Factor analysis of quality of life, dyspnea, and physiologic variables in patients with chronic obstructive pulmonary disease before and after rehabilitation.

OBJECTIVE: To identify the relationships between quality of life (QOL) and the clinical state using factor analysis pre- and postrehabilitation. Patients with chronic obstructive pulmonary disease (COPD) suffer from a significant physiologic impairment associated with an altered QOL. Comprehensive rehabilitative programs, including exercise training, have beneficial effects on exercise tolerance and QOL for these patients. DESIGN: Factor analysis (n = 6) was conducted using the data of 32 patients with COPD. Patients had been evaluated for QOL using the Nottingham Health Profile (NHP), spirometric values, dyspnea, and the variables assessed by an incremental exercise test at three levels of activity. All measurements were obtained pre- and postrehabilitation. RESULTS: Factor analysis showed that the following two factors characterize the pathophysiologic condition of patients with COPD: (1) the specific cardiorespiratory responses to incremental exercise test and the spirometric values; and (2) the QOL results. The factor analysis results differed with the testing time (pre, post) and the level of activity. CONCLUSIONS: QOL, as evaluated by a generic questionnaire and the clinical state of patients with COPD, was independent; this independence characterized the pathophysiologic condition of our patients. Our results reinforce the usefulness of different types of evaluation, especially pre- and postrehabilitation, because they reflect independent benefits used to understand the success and follow-up of rehabilitative programs.

Effect of NaHCO3 on lactate kinetics in forearm muscles during leg exercise in man.

We investigated NaHCO3 infusion effects on plasma lactate removal by forearm muscles and performance during intensive leg exercise. Seven subjects performed the force-velocity (FV) test with placebo and NaHCO3 (2 mEq.min-1) with a double-blind crossover protocol. Blood samples for arterial ([LA]A) and venous ([LA]V) lactate determinations were taken 1) at rest before infusion, and 2, 6, 10, 14, 18, and 22 min following its start; and 2) at the end of each exercise bout. The arteriovenous difference ([LA]A-V) was determined for each sampling. NaHCO3 significantly increased arterial bicarbonate concentration and pH during rest (P < 0.001; P < 0.001) and the FV test (P < 0.001; P < 0.05). During the test, [LA]A and [LA]V were significantly higher with NaHCO3 (P < 0.05, P < 0.001). At test onset, [LA]A-V became positive and increased until the braking force of 6 kg, with NaHCO3 and placebo, with values significantly lower for NaHCO3 (P < 0.001). Peak anaerobic power (Wanae, peak) and the corresponding braking force (Fmax) were also determined. Fmax was significantly increased with NaHCO3 (P < 0.001). In conclusion, the increasing rise in [LA]A and [LA]V induced by NaHCO3 may be partly explained by a decreased rate of lactate uptake by forearm skeletal muscles. NaHCO3 did not improve Wanae, peak, but improved Fmax, thus increasing FV duration.

Effects of two successive maximal exercise tests on pulmonary gas exchange in athletes.

Pulmonary extravascular water accumulation may be involved in exercise-induced hypoxaemia in highly aerobically trained athletes. We hypothesized that if such an alteration were present in elite athletes performing a maximal exercise test, the impairment of gas exchange would be worse during a second exercise test following the first one. Eight male athletes performed two incremental exercise tests separated by a 30-min recovery period. Pulmonary gas exchange and ventilatory data were measured during exercise tests performed in normoxia. Arterial blood samples were drawn each minute during rest, exercise, and recovery. Pulmonary diffusing capacity for CO (DLCO) was measured at rest, after the first (T1) and the second (T2) test. All the subjects underwent a spirometric test at rest and after T2. Maximal and recovery data for O2 uptake and minute ventilation were not statistically different between T1 and T2. Partial pressure of arterial O2 (PaO2) decreased during both tests but was lower during T2 for rest, 60 W, and 120 W (P < 0.02). Alveolar-arterial difference in partial pressure of O2 (PA-aO2) increased during both the tests but was significantly larger during T2 for rest, 60 W, and 120 W (P < 0.01). The PaO2 and PA-aO2 data at maximal exercise were not significantly different between T1 and T2. Compared to rest, PA-aO2 remained significantly larger during recovery for both T1 and T2 (P < 0.0001). The PA-aO2 during T2 recovery was larger than T1 recovery (P < 0.008). Spirometric data did not change. The DLCO measurements after T1 and T2 were not significantly different from rest. These results showed an alteration of PaO2 and PA-aO2 during T1, which tended to be worse during and after T2; however, these data do not allow us to make a definitive statement as to the cause of the hypoxaemia. Our study confirmed that exhausting exercise caused hypoxaemia. It also demonstrated that the disturbance in pulmonary gas exchange persisted for at least 30 min following the end of the exercise period and became worse during submaximal intensities of the following incremental exercise test.

