Effects of sodium bicarbonate administration on the exercise tolerance of normal subjects breathing through dead space.

STUDY OBJECTIVE: The purpose of this study was to determine whether the administration of sodium bicarbonate to normal individuals would increase their PaCO2 and thereby decrease the ventilatory requirements at a given workload. DESIGN: In this double-blind crossover study, six normal men ingested either 3 mEq/kg NaHCO3 or 1 mEq/kg NaCl once a day for 5 days, in addition to 40 mg of furosemide and 40 mEq KCl. After each 5-day treatment, the subjects underwent a symptom-limited maximal bicycle ergometer exercise test while breathing through external dead space (with a volume of approximately 50% of their FEV1), a second exercise test without any external dead space, and an assessment of their respiratory response to hypercapnia. RESULTS: The administration of the NaHCO3 resulted in a significant increase in the arterial HCO3- from 20.8 to 24.0 mEq/L and a significant increase in the PaCO2 from 31.7 to 36.9 mm Hg at rest that persisted during exercise. During exercise periods with the added dead space, the Borg scores were significantly lower at each workload after the subjects received bicarbonate, but the maximal exercise level did not increase. The mean (+/-SD) slope of the mouth occlusion pressure response to hypercapnia was significantly lower after the administration of NaHCO3 than after NaCl, respectively: 0.73+/-0.41 vs 1.27+/-0.97 cm H2O/mm Hg. CONCLUSION: From this study we conclude that the administration of NaHCO3 results in a significant increase in the PaCO2, decreases the ventilation and the Borg score at equivalent workloads, and decreases the hypercapnic response in normal individuals.

Comparison of oxygen saturation by pulse oximetry and co-oximetry during exercise testing in patients with COPD.

INTRODUCTION: Measurement of oxygen saturation by pulse oximetry (SpO2) is frequently performed during exercise testing of patients with COPD to monitor for hypoxemia. The purpose of this study was to assess the accuracy and precision of pulse oximetry during exercise. We hypothesized that the SpO2 would more closely reflect oxygen saturation as measured by co-oximetry (SaO2) when it was corrected for carboxyhemoglobin (COHb). We also hypothesized that SpO2 would more closely reflect SaO2 when the pulse rate by oximeter was equivalent to the heart rate by ECG. Finally, we hypothesized that SpO2 would be a better measure of SaO2 at maximal workloads than at rest or submaximal workloads. METHODS: Eight white men with severe COPD (mean +/- SD FEV1, 0.91 +/- 0.37) underwent progressive, symptom-limited exercise testing by cycle ergometry. SaO2 was measured from arterial blood at each workload using a co-oximeter. SpO2 and pulse rate were obtained by a pulse oximeter (Ohmeda 3700). Heart rate was continuously monitored by ECG. RESULTS: Reliable oximetric values as determined by a dicrotic notch in each waveform and adequate signal intensity were obtained in all eight patients. SpO2 was a moderately accurate measure of SaO2 (bias, 1.7%; precision, 2.9). The bias actually increased (4.1%) when SpO2 was corrected for COHb. Accuracy of SpO2 was not improved when pulse rate by oximetry and heart rate by ECG were equivalent, nor was the accuracy improved at maximal workloads relative to submaximal workloads during the exercise test. CONCLUSION: Oxygen saturation as measured by pulse oximetry (SpO2) in patients with COPD undergoing exercise testing is not sufficiently accurate to replace SaO2 as the gold standard for oxygen saturation.

Effect of 30 mg of morphine alone or with promethazine or prochlorperazine on the exercise capacity of patients with COPD.

