Effects of hyperoxia on ventilatory limitation during exercise in advanced chronic obstructive pulmonary disease. Factors contributing to relief of exertional breathlessness during hyperoxia in chronic airflow limitation. Oxygen relieves breathlessness in "pink puffers". Ventilatory muscle function during exercise in air and oxygen in patients with chronic air-flow limitation. Supplemental oxygen and exercise ability in chronic obstructive airways disease. Relationship between ventilation and breathlessness during exercise in chronic obstructive airways disease is not altered by prevention of hypoxaemia. Exercise tolerance breathing a low density gas mixture, 35 per cent oxygen and air in patients with chronic obstructive bronchitis. Response to exercise in patients with chronic airway obstruction. II. Effects of breathing 40 per cent oxygen. Ambulatory oxygen improves quality of life of COPD patients: a randomised controlled study. Physical training with and without oxygen in patients with chronic obstructive pulmonary disease and exercise-induced hypoxaemia. The effects of 30 per cent oxygen on the respiratory response to treadmill exercise in chronic respiratory failure. Oxygen may lower the O2 cost of ventilation in chronic obstructive lung disease. Effects of oxygen on lower limb blood flow and O2 uptake during exercise in COPD. Relationship between improvement in exercise performance with supplemental oxygen and hypoxic ventilatory drive in patients with chronic airflow obstruction. Portable oxygen and exercise tolerance in patients with chronic hypoxic cor pulmonale. Oxygen-assisted exercise in chronic obstructive lung disease. The effect on exercise capacity and arterial blood gas tensions. Benefits of oxygen on exercise performance and pulmonary hemodynamics in patients with COPD with mild hypoxemia. Ventilatory muscle recruitment in exercise with O2 in obstructed patients with mild hypoxemia. Exertional oxygen of limited benefit in patients with chronic obstructive pulmonary disease and mild hypoxemia. Dose-response effect of oxygen on hyperinflation and exercise endurance in nonhypoxaemic COPD patients. Evaluation of pulsed dose oxygen delivery during exercise in patients with severe chronic obstructive pulmonary disease. Oxygen effect on O2 deficit and VO2 kinetics during exercise in obstructive pulmonary disease. Effect of acute hyperoxia during exercise on quadriceps electrical activity in active COPD patients. Supplemental oxygen during pulmonary rehabilitation in patients with COPD with exercise hypoxaemia. Mechanisms of oxygen effects on exercise in patients with chronic obstructive pulmonary disease. Dyspnea management in alpha-1 antitrypsin deficiency: effect of oxygen administration. Oxygen may improve dyspnea and endurance in patients with chronic obstructive pulmonary disease and only mild hypoxemia.
We studied interrelationships between exercise endurance, ventilatory demand, operational lung volumes, and dyspnea during acute hyperoxia in ventilatory-limited patients with advanced chronic obstructive pulmonary disease (COPD). Eleven patients with COPD (FEV(1.0) = 31 +/- 3% predicted, mean +/- SEM) and chronic respiratory failure (Pa(O(2)) 52 +/- 2 mm Hg, Pa(CO(2 ))48 +/- 2 mm Hg) breathed room air (RA) or 60% O(2) during two cycle exercise tests at 50% of their maximal exercise capacity, in randomized order. Endurance time (T(lim)), dyspnea intensity (Borg Scale), ventilation (V E), breathing pattern, dynamic inspiratory capacity (IC(dyn)), and gas exchange were compared. Pa(O(2)) at end-exercise was 46 +/- 3 and 245 +/- 10 mm Hg during RA and O(2), respectively. During O(2), T(lim) increased 4.7 +/- 1.4 min (p < 0.001); slopes of Borg, V E, V CO(2), and lactate over time fell (p < 0.05); slopes of Borg-V E, V E-V CO(2), V E-lactate were unchanged. At a standardized time near end-exercise, O(2) reduced dyspnea 2.0 +/- 0.5 Borg units, V CO(2) 0.06 +/- 0.03 L/min, V E 2.8 +/- 1.0 L/min, and breathing frequency 4.4 +/- 1.1 breaths/min (p < 0.05 each). IC(dyn) and inspiratory reserve volume (IRV) increased throughout exercise with O(2) (p < 0.05). Increased IC(dyn) was explained by the combination of increased resting IRV and decreased exercise breathing frequency (r(2) = 0.83, p < 0.0005). In conclusion, improved exercise endurance during hyperoxia was explained, in part, by a combination of reduced ventilatory demand, improved operational lung volumes, and dyspnea alleviation. The mechanisms of exertional dyspnea relief in response to supplemental oxygen (O2) in chronic airflow limitation (CAL) are not precisely known and are likely multifactorial. To explore factors contributing to the relief of dyspnea after oxygen administration, 11 patients with severe CAL (FEV1.0 = 39 +/- 3% predicted, mean +/- SEM) and mild hypoxemia (resting PaO2 = 74 +/- 2 mm Hg) breathed room air (RA) and 60% O2 during exercise at approximately 50% of their maximal incremental exercise capacity. Breathlessness ratings (Borg scale), endurance time, respiratory drive (change in