Cardiopulmonary exercise testing. Determinants of dyspnea due to cardiac or pulmonary limitation.

The aim of this study was to bring to light new and simple criteria, obtained during cardiopulmonary exercise testing, in order to demonstrate in patients the cardiac or the pulmonary origin of a comparable exertional dyspnea. Forty male subjects were compared, who exercised with a 30-W/3-min protocol and were divided into three groups: the cardiac heart failure (CHF) group (n = 15), the chronic obstructive lung disease (COLD) group (n = 15), and the control group (n = 10). The two groups of patients differed totally from the control group concerning their spirometric values at rest and a clear inability during effort which was confirmed by all the studied cardiopulmonary parameters at maximal exercise. The CHF and COLD groups differed slightly concerning their maximum symptom-limited oxygen uptake, only when related to body mass (13.26 +/- 0.69 ml/kg/min in CHF group, 17.05 +/- 1.59 ml/kg/min in COLD group; p < 0.05), and concerning their maximum ventilatory equivalent for oxygen which tended to be higher in the CHF group in comparison with the COLD group (p = 0.082). Furthermore, and as foreseen, the two groups of patients clearly differed at maximum exercise concerning the ventilatory reserve respiratory parameter (49.73 +/- 3.18 percent in CHF group, 8.38 +/- 5.85 percent in COLD group; p < 0.01). On the other hand, they did not differ concerning cardiac parameters or those considered as such (maximum heart rate [HR], HR reserve, HR response, maximum O2 pulse measurement). While their maximum ventilation was similar in the CHF and COLD groups, a difference in adaptation during exercise was found by observing their breathing pattern. In the CHF group, this was demonstrated by a significantly lower breathing frequency at maximum exercise (31.24 +/- 1.53 beats/min vs 37.75 +/- 2.24 beats/min; p < 0.05) and a tidal volume that tended to be higher at maximum exercise (p = 0.077) and significantly higher at 60-W work load (p < 0.05). This work shows that the study of ventilatory reserve and breathing pattern during exercise testing allows one to discriminate if dyspnea on exertion in patients is due to cardiac or respiratory disease.

Effects of benzodiazepine during a Wingate test: interaction with caffeine.

To assess the effects of benzodiazepine alone and associated with caffeine on performance and substrate responses during supramaximal exercise, seven healthy volunteers performed the Wingate test after ingestion of placebo (Pla), benzodiazepine alone, i.e., 1 mg of lorazepam (Bz), and benzodiazepine followed by 250 mg of caffeine (Bz-Caf). Peak power (PP), mean power (MP), and percentage of power decrease (%PD) were determined, and substrate responses were estimated by blood lactate and catecholamine concentrations. Four hours after Bz ingestion, there was a significant decrease in PP (PPBz: 626 +/- 72 vs PPPla: 669 +/- 78 W), maximal blood lactate (La max) (La maxBz: 9.5 +/- 1.5 vs La maxPla: 12.4 +/- 1.8 mmol.l-1), and end-exercise epinephrine (E) (EBz: 339 +/- 113 vs EPla: 672 +/- 247 ng.l-1). No other changes were noted. Caffeine ingestion 1 h before the test (Bz-Caf) corrected the decrease in La max (La maxBz-Caf: 11.5 +/- 1.4 mmol.l-1) and E (EBz-Caf: 573 +/- 190 ng.l-1) but was unable to prevent the impairment of performance (PPBz-Caf: 625 +/- 68 W vs PPPla). Moderate benzodiazepine intake significantly altered performance and substrate responses during supramaximal exercise. Moderate caffeine intake antagonized the metabolic but not the performance effects of 1 mg of lorazepam.

Cardiorespiratory fitness evaluation by the shuttle test in asthmatic subjects during aerobic training.

