Training with supplemental oxygen in patients with COPD and hypoxaemia at peak exercise. Effects of oxygen on lower limb blood flow and O2 uptake during exercise in COPD. Benefits of supplemental oxygen in exercise training in nonhypoxemic chronic obstructive pulmonary disease patients. Benefits of oxygen on exercise performance and pulmonary hemodynamics in patients with COPD with mild hypoxemia. [Effect of oxygen (FI02: 0.35) on the aerobic capacity in patients with COPD]. Oxygen supplementation before or after submaximal exercise in patients with chronic obstructive pulmonary disease. Low intensity peripheral muscle conditioning improves exercise tolerance and breathlessness in COPD. Oxygen supplementation during exercise in cystic fibrosis. Exercise training improves recovery in patients with COPD after an acute exacerbation.
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,O2) <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,O2) 10.5 kPa at rest; Pa,O2 7.3 kPa at peak exercise), or to GET while breathing supplemental oxygen (GET/O2 group: FEV1 29% pred; Pa,O2 10.2 kPa at rest; Pa,O2 7.2 kPa at peak exercise). Sa,O2 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/O2 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'CO2) 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. 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. Supplemental oxygen improves exercise tolerance of normoxemic and hypoxemic chronic obstructive pulmonary disease (COPD) patients. We determined whether nonhypoxemic COPD patients undergoing exercise training while breathing supplemental oxygen achieve higher intensity and therefore improve exercise capacity more than patients breathing air. A double-blinded trial was performed involving 29 nonhypoxemic patients (67 years, exercise SaO2 > 88%) with COPD (FEV1 = 36% predicted). All exercised on cycle ergometers for 45 minutes, 3 times per week for 7 weeks at high-intensity targets. During exercise, they received oxygen (3 L/minute) (n = 14) or compressed air (3 L/minute) (n = 15). Both groups had a higher exercise tolerance after training and when breathing oxygen. However, the oxygen-trained group increased the training work rate more rapidly than the air-trained group. The mean +/- SD work rate during the last week was 62 +/- 19 W (oxygen-trained group) and 52 +/- 22 W (air-trained group) (p < 0.01). After training, endurance in constant work rate tests increased more in the oxygen-trained group (14.5 minutes) than in the air-trained group (10.5 minutes) (p < 0.05). At isotime, the breathing rate decreased four breaths per minute in the oxygen-trained group and one breath per minute in the air-trained group (p = 0.001). We conclude that supplemental oxygen provided during high-intensity training yields higher training intensity and evidence of gains in exercise tolerance in laboratory testing. 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. Disability in patients with chronic obstructive pulmonary disease has led to the development of rehabilitation programs to increase exercise tolerance.
                To determine, if the effect of training can be improved by giving supplemental oxygen during exercise.
                Ten male patients with COPD (mean FEV1 = 43.2 +/- 17.1% pred) underwent a five day per week cycle ergometer training program for four weeks at least 45 minutes per day at a constant workload of 80% of their highest achieved workrate--measured in an incremental exercise test before training. At this workrate all patients performed exercise above their anaerobic threshold. Five patients were breathing 35% oxygen during exercise, five were breathing roomair (randomised, single blind). To evaluate and compare the results of training before and after the program all patients performed an incremental exercise test (continuously increasing workrate) with roomair.
                In the group breathing 35% O2 during training the maximally achieved power in the incremental exercise test after training was 15.9% higher. In the group breathing roomair during training the maximally achieved power after training was 36.3% higher than before (p < 0.05). This group also showed significant reductions in lactate levels (p < 0.05) after training at the maximum workload achieved in the pre-training test.
                Training in the roomair-group resulted in a significant increase in the maximum power and total amount of work. In this group training could induce a physiologic response (increase of aerobic capacity), which was shown by significantly lower lactate levels at a comparable workload. Evidence for improved exercise tolerance or relief of breathlessness by short term use of oxygen before or after exercise in patients with chronic obstructive pulmonary disease (COPD) is scant, and guidelines for this treatment are lacking despite widespread provision in the UK.
                The effect of oxygenation either before or after exercise on perception of breathlessness and walk distance was studied in a group of patients with moderate to severe COPD (mean forced expiratory volume in 1 second (FEV(1)) 34% of predicted, mean 6 minute walk distance on air 283 m), all of whom desaturated by at least 4% on submaximal exercise. Oxygen (28%) or air was delivered double blind and in random order, either for 5 minutes before a standard 6 minute walk test (n=34) or for 5 minutes following the end of the test (n=18). Exercise tolerance was measured as the distance achieved and breathlessness was assessed using visual analogue scales (VAS) which were scored before and after exercise and during recovery.