mouth occlusion pressure over the first 0.1 s of inspiration, P0.1), ventilation (VE), breathing pattern, operational lung volumes, gas exchange, and metabolic parameters were compared during RA and 60% O2. PaO2 at exercise cessation during RA and 60% O2 was 65 +/- 3 mm Hg and 226 +/- 12 mm Hg, respectively (p < 0.001). With 60% O2, the mean of individual Borg/time slopes fell significantly (p < 0.05) by 23 +/- 12% and was associated with a 35 +/- 11% increase (p < 0.01) in endurance time (r = -0.64, p < 0.05). During 60% O2, slopes of P0.1 and lactate over time also fell significantly (p < 0.05), whereas delta PaCO2/time did not change significantly. At a standardized time near end-exercise, Borg, VE, and P0.1 changed during 60% O2 by -0.8 +/- 0.3 (p < 0.05), -4.1 +/- 2.0 L/min (p = 0.07), and -1.3 +/- 0.5 cm H2O/s (p < 0.05), respectively. Slopes of Borg/VE, Borg/lactate, and VE/lactate were essentially superimposable during tests on RA and O2: Borg, lactate, and VE all fell proportionally during hyperoxia. In patients with CAL and mild exercise hypoxemia, relief of exertional breathlessness during hyperoxia is explained by reduced ventilatory demand in association with reduced blood lactate levels. The effect of oxygen on breathlessness and exercise tolerance was examined in "pink and puffing" patients with fixed airways obstruction. When breathing oxygen, patients were less breathless and walked further. This was true whether the cylinder was carried by the patient or by an assistant. It was not possible to identify those patients who would benefit most. The best method of assessing improvement was by comparing breathlessness on a standardised progressive exercise test on a treadmill. Four patients had a greater than 30% reduction in breathlessness on submaximum exercise when breathing oxygen. Breathing oxygen for five or fifteen minutes before exercise but not during exercise (predose) resulted in a similar improvement in exercise tolerance. For short periods of exercise predosing with oxygen provides a convenient alternative to continuous oxygen. For longer periods of exercise the benefits of portable oxygen in selected patients have been previously underestimated. Ventilatory muscle function was examined at rest and during exercise on a cycle ergometer in 8 patients with moderate to severe chronic air-flow limitation (FEV1, 32 +/- 4% predicted) in air and in oxygen. The diaphragmatic electromyogram (EMG) was measured using an esophageal electrode. In addition, measurements of esophageal (Pes), gastric (Pga), and transdiaphragmatic (Pdi) pressures and abdominal wall movements were made. Patients exercised to exhaustion at a constant submaximal workload (80% of maximal power output) inspiring air or 40% O2 in random order on separate days. At end-exercise in air, tidal inspiratory Pes swings were 36 +/- 4% of static maximal inspiratory Pes, and inspiratory Pdi swings were 45 +/- 7% of the static maximal Pdi. Arterial oxygen saturation decreased from 91 +/- 2% at rest to 80 +/- 5% at end-exercise in air. During exercise in air, 5 patients demonstrated a persistent and greater than 20% fall in the ratio of high frequency (150 to 350 Hz) to low frequency (20 to 46 Hz) power (H/L) of the diaphragmatic EMG, indicating impending diaphragmatic fatigue, and 2 patients had paradoxical motion of the abdominal wall. Exercise time at the same constant work load increased from 3.0 +/- 0.6 min in air to 6.4 +/- 1.2 min in O2 (p less than 0.005). At the comparable time during exercise in O2 to end-exercise in air, minute ventilation was less by 13% (p less than 0.005), which was entirely attributable to a lower frequency of breathing. Mean inspiratory and expiratory flows and heart rate were all significantly lower.(ABSTRACT TRUNCATED AT 250 WORDS) The influence of supplemental oxygen on exercise performance was assessed in 17 patients with severe airflow obstruction. Exercise capacity was measured by the six minute walking distance, by an endurance walking test, and by an endurance cycling test and comparison was made with performance when the patient was breathing air. In addition, the relation between the flow rate of supplemental oxygen and cycling endurance time was studied. Portable oxygen (41 min-1) carried by the patient increased the mean endurance walking time by 59% and the six minute walking distance by 17%. The endurance time for cycling at a constant work load was increased by 51% with oxygen at a flow rate of 21 min-1, by 88% at 41 min-1, and by 80% at 61 min-1. Supplemental oxygen prolonged the length of time that the patients were able to walk at a fixed speed. It also increased the mean speed achieved during a six minute walk but this was variable and did not occur in all the subjects. The benefit from supplemental oxygen was not cancelled by the effort of carrying the portable cylinder. We have examined the hypothesis that hypoxaemia contributes to breathlessness by a mechanism distinct from its action as a ventilatory stimulant. Five patients who developed arterial