Ventilatory muscles during exercise in air and oxygen in normal men

Bye, Peter T. P.; Esau, Sharon A.; Walley, Keith R.; Macklem, Peter T.; Pardy, Richard L.

doi:10.1152/jappl.1984.56.2.464

Cited by 91 publications

(58 citation statements)

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“…Firstly, the contribution of hypoxaemia to the exercise limitation is still uncertain, and the mechanisms by which oxygen affects exercise performance are complex [6][7][8][9][10][11]. The present study confirmed previous reports showing that the acute effects of oxygen, as well as the effects of training, correlated poorly with lung function parameters or blood gas values at rest or during exercise [5,6,17].…”

Section: Effects Of Oxygen-supplemented Exercise Trainingsupporting

confidence: 87%

“…These acute effects of oxygen have been observed both in normoxic patients and in patients who are hypoxaemic at rest or during exercise. Several mechanisms may be involved, including reduction in ventilatory response to exercise (reduced ventilatory equivalent for carbon dioxide (V'E/V'CO 2 )) [6], ventilatory muscle recruitment [7] and delayed ventilatory muscle fatigue [8,9], improved aerobic capacity of the working muscles [10] and a reduction in breathlessness [11].…”

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confidence: 99%

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Training with supplemental oxygen in patients with COPD and hypoxaemia at peak exercise

Rooyackers

Dekhuijzen²,

Herwaarden³

et al. 1997

Eur Respir J

148

121

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Supplemental oxygen has acute beneficial effects on exercise performance in patients with chronic obstructive pulmonary disease (COPD). The purpose of this study was to investigate whether oxygen-supplemented training enhances the effects of training while breathing room air in patients with severe COPD.A randomized controlled trial was performed in 24 patients with severe COPD who developed hypoxaemia during incremental cycle exercise (arterial oxygen saturation (Sa,O 2 ) <90% at peak exercise). All patients participated in an in-patient pulmonary rehabilitation programme of 10 weeks duration. They were assigned either to general exercise training while breathing room air (GET/RA group: forced expiratory volume in one second (FEV1) 38% of predicted; arterial oxygen tension (Pa,O 2 ) 10.5 kPa at rest; Pa,O 2 7.3 kPa at peak exercise), or to GET while breathing supplemental oxygen (GET/O 2 group: FEV1 29% pred; Pa,O 2 10.2 kPa at rest; Pa,O 2 7.2 kPa at peak exercise). Sa,O 2 was not allowed to fall below 90% during the training. The effects on exercise performance while breathing air and oxygen, and on quality of life were compared.Maximum workload (Wmax) significantly increased in the GET/RA group (mean (SD) 17 (15) W, p<0.01), but not in the GET/O 2 group (7 (25) W). Six minute walking distance (6MWD), stair-climbing, weight-lifting exercise (all while breathing room air) and quality of life significantly increased in both groups. Acute administration of oxygen improved exercise performance before and after training. Training significantly increased Wmax, peak carbon dioxide production (V'CO 2 ) and 6MWD while breathing oxygen in both groups. Differences between groups were not significant.Pulmonary rehabilitation improved exercise performance and quality of life in both groups. Supplementation of oxygen during the training did not add to the effects of training on room air.

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Section: Effects Of Oxygen-supplemented Exercise Trainingsupporting

confidence: 87%

mentioning

confidence: 99%

Training with supplemental oxygen in patients with COPD and hypoxaemia at peak exercise

Rooyackers

Dekhuijzen²,

Herwaarden³

et al. 1997

Eur Respir J

148

121

View full text Add to dashboard Cite

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“…2b) as well as absolute values of PTPdi signi®cantly decreased compared to SL, suggesting further recruitment of accessory respiratory muscles to assist impending failure of the diaphragm. These observations are indirectly con®rmed by studies on hyperoxic exercise that showed a decrease of accessory muscle activation compared to normoxic exercise [24].…”

Section: Effects Of High Altitude On Diaphragm Fatiguementioning

confidence: 80%

Diaphragm fatigue during exercise at high altitude: the role of hypoxia and workload

et al. 2001

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The effect of high altitude (HA) on exercise-induced diaphragm fatigue in normal subjects was examined.Eight normal subjects completed an incremental exercise test at sea level (SL) and at 3,325 m. Before (baseline), during, and after exercise (recovery), maximal transdiaphragm pressure (Pdi,sniff), breathing pattern, and diaphragmatic effort (PTPdi) were measured. Arterialized blood lactate was measured at baseline and during recovery.At maximal exercise (WRmax) Pdi,sniff fell to 72% and 61% of baseline at SL and HA respectively, recovering to baseline in 60 min at SL, and >60 min at HA. At the 5th min of recovery, circulating lactate was six-fold and seven-fold baseline at SL and HA, respectively. The time course of circulating lactate recovery was as for Pdi,sniff. To conclude, in normal subjects hypoxia-related effects, and not an increase in diaphragm work, hastens exercise-induced diaphragm fatigue and delays its recovery at high altitude compared to sea level. Eur Respir J 2001; 17: 674±680.

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“…The respiratory muscles are probably weaker and more fatiguable under isocapnic, hypoxic conditions than under hyperoxic, hypercapnic conditions. Even under normoxic conditions, the administration of supplemental 02 during exercise reduces inspiratory muscle fatiguability (Bye, Esau, Walley, Macklem & Pardy, 1984). Hence, one possible explanation for the unique relation of AP1es I to Sa, 2 could be that peak pressure development is limited at a given Sa0°2 in order to avoid uncomfortable sensations associated with the act of breathing and/or to avoid high pressure that might predispose to muscle fatigue (Bellemare & Grassino 1982;Buchler, Magder & Roussos, 1985).…”

Section: Subjectsmentioning

confidence: 99%

Influence of body position on pressure and airflow generation during hypoxia and hypercapnia in man.

Xie¹,

Takasaki²,

Popkin³

et al. 1993

The Journal of Physiology

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SUMMARY1. Inspiratory oesophageal pressure and ventilatory responses to hyperoxic, progressive hypercapnic rebreathing (HCVR) and isocapnic, progressive hypoxic rebreathing (HVR) were studied in five normal males in both supine and upright seated positions.2. No significant differences were found in the ventilatory response to hypercapnia between the supine and upright position. The slopes of the relationship between minute ventilation (VI) and the increase of end tidal Pco2 (APET, C02) were 3-27+0-23 and 2-76 + 024 1 min-mmHg-' supine and upright, respectively. However, the change in oesophageal pressure from the end expiratory level observed during quiet breathing to that at peak inspiration (AP.,es I) in relationship to APETCO2 was greater supine than upright (1-23+0 07 versus 0 79+0411 cmH20 mmHg-', P < 0-01).3. In contrast, during hypoxia-stimulated breathing the slope of the minute ventilation versus oxyhaemoglobin saturation curve (VI-Sa, 2) was flatter supine than upright (1P00+0-03 versus 175+0-05 1 min-(percentage fall in Sa, o2)1 P < 0-0001), but ApoI I in relation to Sa°2 during hypoxic rebreathing was similar supine and upright (0-38 + 0-03 versus 0 40 + 0-04 cmH2O (percentage fall in Sa' 02)' respectively).

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Ventilatory muscles during exercise in air and oxygen in normal men

Cited by 91 publications

References 0 publications

Training with supplemental oxygen in patients with COPD and hypoxaemia at peak exercise

Training with supplemental oxygen in patients with COPD and hypoxaemia at peak exercise

Diaphragm fatigue during exercise at high altitude: the role of hypoxia and workload

Influence of body position on pressure and airflow generation during hypoxia and hypercapnia in man.

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