OBJECTIVE: We have shown that the administration of 0.8 mg/kg of morphine (M) to patients with COPD resulted in a 20% increase in the maximum oxygen consumption (Vo2max), but was associated with significant drowsiness and euphoria. The objective of the present study was to ascertain whether lower doses of M alone or in combination with prochlorperazine (PC) or promethazine (P) could elicit significant increases in exercise tolerance. DESIGN: The exercise capacity, psychological status, and reaction times were assessed before and 60 min after the patients received placebo (PLAC), 30 mg M orally, 30 mg M plus 10 mg PC (M-PC), or 30 mg M plus 25 mg P (M-P) in a randomized double-blind crossover study. In a secondary study, nine patients were tested on three separate days before and after receiving PLAC, 25 mg P, or 30 mg M plus 25 mg P. PATIENTS: Seven COPD patients (FEV1=0.99 +/- 0.30 L, Vo2max=990 +/- 315 mL/min) who were ventilatory-limited. SETTING: Veterans Affairs medical center. RESULTS: After the patients ingested M-P, the increase in the Vo2max (129.0 +/- 104 mL/min), the workload (10.0 +/- 6.5 W) and the maximum minute ventilation (4.0 +/- 3.9 L/min) were significantly greater (p<0.05) than after PLAC ingestion (-4.8 +/- 79 mL/min, 1.4 +/- 6.9 W, and -1.6 +/- 2.4 L/min, respectively). Changes after the ingestion of M, P, o r M-PC were intermediate. The M-PC combination adversely affected the patient's reported mental status (Bond visual analog scale) more than the M-P or M regimens. No regimen significantly affected the reaction time. CONCLUSIONS: We conclude that the administration of 30 mg of M plus 25 mg of P significantly improves the exercise tolerance of patients with COPD, without significantly impairing the mental capabilities of the subjects. The utility of this regimen over longer time periods needs to be evaluated.

The effects of pentoxifylline on oxygenation, diffusion of carbon monoxide, and exercise tolerance in patients with COPD.

Pentoxifylline has been reported previously in an unblinded study to improve oxygen saturation, treadmill walk time, and resting diffusion of carbon monoxide (Dco) in patients with COPD. We recruited 12 patients with moderate to severe COPD whose exercise capacity was limited by ventilation or who developed hypoxemia with exercise. Patients were randomized to receive pentoxifylline or placebo, each for a 12-week period in a prospective, double-blind, crossover design study, to assess the effects of pentoxifylline on oxygenation, resting Dco, and exercise tolerance using arterial blood gas analysis. Eleven patients with a mean FEV1 of 0.94 L and a mean Dco of 9.85 mL/min/mm Hg completed the study. One patient withdrew from the study after developing pneumonia. There were no significant differences in resting oxygenation, resting Dco, or spirometry after 12 weeks of pentoxifylline relative to placebo. The 12-min walk test and dyspnea index for activities of daily living were also not significantly different while taking pentoxifylline. Finally, at maximal exercise, there were no differences in workload attained, exercise duration, oxygen consumption, carbon dioxide production, minute ventilation, oxygen saturation, PO2, alveolar-arterial oxygen pressure difference, or Borg score while taking pentoxifylline relative to placebo. We conclude that pentoxifylline does not improve oxygenation, resting Dco, exercise tolerance, or dyspnea in patients with moderate to severe COPD.

Reanalysis of the 12-minute walk in patients with chronic obstructive pulmonary disease.

The purpose of this study was to determine the correlation between different intervals in the 12-min walk test, to determine which of the intervals best correlated with maximal oxygen intake (VO2max) and maximal CO2 expelled (VCO2max) and to determine the degree of correlation between changes in the VO2max and changes in the walk test and spirometry. Nine elderly (age, 67 +/- 4 years) patients with moderate COPD (FEV1, 1.32 +/- 0.28 L) who were ventilatory limited were seen 6 times over a 14-week period. At each visit they performed spirometry, a 12-min walk, and a symptom-limited maximal exercise test. During the 12-min walk the distances traversed in each 2-min interval were recorded. A Borg score was obtained at the end of each 2 min. The distances that the patients walked in each 2-min interval were very similar, but the mean Borg score became higher the longer the patient walked. The Borg score after 2 min was 1.64 +/- 1.15, while the Borg score after 12 min was 5.70 +/- 3.59. The correlation coefficients between the distance walked at various intervals and the oxygen consumption (VO2)/kg (approximately 0.65) and the VCO2/kg (approximately 0.52) were very similar. However, changes in the VO2/kg were more closely correlated with changes in the 12-min walk (r = 0.72), than with changes in the 6-min walk (r = 0.64), the 4-min walk (r = 0.59), or the 2-min walk (r = 0.53). This latter observation suggests that the 12-min walk may be preferable to tests in which the patient walks 4 or 6 min for documenting changes in the exercise capabilities.