oxygen desaturation during incremental exercise were studied. Exercise tests were performed on a cycle-ergometer. Breathlessness was measured by using a visual analogue scale technique. All five patients had considerable previous experience of these procedures. Two identical exercise tests were performed by each patient, breathing either room air or 60% oxygen in a blind randomized study. Breathing air, arterial saturation at rest was 93% and fell by 7% during exercise. Breathing 60% oxygen, resting saturation was 98% and there was no fall during exercise. Breathing oxygen, ventilation for a given work load was reduced and exercise duration was increased when compared with air breathing. In each of the five patients the relationship between breathlessness and minute ventilation was the same whether breathing air or 60% oxygen, despite the reduction in ventilation for a given work rate. nan nan It is unknown whether acute response to ambulatory oxygen (O2) predicts longer term improvement in health-related quality of life (HRQL) in chronic obstructive pulmonary disease (COPD) patients. The aims of this study were 1) to assess the short-term clinical impact, as determined by HRQL, of ambulatory O2 in a 12-week, double-blind, randomised crossover study of O2 (versus cylinder compressed air) of dyspnoeic but not chronically hypoxic COPD patients with exertional desaturation < or = 88% (n=41), and 2) to determine whether either baseline characteristics or acute response to O2 predicts short-term (12 weeks) response. Primary outcome measures were Chronic Respiratory Questionnaire (CRQ), Hospital Anxiety and Depression scale and the short form (SF)-36. Improvements were seen in all domains of the CRQ for cylinder O2 compared with cylinder air. Significant improvements were also noted in anxiety and depression and in certain domains of the SF-36. There were 28 (68%) acute responders to cylinder O2 (defined as increase in 6-min walk > or = 54 m or decrease in post-Borg dyspnoea > or = 1) and 23 (56%) short-term responders (defined as clinically significant improvement in CRQ). However, acute and short-term responses were not correlated with no predictors of short-term response identified. At study completion, 14 (41%) of acute or short-term responders did not want to continue therapy, with 11 citing poor acceptability or tolerability. Short-term ambulatory oxygen is associated with significant improvements in health-related quality of life. These benefits cannot be predicted by baseline characteristics or acute response. Despite acute or short-term response, a substantial proportion of patients declined ambulatory oxygen. A randomized, controlled, single-blind study was performed on 20 patients with chronic obstructive pulmonary disease and exercise-induced hypoxaemia. Ten patients each were randomly assigned to one of two groups, one training with air and the other training with oxygen. There were no significant differences between the groups regarding values measured prior to the study. The patients trained 3 times per week for 30 minutes each time for a duration of 8 weeks. The training consisted of interval walking on a treadmill (intensity set according to Borg ratings) with either air or oxygen administered through a nasal cannula at a rate of 5 l/min. Training significantly improved the 6-minute walking distance by 20% and 14% in the air and oxygen group, respectively, when the patients were tested on air. In the same test the air group significantly decreased Borg ratings for perceived exertion. Borg ratings for dyspnoea and perceived exertion significantly decreased in the oxygen group when they were tested on oxygen. It was concluded that oxygen supplementation did not further improve the training effect, compared with training with air, in patients with chronic obstructive pulmonary disease and exercise-induced hypoxaemia. nan It is known that the O2 COV in COLD is high; O2 administration to these patients lowers airway resistance, a major determinant of the COV. Thus, O2 should lower the COV. We measured the COV in ten stable COLD patients and five normal control subjects breathing room air and 30 percent O2. Results indicate that the COV of our patients was elevated above that of control subjects, was related to disease severity, and was decreased with 30 percent O2. The COV of control subjects also was lowered by O2. At rest, O2 lowered VE, VEQ O2 and HR. During submaximal exercise O2 lowered VE, reduced VEQ O2 and extended total exercise time. An inverse correlation was noted between COV and maximal O2 uptake. Thus, in stable COLD, the COV is elevated in proportion to the degree of airway obstruction, inversely related to exercise capacity and lowered by O2 administration. To quantify the effects of acute oxygen supplementation on lower limb blood flow (QLEG), O2 delivery (QO2LEG), and O2 uptake (VO2LEG) during exercise and to determine whether the metabolic capacity of the lower limb is exhausted at peak exercise during room air breathing in patients with COPD.