                No increase in mean walk distance after oxygen (288 v 283 m) and no improvement in mean breathlessness scores (58 v 54 mm) or recovery times occurred with oxygen taken either before (177 v 184 seconds) or after exercise (182 v 151 seconds).
                This group of patients with COPD derived no physiological or symptomatic benefit from oxygen breathed for short periods before or after submaximal exercise. Domiciliary oxygen should only be prescribed for such patients if they have shown objective evidence of benefit on exercise testing. This randomized, controlled study investigated the physiological effects of a specially designed 12 week programme of isolated conditioning of peripheral skeletal muscle groups. The programme required minimal infrastructure in order to allow continued rehabilitation at home after familiarization within hospital. Forty eight patients, aged 40-72 yrs with chronic obstructive pulmonary disease (COPD) (mean (SD) forced expiratory volume in one second (FEV1) 61 (27)% of predicted normal) were randomly allocated into training (n = 32) and control (n = 16) groups. Physiological assessments were performed before and after the 12 week study period, and included peripheral muscle endurance and strength, whole body endurance, maximal exercise capacity (maximum oxygen consumption (V'O2,max)) and lung function. The training group showed significant improvement in a variety of measures of upper and lower peripheral muscle performance, with no additional breathlessness. Whole body endurance measured by free arm treadmill walking increased by 6,372 (3,932-8,812) 3 (p < 0.001). Symptom-limited maximal V'O2 was unchanged. However, the training group showed a reduction in ventilatory equivalents for oxygen and carbon dioxide, both at peak exercise and at equivalent work rate (Wmax). In summary, low intensity isolated peripheral muscle conditioning is well-tolerated, simple and easy to perform at home. The various physiological benefits should enable patients across the range of severity of chronic obstructive pulmonary disease to improve daily functioning. Fourteen female and 22 male patients with cystic fibrosis (CF), 8 to 29 yr of age, performed two progressive exercise tests to exhaustion on a cycle ergometer, breathing normoxic air (21% O2) for one test, and hyperoxic air (30% O2) for the other test. The order of gas administration was randomized. Minute ventilation (VE), oxygen uptake (VO2), end-tidal CO2 tension (PETCO2), work rate, oxyhemoglobin saturation (SAO2), and heart rate (HR) were measured throughout the tests. The SaO2 of 11 patients at peak exercise was 90% or less ("Low Sat" group). The SaO2 of 23 patients remained above 90% throughout the exercise ("High Sat" group). Hyperoxic air minimized desaturation during exercise in the Low Sat group to 2 +/- 2% compared to a decrease of 10 +/- 5% with normoxic air. The decrease in saturation was not significant for the High Sat group (1 +/- 1% for both 21% and 30% O2). Peak work rate and VO2 did not differ significantly between normoxic and hyperoxic conditions. However, VE and HR at peak exercise tended to be lower, and PETCO2 was higher during peak exercise with 30% O2 than 21% O2 for both groups. During submaximal exercise, O2 desaturation was diminished and HR was significantly lower with supplemental O2, specifically in the Low Sat group. VE was significantly lower for both groups during submaximal exercise with hyperoxic air. The results suggest that O2 supplementation minimizes O2 desaturation and enables patients with CF to exercise with reduced ventilatory and cardiovascular work. Clinical experience suggests that exercise is beneficial for recovery after an acute exacerbation in patients with severe chronic obstructive pulmonary disease (COPD). The aim of this study was to quantify the clinical benefit of exercise in these patients. Twenty-nine inpatients were randomly assigned to a training group (n = 15, FEV1 34% pred) or a control group (n = 14, FEV1 38% pred). On ten consecutive days, patients in the training group performed a 6-min treadmill walking test and, in addition, five walking sessions per day at > or = 75% of the respective treadmill walking distance. Patients in the control group performed only treadmill walking tests on days 1, 5, and 10. To directly compare the possible benefit of exercise training all patients had an exercise test on day 11 at the same work load as on day 1. In the training group, 6-min walking distance increased from 237 to 420 m, in the control group from 230 to 255 m over the 10 day period which was significantly different (P < 0.0001). Minute ventilation and oxygen uptake increased significantly (P < 0.05) in the training but not in the control group. When comparing exercise tests on days 1 and 11, minute ventilation, oxygen uptake, PaCO2, lactic acid concentration, and Borg scale were significantly reduced to achieve the same work load (P < 0.01) only in the training group. Intrathoracic gas volume and residual volume decreased, and FEV1 and vital capacity increased in the training (P < 0.05) but not in the control group. Our data demonstrate that exercise training significantly improves the exercise capacity in patients with severe COPD after an acute exacerbation of their disease.
This review provides little support for oxygen supplementation during exercise training for individuals with COPD, but the evidence is very limited. Studies with larger number of participants and strong design are required to permit strong conclusions, especially for functional outcomes such as symptom alleviation, health-related quality of life and ambulation.