eight male participants (age: 23 ± 4 years, VO2peak: 46.5 ± 4.4 mL·kg-1·min-1) received one week of NR or cellulose placebo (PLA) supplementation (1000 mg·d-1) before performing one hour of cycling at 60% Wmax. Muscle biopsies were collected prior to supplementation and pre-, immediately and three-hours post-exercise from the medial vastus lateralis, whilst venous blood samples were collected throughout the trial. Global acetylation, auto-PARylation of PARP1, acetylation of p53Lys382 and MnSODLys122 were unaffected by NR supplementation or exercise. Exercise led to an increase in AMPKThr172 (1.6-fold), and ACCSer79 (4-fold) phosphorylation, in addition to an increase in PGC-1α (∼5-fold) and PDK4 (∼10-fold) mRNA expression, however NR had no additional effect on this response. There was also no effect of NR supplementation on substrate utilisation at rest or during exercise or on skeletal muscle mitochondrial respiration. Finally, NR supplementation blunted the exercise induced activation of skeletal muscle NNMT mRNA expression, but had no effect on mRNA expression of NMRK1, NAMPT or NMNAT1, which were not significantly affected by NR supplementation or exercise. In summary, one week of NR supplementation does not augment skeletal muscle signal transduction pathways implicated in mitochondrial adaptation to endurance exercise.

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

Journal of Applied Physiology ◽

10.1152/japplphysiol.00870.2017 ◽

2018 ◽

Vol 124 (3) ◽

pp. 805-811 ◽

Cited By ~ 2

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.

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Effects of respiratory muscle unloading on exercise-induced diaphragm fatigue

Journal of Applied Physiology ◽

10.1152/japplphysiol.00612.2001 ◽

2002 ◽

Vol 93 (1) ◽

pp. 201-206 ◽

Cited By ~ 99

Author(s):

Mark A. Babcock ◽

David F. Pegelow ◽

Craig A. Harms ◽

Jerome A. Dempsey

Keyword(s):

Oxygen Consumption ◽

Nerve Stimulation ◽

Phrenic Nerve ◽

Respiratory Muscle ◽

Respiratory Muscles ◽

Whole Body ◽

Phrenic Nerve Stimulation ◽

Muscle Work ◽

Diaphragmatic Fatigue ◽

Exercise Induced

We previously compared the effects of increased respiratory muscle work during whole body exercise and at rest on diaphragmatic fatigue and showed that the amount of diaphragmatic force output required to cause fatigue was reduced significantly during exercise (Babcock et al., J Appl Physiol 78: 1710, 1995). In this study, we use positive-pressure proportional assist ventilation (PAV) to unload the respiratory muscles during exercise to determine the effects of respiratory muscle work, per se, on exercise-induced diaphragmatic fatigue. After 8–13 min of exercise to exhaustion under control conditions at 80–85% maximal oxygen consumption, bilateral phrenic nerve stimulation using single-twitch stimuli (1 Hz) and paired stimuli (10–100 Hz) showed that diaphragmatic pressure was reduced by 20–30% for up to 60 min after exercise. Usage of PAV during heavy exercise reduced the work of breathing by 40–50% and oxygen consumption by 10–15% below control. PAV prevented exercise-induced diaphragmatic fatigue as determined by bilateral phrenic nerve stimulation at all frequencies and times postexercise. Our study has confirmed that high- and low-frequency diaphragmatic fatigue result from heavy-intensity whole body exercise to exhaustion; furthermore, the data show that the workload endured by the respiratory muscles is a critical determinant of this exercise-induced diaphragmatic fatigue.

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Use of Continuous Blood Volume Monitoring to Detect Inadequately High Dry Weight

The International Journal of Artificial Organs ◽

10.1177/039139889601900706 ◽

1996 ◽

Vol 19 (7) ◽

pp. 411-414 ◽

Cited By ~ 48

Author(s):

F. Lopot ◽

P. Kotyk ◽

J. Bláha ◽

J. Forejt

Keyword(s):

Blood Volume ◽

Vena Cava ◽

Extracellular Fluid ◽

Dry Weight ◽

Whole Body ◽

The Status ◽

Varying Length ◽

Group 3 ◽

Group 2 ◽

Total Body

A continuous blood volume monitoring (CBVM) device (Inline Diagnostics, Riverdale, USA) was used to study response to prescribed ultrafiltration during haemodialysis (HD) in 66 stabilised HD patients. Fifty percent of patients showed the expected linear decrease in BV right from the beginning of HD (group 1), 32% exhibited no decrease at all (group 2), while eighteen percent formed the transient group 3 which showed a plateau of varying length after which a decrease occurred. The correct setting of dry weight was verified through evaluation of the ratio of extracellular fluid volume to total body water (VEC/TBW) in 26 patients by means of whole body multifrequency impedometry MFI (Xitron Tech., San Diego, USA) and through measurement of the Vena Cava Inferior diameter (VCID) pre and post HD (in 6 and 5 patients from groups 1 and 3 and from group 2, respectively). The mean VEC/TBW in groups 1 and 3 was 0.56 pre and 0.51 post HD as compared to 0.583 and 0.551 in group 2. VCID decreased on average by 14.1% in groups 1 and 3 but remained stable in group 2. Both findings thus confirmed inadequately high estimation of dry weight. Since CBVM is extremely easy to perform it can be used as a method of choice in detecting inadequately high prescribed dry weight. The status of the cardiovascular system must always be considered before final judgement is made.

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Exercise and MEF2–HDAC interactions

Applied Physiology Nutrition and Metabolism ◽

10.1139/h07-082 ◽

2007 ◽

Vol 32 (5) ◽

pp. 852-856 ◽

Cited By ~ 21

Author(s):

Sean L. McGee

Keyword(s):

Skeletal Muscle ◽

Protein Kinase ◽

Nuclear Export ◽

Energy Homeostasis ◽

Whole Body ◽

Positive Health ◽

Exercise Induced ◽

Amp Activated Protein Kinase ◽

Body Energy ◽

Skeletal Muscle Adaptations

Exercise increases the metabolic capacity of skeletal muscle, which improves whole-body energy homeostasis and contributes to the positive health benefits of exercise. This is, in part, mediated by increases in the expression of a number of metabolic enzymes, regulated largely at the level of transcription. At a molecular level, many of these genes are regulated by the class II histone deacetylase (HDAC) family of transcriptional repressors, in particular HDAC5, through their interaction with myocyte enhancer factor 2 transcription factors. HDAC5 kinases, including 5′-AMP-activated protein kinase and protein kinase D, appear to regulate skeletal muscle metabolic gene transcription by inactivating HDAC5 and inducing HDAC5 nuclear export. These mechanisms appear to participate in exercise-induced gene expression and could be important for skeletal muscle adaptations to exercise.

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