                Oxygen (FIO2 = 0.75) and air were randomly administered to 14 patients with COPD (FEV1: 35 +/- 2% pred, mean +/- SEM) during two symptom-limited incremental cycle exercise tests. Before exercise, a cannula was installed in a radial artery and a thermodilution catheter inserted in the right femoral vein. At each exercise step, five-breath averages of respiratory rate, tidal volume, and ventilation (VE), dyspnea and leg fatigue scores, arterial and venous blood gases, and QLEG were obtained. From these measurements, VO2LEG was calculated.
                Peak exercise capacity increased from 46 +/- 3 W in room air to 59 +/- 5 W when supplemental oxygen was used (P < 0.001). QLEG, QO2LEG, and VO2LEG were greater at peak exercise with O2 than with air (P < 0.05). During submaximal exercise, dyspnea score and VE were significantly reduced with O2 (P < 0.05), whereas QLEG, VO2LEG, and leg fatigue were similar under both experimental conditions. The improvement in peak exercise work rate correlated with the increase in peak QO2LEG (r = 0.66, P < 0.01), peak VO2LEG (r = 0.53, P < 0.05), and reduction in dyspnea at iso-exercise intensity (r = 0.56, P < 0.05).
                The improvement in peak exercise capacity with oxygen supplementation could be explained by the reduction in dyspnea at submaximal exercise and the increases in QO2LEG and VO2LEG, which enabled the exercising muscles to perform more external work. These data indicate that the metabolic capacity of the lower limb muscles was not exhausted at peak exercise during room air breathing in these patients with COPD. The purpose of this study was to determine if there is a relationship between improvement in exercise capacity with supplemental oxygen and the magnitude of hypoxic ventilatory drive in patients with CAO. We hypothesized that those patients with the highest hypoxic drives would be the most likely to have increased exercise tolerance with supplemental oxygen. Seventeen patients with CAO (mean FEV1 = 0.99 +/- 0.45 L) underwent identical maximal cycle ergometry exercise tests on two occasions 45 minutes apart while breathing either air or 30 percent oxygen in a randomized single-blind fashion. With supplemental oxygen, the ventilation decreased and the PaCO2 increased significantly at rest. The patients had a significantly greater exercise tolerance on supplemental oxygen (76.7 vs 69.1 watts, p less than 0.005) but no increase in the maximal ventilation. When the nine patients who improved were compared to the eight patients who did not improve, the two groups were basically identical. Specifically, there were no significant differences in the mean ventilatory or mouth occlusion responses to hypoxia or in the blood gases. The patients who did improve tended to have a greater reduction in their ventilatory response to exercise while exercising on oxygen as compared to when they were exercising on room air. From this study, it was concluded that measurements of hypoxic ventilatory drive are not helpful in predicting which patients with CAO are likely to have improved exercise capability while breathing supplemental oxygen. Breathing 30% oxygen during exercise alleviated arterial hypoxaemia and reduced minute ventilation in patients with severe chronic bronchitis. A similar level of oxygen (2 or 4 litres of oxygen/minute) from nasal prongs also increased their exercise tolerance, as assessed by the distance that they could walk on the level in 12 minutes. Nevertheless, a single-blind controlled study showed that the effort of carrying their portable supply of liquid oxygen, in the Union Carbide Oxygen Walker, abolished this gain in exercise tolerance. The improvement in walking distance was restored when oxygen on exercise was provided by wheeling the oxygen walker on a light-weight shopping trolley. Twenty-six patients with severe chronic obstructive lung disease exercised on a treadmill while breathing either room air, supplementary compressed air, or O2. Endurance was significantly increased by O2, but there was no improvement in maximal work rate. No relation was found between increased endurance and the degree of hypoxia, hypercarbia, or acidosis during exercise or the changes in these while breathing O2. To clarify the effects of oxygen on exercise performance and pulmonary hemodynamics during exercise in patients with COPD with mild hypoxemia at rest.