Effects of nebulized morphine sulfate on the exercise tolerance of the ventilatory limited COPD patient.

We have shown previously that the administration of morphine (0.8 mg/kg) to patients with COPD increases the VO2max by 19.3 percent. A recent study demonstrated that the administration of low-dose nebulized morphine (approximately 2 mg) increased the endurance time of patients with severe lung disease by 1 min (35 percent) with few systemic side effects. This double-blind crossover study evaluated the effects of various doses of nebulized morphine (0, 1, 4, and 10 mg) on the exercise tolerance and the psychologic status of COPD patients. In the present study, eight COPD patients (FEV1 = 0.90 +/- 0.26 L, workload max = 76 +/- 29 W, VO2max = 950 +/- 264 ml, VEmax = 34 +/- 7 L), who were ventilatory limited were tested on four separate days. On each testing day, the patients underwent incremental exercise testing and psychologic testing before and 45 min after receiving the nebulized solution. The mean changes (+/- SD) in the exercise test results after each of the four different regimens were as follows: [table: see text] Although there tended to be larger increases in the workload, VO2max, and VEmax after the largest dose of morphine, none of the changes was statistically significant. Likewise, there were no significant differences in spirometry, resting metabolic measurements, or psychologic test scores after the four different regimens. We conclude that aerosolized morphine in the doses used in this study has no significant beneficial effect on the exercise tolerance of patients with COPD.

Effects of buspirone on anxiety levels and exercise tolerance in patients with chronic airflow obstruction and mild anxiety.

The objective of this study was to determine if buspirone would alleviate anxiety and improve exercise tolerance of anxious patients with chronic airflow obstruction (CAO). Eleven male patients with mild to moderate anxiety and CAO completed this study comparing buspirone, 10 to 20 mg given three times a day, with placebo. Patients were evaluated with State Trait Anxiety Inventory, spirometry, 12-min walk, incremental exercise on a cycle ergometer to symptom limitation and measurement of dyspnea with a modified Borg scale at exercise levels and the end of each 2 min on 12-min walk. There were no significant differences in anxiety scores, work load, maximum oxygen consumption per minute, maximum expired volume per minute, PETCO2, PETO2, 12-min walking distance or dyspnea scores after 6 weeks of buspirone or placebo therapy. We conclude that administration of buspirone has no significant effect on anxiety levels, exercise capabilities or PETO2 or PETCO2 in patients with CAO and mild anxiety.

Does the hypoxic ventilatory response predict the oxygen-induced falls in ventilation in COPD?

The purpose of this study was to determine whether supplemental oxygen-induced decreases in ventilation (VE) and mouth occlusion pressure (P0.1) in patients with COPD are related to the ventilatory or P0.1 responses to hypoxia (delta VE/delta SaO2, delta P0.1/delta SaO2). We measured these responses in 14 patients with a (mean +/- SD) FEV1 of 0.95 +/- .41 L. The VE and P0.1 were also measured while the patients sequentially breathed either room air or supplemental oxygen (1-2 L/min) for 10 min in a randomized single blind fashion. The mean (+/- SEM) SaO2 increased from 90.8 +/- 0.99 percent to 95.2 +/- 0.46 percent and the VE decreased during oxygen breathing from 12.3 +/- 0.46 to 11.6 +/- 0.47 L/min (p < 0.03). However, the individual changes in VE were not significantly related to the corresponding changes in SaO2 (CHG SaO2), (delta VE/delta SaO2), or (delta VE/SaO2) (CHG SaO2). Similarly, the P0.1 decreased from 2.50 +/- 0.27 to 2.26 +/- 0.20 cm H2O (p < 0.05), but the individual changes in P0.1 were not significantly related to (CHG SaO2), (delta P0.1/delta SaO2), or (delta PO.1/delta SaO2) (CHG SaO2).