PURPOSE: The purpose of this study was to assess the validity of the 20-m shuttle test with 1-min stages (20-MST) to estimate maximal oxygen uptake (VO2 max) and its ability to register cardiorespiratory modifications over the course of an individualized aerobic training program for mild to moderately asthmatic children acclimatized to moderate altitude. METHODS: Forty-eight asthmatic subjects aged 12 to 17 years performed both a maximal incremental exercise test on a cycle ergometer and the 20-MST. Ten of the subjects were then randomly chosen and trained three times per week at their ventilatory threshold (Vth) intensity level for three months. Another group of ten asthmatic subjects served as control subjects. Training intensity was adjusted monthly; heart rate values at Vth were increased by the same proportion as the increase in Vo2 max as measured by the 20-MST. At the end of training, both groups were again evaluated with the two tests. The Vo2 max values by direct measurement and by the 20-MST were not significantly different for the entire population (46.5 +/- 1.6 vs 47.2 +/- 2.1 ml.min-1.kg-1). In addition, the two test results were in close agreement (r = 0.84; p < 0.01). After training, a sharp improvement in the direct Vo2 max (44.1 +/- 2.4 to 51.2 +/- 1.9 ml.min-1.kg-1) was noted in the training group as well as an increase in the Vth (25.6 +/- 1.9 to 32.1 +/- 3.4 ml.min-1.kg-1), the maximal power (152 +/- 7.1 to 185 +/- 3.8 W), and the maximal oxygen pulse (0.24 +/- 0.007 to 0.27 +/- 0.008 ml.beat-1.kg-1). CONCLUSION: The indirect measure confirmed these results: a simultaneous increase in VO2 max (43.7 +/- 2.5 to 53.8 +/- 2.1 ml.min-1.kg-1), maximal oxygen pulse (0.22 +/- 0.004 to 0.27 +/- 0.006 ml.beat-1.kg-1), and the number of stages completed (7 +/- 1.4 to 10.1 +/- 1.3) was observed. It was concluded that the 20-MST has sufficient validity to assess VO2 max and to register cardiorespiratory modifications over the course of individualized aerobic training programs in mild and moderately asthmatic children. It thus may be used to adjust training intensities during these programs.

Individualized aerobic and high intensity training for asthmatic children in an exercise readaptation program. Is training always helpful for better adaptation to exercise?

In order to define the role of individualized training intensity in a conditioning program for asthmatic children, we have trained seven asthmatics (age = 11.4 +/- 1.8 years) at their ventilatory threshold (VTh) intensity level for a three-month period (aerobic training) and at maximal intensity also for three months (high intensity training). VTh is the point at which a nonlinear increase of VE occurs. Another group of seven asthmatics (age = 11.4 +/- 1.5) served as control subjects. Cardiopulmonary fitness was determined on a cycle ergometer before and after each training session. This study demonstrated that aerobic training, correctly adapted to the child's physical ability, induces the following: (1) a rapid and marked cardiovascular fitness increase; and (2) a decrease in VE over a given work range so that VTh is increased. This is of great importance because hyperventilation is a major determinant of exercise-induced bronchospasm. In contrast, even if high intensity training is well tolerated in an indoor swimming pool, the long-term effects are unsuitable for asthmatic children because the decrease of VTh will involve an increase of hyperventilation, even when exercise is performed at submaximal intensity.

Ventilatory control during exercise in children with mild or moderate asthma.

The aim of this study was to specify whether during exercise the neural response to increased resistive load in asthmatic children corresponds to a modification of the neuromuscular inspiratory drive, to a modification of the breathing pattern, or to both. Thus, nine children with mild or moderate asthma (aged 10-15 yr) and nine normal children (aged 11-16 yr) were studied during an incremental load exercise with a cyclic ergometer, the load of which was increased by steps of 30 W.3 min-1. During the 3rd min of each workload, we measured the following parameters: O2 consumption (VO2), CO2 production (VCO2), ventilation (VE), tidal volume (VT), respiratory frequency (f), ratio of inspiratory to total time of respiratory cycle (T1/TTOT), mean inspiratory flow (VT/T1) as well as mouth occlusion pressure measured at 100 ms (P0.1), and inspiratory power for breathing (W). At maximum level, the two groups showed identical values for heart rate, ventilation divided by weight (VEBW), T1/TTOT), VT/T1, P0.1, and W. However, asthmatic children had lower maximal power (P less than 0.02), higher tidal volume divided by weight (VTBW) (P less than 0.05), and lower f (P less than 0.01). At a same level of exercise (60, 90, or 120 W), in both groups, we found identical values for P0.1, VEBW, VO2, T1/TTOT, and VTBW/T1. However, asthmatic patients exhibited higher VTBW and lower f(limit of significance). This resulted from higher inspiratory and total time durations. Furthermore, they showed a higher inspiratory power for breathing. It was the same for f and VTBW if the results were expressed in relation to the VO2 in ml.kg-1.(ABSTRACT TRUNCATED AT 250 WORDS)