                Seventy-five male patients with stable COPD ("pink puffer" type), accompanied by mild hypoxemia (> 60 mm Hg) at rest and with mild (percentage of predicted FEV1 [%FEV1] > 50%, n = 16), moderate (%FEV1 > 35% to < or = 50%, n = 25), and severe (%FEV1 < or =35%, n = 34) airflow obstruction were recruited from an outpatient clinic. A 6-min walking distance (6MD) test was administered to 75 patients, and the pulmonary hemodynamics of 43 subjects were determined during exercise on a supine bicycle ergometer at 25 W and breathing compressed air and oxygen at 2 L/min.
                Supplemental oxygen resulted in a significant increase in 6MD, except for patients with mild airflow obstruction and mild desaturation. This increase in 6MD produced by oxygen was greater as the restriction of the airflow was more severe, and correlated negatively with %FEV1, but not with PaO2 at rest or exercise hypoxemia. Pulmonary artery pressure (Ppa) and pulmonary artery occlusion pressure (Pop) increased with exercise, while the rates of increase in both types of pressure were significantly higher for severe COPD than for mild COPD and moderate COPD. Oxygen inhalation significantly reduced the increases in Ppa and Pop during exercise in patients with moderate-to-severe COPD, and the effect of oxygen on the increase in Pop correlated positively with airtrapping (vital capacity - FVC).
                These findings suggest that supplemental oxygen benefits patients with COPD with moderate-to-severe airflow obstruction and mild hypoxemia at rest, as reflected in improvement in exercise performance and pulmonary hypertension during exercise. Respiratory muscle dysfunction limits exercise endurance in severe chronic airflow obstruction (CAO). To investigate whether inspiring O2 alters ventilatory muscle recruitment and improves exercise endurance, we recorded pleural (Ppl) and gastric (Pga) pressures while breathing air or 30% O2 during leg cycling in six patients with severe CAO, mild hypoxemia, and minimal arterial O2 desaturation with exercise. At rest, mean (+/- SD) transdiaphragmatic pressure (Pdi) was lower inspiring 30% O2 compared with air (23 +/- 4 vs. 26 +/- 7 cmH2O, P less than 0.05), but the pattern of Ppl and Pga contraction was identical while breathing either gas mixture. Maximal transdiaphragmatic pressure was similar breathing air or 30% O2 (84 +/- 30 vs. 77 +/- 30 cmH2O). During exercise, Pdi increased similarly while breathing air or 30% O2, but the latter was associated with a significant increase in peak inspiratory Pga and decreases in peak inspiratory Ppl and expiratory Pga. In five out of six patients, exercise endurance increased with O2 (671 +/- 365 vs. 362 +/- 227 s, P less than 0.05). We conclude that exercise with O2 alters ventilatory muscle recruitment and increases exercise endurance. During exercise inspiring O2, the diaphragm performs more ventilatory work which may prevent overloading the accessory muscles of respiration. It is unclear whether short-term benefits from supplemental oxygen translate into improved quality of life in patients with severe COPD. In a 12 wk double-blind randomized crossover study, we assessed the effects of supplemental air and oxygen on exercise performance (step tests and 6 min walking distance [6MWD]) initially and after two 6 wk periods at home using exertional cylinder air or oxygen. We measured quality of life at baseline and after the two 6 wk domiciliary periods. The 26 patients (24 males) had a mean age of 73 +/- 6 yr; mean FEV1, 0.9 +/- 0.4 L; mean DLCO, 10.6 +/- 2.4 ml/min/mm Hg; mean resting PO2, 69 +/- 8.5 (range 58 to 82) mm Hg; mean PCO2, 41 +/- 3.3 mm Hg; and mean resting SaO2, 94 +/- 2.1 (mean +/- SD). Laboratory tests were performed breathing intranasal air or oxygen at 4 L/min, and measurements were made of SaO2 and Borg dysnea scores. Supplemental oxygen increased 6MWD and steps by small, statistically significant increments acutely at baseline and after 6 and 12 wk, without corresponding falls in