Effects of high- and low-carbohydrate meals on maximum exercise performance in chronic airflow obstruction.

The purpose of this study was to compare the effects of isocaloric liquid meals with high fat (55 percent) and low carbohydrate (28 percent) content (Pulmocare) to meals with low fat (30 percent) and high carbohydrate (53 percent) content (Ensureplus) on exercise performance in subjects with chronic airflow obstruction (CAO). Twelve stable subjects with CAO (FEV1 = 1.30 +/- 0.47 L) underwent incremental symptom-limited exercise tests 90 minutes following the ingestion of 920 calories of EnsurePlus HN (E), 920 calories of Pulmocare (P), or a noncaloric placebo (C). Tests were performed on three days, in a double-blind randomized fashion. Expired gases were collected continuously and analyzed every 30 seconds. The mean maximal work load after E (81 +/- 24 W) was significantly less than that after P (88 +/- 21 W) or C (88 +/- 24 W). The mean ventilation at exhaustion was similar after E (48 +/- 13 L/min), P (51 +/- 11 L/min), and C (49 +/- 10 L/min). In comparison to C, six of the 12 individuals had a decreased work load following E, while only one had a decreased maximal tolerated work load following P. The results of this study suggest that meals with a higher fat and lower carbohydrate content may be less likely to impair work performance of patients with CAO in the absorptive phase than meals with a lower fat and higher carbohydrate content. These findings may have clinical significance to patients with CAO who complain of postprandial exertional dyspnea.

Lack of effect of dextromethorphan on breathlessness and exercise performance in patients with chronic obstructive pulmonary disease (COPD).

We have previously shown that the exercise performance of patients with severe chronic obstructive pulmonary disease (COPD) can be increased with the administration of oral morphine (0.8 mg.kg-1). The purpose of this study was to determine whether the administration of dextromethorphan (DXT), an antitussive structurally similar to codeine, would result in increased exercise performance and decreased dyspnoea in patients with COPD, without the side-effects of opiates. Six eucapnic patients (mean age = 66 +/- 3.8 yrs) with COPD (mean forced expiratory volume in one second (FEV1) = 1.01 +/- 0.07 l) underwent two incremental cycle ergometer tests to exhaustion (Emax) and assessment of their hypercapnic and hypoxic ventilatory responses and mouth occlusion pressure responses following first the oral administration of placebo (P) and then dextromethorphan (60 mg) in a single-blind fashion. There was no statistically significant difference in the maximal exercise performance, perceived dyspnoea (modified Borg scale), breathing pattern or expired gases after the two different treatments. In addition, the ventilatory response to CO2 production during exercise (delta VE/VCO2) and the ventilatory and mouth occlusion pressure responses to hypoxia and hypercapnia did not differ significantly after DXT as compared with after P. Indeed the exercise performance was poorer and the ventilatory responses were brisker after DXT. We conclude from this study that the administration of this opiate analogue does not improve the exercise capacity or decrease the ventilatory response of patients with COPD.

Exercise performance of polycythemic chronic obstructive pulmonary disease patients. Effect of phlebotomies.

The purpose of this study was to determine the effects of phlebotomy on the exercise tolerance and right and left ventricular ejection fraction of polycythemic patients with chronic obstructive pulmonary disease. Ten patients with COPD (mean FEV1 = 1.32 +/- 0.55 L) and polycythemia (mean Hct = 62 +/- 3 percent) were studied before and after their hematocrits had been reduced to approximately 50 percent. Post-phlebotomy the maximal oxygen consumption increased from 1.09 +/- 0.34 L/min to 1.26 +/- 0.43 L/min (p less than 0.05) and the maximum workload increased from 56.5 +/- 32.6 watts to 74.5 +/- 23.4 watts (p less than 0.05). The increase in the exercise tolerance appeared to be primarily due to an increased cardiac output at Emax. There was no relationship between the increases in the upright exercise capacity and changes in the supine ejection fractions of the right or left ventricular either at rest or during exercise.

