The effects of two 8 week programmes of reconditioning in chronic obstructive pulmonary disease (COPD) patients were studied. Forty one subjects (mean+/-SD) 644.5) yrs; forced expiratory volume in one second (FEV1) 1.09+/-0.16 L; 40.6+/-6.2% predicted were randomly assigned either to supervised training on a treadmill, 4 days x week(-1) (group S; n=21) or walking 3 or 4 km in 1 h 4 days x week(-1), self-monitored with a pedometer, with weekly visits to encourage adherence (group SM; n=20). Patients were evaluated with the chronic respiratory diseases questionnaire (CRQ) and two exercise tests on a treadmill: incremental (IT) and constant (CT), above lactic threshold or 70% of maximal oxygen uptake (VO2, max) with arterial blood lactate determinations. Estimated mean work rate of training was 69+/-27 W and 25+/-5 W respectively for groups S and SM. Both types of training produced similar changes in the four dimensions of the CRQ. In group S reconditioning yielded significant (p<0.05) increases in VO2, max and increases in duration, with decreased lactate accumulation, ventilation, CO2 output (VCO2), heart rate (HR) and diastolic blood pressure (DBP) at the end of CT. They also adopted a deeper slower pattern of breathing during exercise. The SM group showed significant (p<0.05) increases in duration, lower HR and DBP at the end of CT. Significantly (p<0.05) different effects between S and SM programmes were changes in VO2, max 100+/-101 mL x min(-1) versus 5+/-101 mL x min(-1)), duration of the CT (8.1+/-4.4 min versus 3.9+/-4.7 min), VCO2 (-94+/-153 mL x min(-1) versus 48+/-252 mL x min(-1)), lactate accumulation (-1.3+/-2.2 mmol x L(-1) versus 0+/-1.2 mmol x L(-1) and respiratory rate at the end of CT (4.3+/-3.4 min(-1) versus -1+/-4.2 min(-1)). Supervised, intense training yields physiological improvements in severe chronic obstructive pulmonary disease patients not induced by self-monitored training. The self-monitored, less intense training, increases submaximal exercise endurance, although to a lesser degree.

The endurance time during constant high work-rate exercise (tLIM) is used to assess exercise capacity in patients with chronic obstructive pulmonary disease and as an outcome measure for pulmonary rehabilitation. Our study was designed to establish the minimum clinically important difference for the tLIM. tLIM was measured in 105 patients (86 males) before and after an 8-week outpatient pulmonary rehabilitation programme. Subjects were asked to identify, from a five-point Likert scale, the perceived change in their exercise performance immediately upon completion of the exercise tests. The scale ranged from ''better'' to ''worse''.The mean¡SD age was 64¡5 yrs, forced expiratory volume in 1 s (FEV1) 47¡10% and FEV1/ forced vital capacity 54.7¡16.3%. Baseline tLIM at 75% of the peak work rate was 397¡184 s, which increased by 62¡63% after rehabilitation. In subjects who felt their exercise tolerance was ''slightly better'', the mean improvement was 34% in the relative improvement over the baseline value (95% CI 29-39)% or 101 (86-116) s compared with 121 (109-134)% in those who reported that their exercise tolerance was ''better'' and 8 (2-14)% in those who felt their exercise tolerance was ''about the same''.Minimum clinically important improvement for tLIM averaged ,33% of baseline. Patients were able to distinguish at least one further additional level of benefit at 120% of baseline.

The effects of two 8-week programmes of exercise reconditioning on the time constants (tau) of the pulmonary gas exchange, ventilatory and heart rate responses to moderate intensity exercise in patients with chronic obstructive pulmonary disease (COPD) were studied. Thirty-five subjects (mean+/-SD 64+/-5 yrs; forced expiratory volume in one second (FEV1) 1.09+/-0.17 L; 41+/-6.2% predicted) were randomly assigned either to supervised (s) training on a treadmill, 4 days x week(-1) (group S; n=21) or self-monitored (SM) walking 3 or 4 km in 1 h 4 days x week(-l) (group SM; n=20). The different levels of supervision resulted in a different estimated intensity of training (35+/-10 W in the SM group and 70+/-22 W in the S group). The kinetics were evaluated with a constant-load exercise test on a cycle-ergometer at a work rate corresponding to 80% the highest oxygen consumption (V'O2) that can be achieved without blood lactic acidosis (V'O2,LAT) or 50% of V'O2,max, if maximum oxygen consumption V'O2,LAT was not found. Mean endurance time at a work rate equivalent to 70% of the pretraining V'O2,max increased by 493+/-281 s in the S group and 254+/-283 s in the SM group (p<0.001). Mean tauV'O2 decreased from 83+/-17 s to 67+/-11 s (p<0.0001) in the S group and from 84+/-12 to 79+/-16 (p=0.04) in the SM group. Mean tau for carbon dioxide output minute ventilation and heart rate were also speeded after training, again more markedly in the S group. In the S group there was a significant correlation between the decrease in tauV'O2 and the increase in endurance time (r=-0.56, SEM=0.21). It is concluded that training speeds the kinetic response of oxygen consumption, carbon dioxide production, minute ventilation and heart rate to moderate exercise and that the effect is greater after supervised, more intense training.

To be clinically useful as indices reflective of altered physiological function consequent to interventions in patients with chronic obstructive pulmonary disease (COPD), the time constant (tau) and steady-state amplitude of the kinetic responses for oxygen uptake (VO2) carbon dioxide output (VCO2) ventilation (VE) and heart rate (HR) have to be appropriately differentiable and reproducible. We therefore assessed the reproducibility of tau and steady state amplitude values in 41 patients with severe COPD [mean (SD)] [forced expiratory volume in 1 s = 41 (7)% predicted], aged 64 (5) years. Of the total, 6 of the patients (15%) did not produce breath-by-breath data of sufficient quality to warrant kinetic analysis. The remaining 35 patients completed two moderate-intensity 10 min square-wave exercise tests separated by 2 h, both before and after an endurance training programme. Tests were conducted on an electromagnetically-braked cycle ergometer at an exercise intensity corresponding to 80% of the estimated lactate threshold (thetaLa) or 50% of peak oxygen uptake if thetaLa was insufficiently differentiable. Breath-by-breath measurements of VO2, VCO2, VE and HR were averaged into 10 s bins and the on-transient response kinetics were estimated using a mono-exponential model. Analysing the pre-training and the post-training test 1 and test 2 comparisons together, the test 1- test 2 differences were not significantly different from 0 for either tau or A. The standard deviation of the test 1- test 2 differences allowed us to define the magnitude of change that would reach statistical significance. For tau, this averaged some 8, 10, 11 and 8 s, for VO2, VCO2, VE and HR, respectively, for a one-tailed paired-comparisons test (i.e. appropriate for assessing hypothesised improvements resulting from an intervention); for a two-tailed comparison, the differences were approximately 2 s greater. The corresponding one-tailed values for A were 100 ml x min(-1), 95 ml x min(-1), 2.5 1 x min(-1) and 4 beats x min(-1), respectively; the two-tailed values were 10%-15% greater. We therefore conclude that both tau and A for moderate-intensity exercise can be reproducibly estimated in patients with COPD when the data set provides a sufficiently large amplitude of response and sufficiently low sample variability to allow appropriate parameter estimation.

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