Borg score. Degree of desaturation at baseline did not correlate with increase in 6MWD or steps achieved at baseline or at 6 or 12 wk, nor with the domiciliary gas used. There was no difference in 6MWD or steps achieved while breathing supplemental oxygen after 6 wk of domiciliary oxygen compared with domiciliary air. Small improvements in quality of life indices were found after domiciliary oxygen, and mastery also improved after domiciliary air. There were no differences in quality of life, however, when domiciliary oxygen was compared with domiciliary air. Although oxygen supplementation induced small acute increments in laboratory exercise performance, such improvements had little impact on the patients' daily lives. Dynamic hyperinflation contributes to exertional breathlessness and reduced exercise tolerance in chronic obstructive pulmonary disease (COPD) patients. This study examined whether oxygen supplementation results in a dose-dependent decrease in hyperinflation associated with functional and symptomatic improvement. Ten severe COPD patients without clinically significant oxygen (O2) desaturation during exercise, and seven healthy subjects, performed five exercise tests at 75% of maximally tolerated work rate. Inspired oxygen fraction (FI,O2) was varied (0.21, 0.3, 0.5, 0.75 and 1.0) among tests in a randomized order. Ventilation (V'E) was measured, and end-inspiratory (EILV) and end-expiratory (EELV) lung volume changes were assessed from inspiratory capacity manoeuvres. In the patients, compared to room air, endurance time increased with FI,O2=0.3 (mean+/-SEM 92+/-20%) and increased further with FI,O2=0.5 (157+/-30%). At isotime, compared to room air, there were significant reductions in dyspnoea score, EELV, EILV, V'E and respiratory frequency (fR) with FI,O2=0.3. Improved endurance time negatively correlated with change in EELV (r=0.48, p=0.002) and EILV (r=0.43, p=0.005). The dyspnoea rating decrease correlated with fR decrease. In healthy subjects, smaller V'E and fR decreases were observed at FI,O2=0.5, accompanied by more modestly increased endurance. Oxygen supplementation during exercise induced dose-dependent improvement in endurance and symptom perception in nonhypoxaemic chronic obstructive pulmonary disease patients, which may be partly related to decreased hyperinflation and slower breathing pattern. This effect is maximized at an inspired oxygen fraction of 0.5. Oxygen conserving devices may lead to substantial increases in the duration of oxygen provided. A study was undertaken to compare the performance of a pulsed dose oxygen delivery (PDOD) system with continuous flow oxygen or air during a maximal walking test.
                Fourteen patients with chronic obstructive pulmonary disease (COPD) and arterial oxygen desaturation on exercise (mean (SD) forced expiratory volume in one second (FEV1) 0.83 (0.28) 1, arterial oxygen pressure (PaO2) 8.38 (1.24) kPa, arterial carbon dioxide pressure (PaCO2) 5.95 (0.86) kPa) were randomised to perform a walking test using air administered via a cylinder or continuous flow oxygen at 2 l/min or by a PDOD system.
                There was no significant difference in the mean arterial oxygen saturation (SaO2) using the PDOD system or with continuous flow oxygen (p = 0.33). Patients showed greatest desaturation whilst walking with the air cylinder (SaO2 79.2 (8.59)%) which was significantly different from the desaturation with both continuous flow oxygen (87.6 (5.85)%, p = 0.001) and PDOD (85.6 (7.36)%, p = 0.004). There was no significant difference between the distance walked using oxygen delivered at 2 l/min by continuous flow or via the PDOD (p = 0.72; CI 0.34 to 1.08). The mean (SD) distance walked on continuous flow oxygen (203.6 (106.1) m) and PDOD (207.9 (109.8) m) was significantly greater than the distance walked with the air cylinder (188.6 (110.02) m); (1.12 fold increase in distance, CI 1.01 to 1.23, p = 0.02, and 1.14 fold increase in distance, CI 1.01 to 1.28, p = 0.03, respectively).