Effect of naloxone on maximal exercise performance and control of ventilation in COPD.

Elevated endorphin levels in patients with COPD may act to diminish the sensation of dyspnea. Exogenous opioids decrease exertional dyspnea and increase exercise capacity in COPD patients. The purpose of this study was to determine the effects of endogenous opioids on the exercise capacity and control of breathing in patients with COPD. We hypothesized that naloxone, an opioid antagonist, would block the endogenous endorphins and decrease the exercise capacity of our patients. Six patients (mean age, 58.8 +/- 3.2 years) with COPD (mean FEV1, 1.28 +/- 0.46 L) underwent identical incremental cycle ergometer tests to exhaustion (Emax) and assessment of their hypercapnic and hypoxic ventilatory responses and mouth occlusion pressure responses following the IV administration of naloxone (0.4 mg/kg) (N) or placebo (P) in a randomized, double-blind fashion. Perceived dyspnea (modified Borg scale), breathing patterns, and expired gas levels were compared at rest and at maximal workload (WL). There was no significant difference after N compared with after P in the WL or the duration of work. At Emax there were no significant differences after N compared with after P in ventilation, the level of dyspnea, P0.1, VO2, or VCO2. The ventilatory response to CO2 production during exercise (delta VE/delta VCO2) and the ventilatory and mouth occlusion pressure responses to hypoxia and hypercapnia did not differ significantly after N compared with after P. This study does not support the hypothesis that endogenous opioids play a significant role in dampening dyspnea and facilitating exercise in patients with COPD.

Relationship between improvement in exercise performance with supplemental oxygen and hypoxic ventilatory drive in patients with chronic airflow obstruction.

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.

Effects of oral morphine on breathlessness and exercise tolerance in patients with chronic obstructive pulmonary disease.

Previous studies have shown that opiates increase the maximal external work performed at exhaustion in patients with chronic obstructive pulmonary disease (COPD). The mechanism responsible for this improvement in exercise tolerance is unknown. The purpose of this study was to determine the effects of an oral morphine solution (0.8 mg/kg) on the exercise tolerance, perception of dyspnea, and arterial blood gases of patients with COPD. Thirteen eucapnic patients with stable COPD (FEV1 = 0.99 +/- 0.48) underwent duplicate incremental cycle ergometer tests to exhaustion (Emax) after the ingestion of placebo and after the ingestion of morphine. After the ingestion of morphine, the maximal workload increased by 18% (p less than 0.001) and the VO2 increased by 19.3% (p less than 0.001). Ten of the 13 patients had a higher ventilation at Emax after morphine ingestion. Despite the higher ventilation at Emax after morphine, the mean Borg score was not significantly higher. At Emax after morphine ingestion, the PaO2 (65.8 +/- 11.6 mm Hg) was significantly lower and the PaCO2 (43.5 +/- 8.3 mm Hg) was significantly higher than at Emax after placebo (71.9 +/- 15.5 and 38.3 +/- 8.5, respectively). When data at the highest equivalent workload were analyzed, the ventilation and the Borg scores were significantly lower, whereas the VO2 and VCO2 were comparable. From this study, we conclude that the administration of opiates can substantially increase the exercise capacity of patients with COPD. The improved exercise tolerance appears to be related to both a higher PaCO2 resulting in lowered ventilation requirements for a given workload and also to a reduced perception of breathlessness for a given level of ventilation.

Indomethacin and perception of dyspnea in chronic airflow obstruction.

A recent study showed that indomethacin reduces the perception of dyspnea during submaximal exercise in normal subjects (1). The purpose of this study was to determine whether indomethacin alters the perception of dyspnea in patients with chronic airflow obstruction during exercise. In a randomized double-blind crossover fashion, 11 subjects (FEV1 = 0.97 +/- 0.58 L) performed an incremental (15 W/min) cycle ergometer exercise test to exhaustion on 2 study days. Testing was performed 3 to 4 h after placebo or 50 mg of indomethacin. Perception of dyspnea was measured using the modified Borg scale. Minute ventilation, workload, and Borg scale measurements at exhaustion and during moderate exercise were determined. The data demonstrated no statistically significant differences between values obtained for minute ventilation, workload, or Borg scale measurements on placebo and indomethacin study days. Contrary to the previous findings in normal subjects, indomethacin failed to significantly alter perceived dyspnea during exercise in patients with chronic airflow limitation. This suggests that prostanoids do not play a major role in the perception of dyspnea in these patients during exercise.

The relationship between pleural pressures and changes in pulmonary function after therapeutic thoracentesis.

The purpose of this study was to determine whether changes in pulmonary function after therapeutic thoracentesis are related to the pleural pressure or to changes in pleural pressure during thoracentesis. Spirometry was obtained before and 24 h after thoracentesis in 26 patients. Pleural pressures were measured with a U-shaped manometer initially and after each 400-ml aliquot of pleural fluid was removed. Thoracentesis was continued until the patient developed severe symptoms (chest pain or coughing), the pleural pressure dropped below -20 cm H2O, or no more fluid could be obtained. The mean vital capacity improved 410 +/- 390 ml in this group of patients who had 1,740 +/- 900 ml fluid removed. The improvement in the VC most closely correlated with the pleural pressure after 800 ml fluid had been withdrawn (r = 0.57, p less than 0.005). The ratio of the improvement in the VC to the amount of fluid removed most closely correlated with the pressure change after 800 ml fluid had been removed (r = -0.43, p less than 0.05). From this study we conclude that the improvement in the FVC after therapeutic thoracentesis is small relative to the amount of fluid withdrawn. Patients with higher pleural pressures after the removal of 800 ml pleural fluid and patients with smaller decreases in the pleural pressure after removal of 800 ml pleural fluid have greater improvements in their pulmonary functions after thoracentesis.

Cardiopulmonary responses to exercise in chronic airflow obstruction. Effects of inhaled atropine sulfate.

The purpose of this study was to evaluate the effects of inhaled atropine sulfate on the exercise capacity and cardiopulmonary responses to exercise in patients with chronic airflow obstruction (CAO). Eighteen patients underwent duplicate incremental (15 watts/min) maximal cycle ergometer exercise tests 60 minutes after either inhaled atropine (0.075 mg/kg) or placebo, in double blind randomized fashion on consecutive days. Bronchodilator medications were withheld before each study. Spirograms were obtained before and 60 minutes after each aerosol treatment. Atropine increased the FEV1 by 25 percent, from 1.37 +/- 0.49 to 1.71 +/- 0.52 L (p less than 0.001), as compared to placebo. Although the ventilation at exhaustion (VEmax) increased significantly (from 52.3 +/- 11.5 to 55.9 +/- 10.0 L/min, P less than 0.05) after atropine, the increase in the mean maximum work load (95 +/- 28 vs 101 +/- 19 watts) did not achieve significance. The drug resulted in a significant decrease in oxygen consumption at all equivalent workloads greater than "0" watts (unloaded cycling), presumably because the improvement in airway mechanics decreased the oxygen cost of ventilation. Atropine-induced increases in FEV1 did not result in a significant group mean increase in maximum exercise capacity, but the drug did result in a lower oxygen cost of performing work in patients with CAO.

Effects of a large carbohydrate load on walking performance in chronic air-flow obstruction.