                These findings suggest that the pulsed dose oxygen conserving device was as effective as continuous flow oxygen in maintaining arterial oxygen saturation and that the use of this device was associated with similar improvements in exercise tolerance to patients taking continuous flow oxygen therapy. We evaluated the effect of supplemental O2 on energy metabolism of hypoxemic humans by measuring O2 uptake (VO2) kinetics and other cardiorespiratory parameters in nine male chronic obstructive pulmonary disease (COPD) patients and seven age-matched control subjects (on air and on 30% O2) at rest and during moderate cycle ergometer exercise. Heart rate, ventilation, VO2, CO2 output, respiratory exchange ratio, O2 cost of work, and work efficiency were measured with a computerized metabolic cart; O2 deficit and VO2 time courses were calculated. In COPD patients, 30% O2 breathing resulted in 1) reduction of O2 deficit (from 488 +/- 34 ml in air to 398 +/- 27 ml in O2; P < 0.05) and phase 2 VO2 time constant (from 116 +/- 13 s in air to 74 +/- 12 s in O2; P < 0.05); 2) a smaller steady-state increment in CO2 output than in room air (315 +/- 17 ml/min in O2 vs. 358 +/- 27 ml/min in air; P < 0.02), which resulted in a lower exercise respiratory exchange ratio (0.75 +/- 0.02 in O2 vs. 0.80 +/- 0.02 in air; P < 0.02); and 3) reduced steady-state ventilation (22.6 +/- 1.0 l/min in O2 vs. 25.4 +/- 1.1 l/min in air; P < 0.05). In conclusion, 30% O2 breathing accelerated exercise VO2 kinetics in mildly hypoxemic COPD patients. The observed VO2 kinetics improvement with O2 supplementation is consistent with an enhancement of aerobic metabolism in skeletal muscles during moderate exercise. This study investigated whether acute hyperoxia improves electrical muscle activity in active chronic obstructive pulmonary disease (COPD) patients with mild hypoxemia (rest PaO(2) = 9.1 +/- 0.4 kPa).
                Two identical incremental exercise tests were performed by nine patients while breathing either air or 30% oxygen. Pulmonary gas exchanges, venous concentrations of lactate and pyruvate, and the electromyographic signal of the quadriceps muscle (vastus lateralis and vastus medialis) were sampled each minute.
                Peak working capacity increased significantly in hyperoxia (94.4 +/- 5.2W) compared with normoxia (85.4 +/- 5.8W, P < 0.01). During hyperoxic exercise and for a given work load, oxygen uptake was increased (P < 0.001) and ventilation decreased (P < 0.05). Lactate concentration was significantly decreased (P < 0.01) at isowork level and during recovery (respectively - 26% and at least - 15%). In the quadriceps muscle, M-wave amplitude (P < 0.05), root mean square (P < 0.01) and root mean square/oxygen uptake ratio (P < 0.001) were significantly increased during hyperoxic exercise compared with room air. Although median frequency values did not differ between conditions, the median frequency was significantly decreased for higher exercise intensity in hyperoxic condition. These modifications reflected better aerobic metabolism, later emergence of muscle fatigue, and greater muscle excitability and activation for the same level of exercise under hyperoxic condition.
                These data suggest that the acute addition of oxygen in active COPD patients improves their muscle electrical activity during dynamic exercise. Hypoxemia-induced skeletal muscle dysfunction most probably acts through mechanisms based on oxygen availability. Supplemental oxygen in patients with chronic obstructive pulmonary disease (COPD) and exercise hypoxaemia improves exercise capacity and dyspnoea. However, the benefit of oxygen during pulmonary rehabilitation in these patients is still unknown.
                Twenty five patients with stable COPD (mean (SD) forced expiratory volume in one second (FEV(1)) 0.76 (0.29) l and 30.0 (9.89)% predicted, arterial oxygen tension (PaO(2)) 8.46 (1.22) kPa, arterial carbon dioxide tension (PaCO(2)) 6.32 (1.01) kPa) and significant arterial desaturation on exercise (82.0 (10.4)%) were entered onto a pulmonary rehabilitation programme. Patients were randomised to train whilst breathing oxygen (OT) (n = 13) or air (AT) (n = 12), both at 4 l/min. Assessments included exercise tolerance and associated dyspnoea using the shuttle walk test (SWT) and Borg dyspnoea score, health status, mood state, and performance during daily activities.
                The OT group showed a significant reduction in dyspnoea after rehabilitation compared with the AT group (Borg mean difference -1.46 (95% CI -2.72 to -0.19)) but there were no differences in other outcome measures: SWT difference -23.6 m (95% CI -70.7 to 23.5), Chronic Respiratory Disease Questionnaire 3.67 (95% CI -7.70 to 15.1), Hospital Anxiety and Depression Scale 1. 73 (95% CI -2.32 to 5.78), and London Chest Activity of Daily Living Scale -2.18 (95% CI -7.15 to 2.79). At baseline oxygen significantly improved SWT (mean difference 27.3 m (95% CI 14.7 to 39.8) and dyspnoea (-0.68 (95% CI -1.05 to -0.31)) compared with placebo air.
                This study suggests that supplemental oxygen during training does little to enhance exercise tolerance although there is a small benefit in terms of dyspnoea. Patients with severe disabling dyspnoea may find symptomatic relief with supplemental oxygen. nan A deficiency of alpha-1 antitrypsin (AAT) can lead to pulmonary disease in middle-aged adults in whom dyspnea management can be a significant issue.
                The research addressed whether short-term oxygen (O2) administration during activities might decrease dyspnea and improve exercise performance in nonhypoxemic patients with emphysema caused by a deficiency of alpha-1 antitrypsin.
                This was a double-blind, randomized crossover study of 31 subjects with a deficiency of AAT (mean + SD, age = 47 +/- 7), moderate emphysema and a resting PaO2 > 70 mm Hg. Oxygen saturation (SpO2), 6-minute walk distance, and end of walk dyspnea were measured during three practice walks and during walks with nasal cannula administration of O2 (intervention) and compressed air (control).
                Repeated measures analysis of variance (ANOVA) showed significant differences across the walks for SpO (F= 18.9, p = 0.0001), 6-minute walk distance (F= 6.07, p = 0.004), and dyspnea (F= 4.44, p = 0.016). Using post hoc contrasts, SpO2 was the only variable that differed between 20, and compressed air (p < 0.0001). There was, however, an interaction effect of gender with O2 for dyspnea (F= 9.85, p = 0.004). Mean values showed that men did not benefit from O2 (p = 0.87). However, women experienced less dyspnea when receiving O2 as compared with compressed air (p = 0.0025), and although not statistically significant, the lower dyspnea with O2 corresponded with an increased walk distance of 79 feet.
                O2 administration may be useful for reducing dyspnea during exercise in selected populations. Oxygen (O2) has been reported to improve exercise tolerance in some patients with chronic obstructive pulmonary disease (COPD) despite only mild resting hypoxemia (PaO2 greater than 60 mm Hg). To confirm these prior studies and evaluate potential mechanisms of benefit, we measured dyspnea scores by numeric rating scale during cycle ergometry endurance testing and correlated the severity of dyspnea with right ventricular systolic pressure (RVSP) measured by Doppler echocardiography during a separate supine incremental exercise test. Both sets of exercise were performed according to a randomized double-blind crossover protocol in which patients breathed compressed air or 40% O2. We studied 12 patients with severe COPD (FEV1 0.89 +/- 0.09 L [mean +/- SEM], FEV1/FVC 37 +/- 2%, DLCO 9.8 +/- 1.5 ml/min/mm Hg[47% of predicted], PaO2 71 +/- 2.6 mm Hg). With endurance testing on compressed air, PaO2 did not change significantly in the group as whole (postexercise PaO2 63 +/- 5.1 mm Hg, p = NS), but did fall to less than 55 mm Hg in four patients from this group. Duration of exercise increased on 40% O2 from 10.3 +/- 1.6 to 14.2 +/- 1.5 min (p = 0.005), and the rise in dyspnea scores was delayed. Oxygen delayed the rise in RVSP with incremental exercise in all patients and lowered the mean RVSP at maximum exercise from 71 +/- 8 to 64 +/- 7 mm Hg (p less than 0.03). Improvement in duration of exercise correlated with decrease in dyspnea (r2 = 0.66, p = 0.001) but not with decreases in heart rate, minute ventilation, or RVSP.(ABSTRACT TRUNCATED AT 250 WORDS)
This review provides some evidence from small, single assessment studies that ambulatory oxygen improves exercise performance in people with moderate to severe COPD. The results of the review may be affected by publication bias, and the small sample sizes in the studies. Although positive, the findings of the review require replication in larger trials with more distinct subgroups of participants. Maximal or endurance tests can be used in ambulatory oxygen assessment. Consideration should be given to the measurement of SaO2 and breathlessness at isotime as these provide important additional information. We recommend that these outcomes are included in the assessment for ambulatory oxygen. Future research needs to establish the level of benefit of ambulatory oxygen in specific subgroups of people with COPD.