The purpose of this study was to determine whether a single large liquid carbohydrate (CHO) load (920 calories) affects walking performance in patients with chronic air-flow obstruction (CAO). Walking performance was measured using the 12-min walking test. Fifteen patients with stable CAO (FEV1, 1.30 +/- 0.41 L; FVC, 3.26 +/- 0.46 L) underwent 12-min walking tests 40 min after ingestion of either CHO or placebo on consecutive days in randomized double-blind fashion. Three practice walks were performed on a preliminary day in order to eliminate learning effects. Resting measurements of ventilation (VE) and carbon dioxide output (VCO2) were obtained prior to each walking test. Carbohydrate significantly increased both VCO2 (from 0.288 +/- 0.060 to 0.372 +/- 0.057 L/min, p less than 0.001) and VE (from 15.2 +/- 3.5 to 18.5 +/- 3.1 L/min, p less than 0.001) at rest. The total 12-minute walking distance decreased from 894 +/- 199 to 847 +/- 191 m following CHO (p less than 0.005). This distance decreased in 14 of the 15 study patients. The decrease in walking distance ranged from 1.5 to 168 m (0.2 to 15.2%). From this study we conclude that a large liquid carbohydrate load adversely affects walking performance in patients with CAO. This potential impairment of functional capacity should be considered when caloric intake is increased in attempts to improve nutritional status in this patient population.

Reproducibility of VO2max in patients with chronic air-flow obstruction.

The purpose of this study was to determine the variability in maximal oxygen consumption (VO2 max) determined from repeated exercise tests in patients with chronic air-flow obstruction (CAO). Three incremental maximal cycle ergometer tests were performed in each of 11 CAO patients who were familiar with such testing. Two tests (Test 1, Test 2) were carried out on the same day, separated by a 60-min rest period, and 1 (Test 3) was performed on a consecutive day. Group mean values for VO2 max were: 1.313 +/- 0.259, 1.311 +/- 0.281, 1.306 +/- 0.288 L/min, for Tests 1 to 3, respectively. These nearly identical values did not differ significantly. There was no systematic "fatigue" or "learning" effect from test to test. Other mean measurements obtained at maximal exercise were likewise not significantly different among the 3 tests. For tests performed on the same day, the mean of the absolute values of the individual patient VO2 max differences (delta VO2 max) was 53 +/- 30 ml. The delta VO2 max was less than 6% in 10 of the 11 patients and less than 10% in the remaining patient. For tests performed on consecutive days, delta VO2 max was 93 +/- 81 ml; delta VO2 max was less than 6% in 6 patients and less than 10% in 9 patients. From this study we concluded that repeated maximal exercise testing is highly reproducible for groups of CAO patients, although some individual patient variability is seen. Individual patient differences in delta VO2 max are less when the 2 tests are performed on the same day than when duplicate testing is performed on consecutive days.

Exercise performance with added dead space in chronic airflow obstruction.

Individuals with chronic airflow obstruction (CAO) are thought to have limited exercise tolerance primarily because of impaired ventilatory mechanics. We studied the effects of added external dead space (DS) on exercise capacity [maximum O2 consumption (VO2max)], maximum exercise ventilation (VEmax), and blood gases (arterial PO2, PCO2, pH) in 22 patients with CAO [forced expired volume at 1 s (FEV1) = 0.96 +/- 0.41 liter]. Maximum exercise testing (Emax) was performed by incremental cycle ergometry. Patients exercised at base line (BL) and with DS (0.25 liter if FEV1 less than 0.8, and 0.50 liter if FEV1 greater than 0.8 liter), in random-order single-blind fashion. DS resulted in a 12.2% increase in VEmax (P less than 0.001); tidal volume increased (P less than 0.025) while respiratory frequency was unchanged. The VO2max and maximum CO2 production decreased (P less than 0.001) with DS. Arterial PCO2 at rest and at exhaustion increased with DS (P less than 0.001). The pH and arterial PO2 showed small declines at rest and at Emax. Thus, at the lower maximum work load achieved with DS, the patients ventilated more and tolerated a higher arterial PCO2 and a lower arterial PO2 and pH before stopping from dyspnea as compared with the BL exercise run. In contrast, the VO2max of nine normal control subjects was unaffected by the addition of DS. Although VEmax can be increased in CAO patients with DS, this increase is not sufficient to prevent further CO2 retention or a decrease in exercise capacity. We conclude that exercise performance is limited primarily by impaired ventilatory mechanics in CAO.