Physiological Response to Moderate Exercise Workloads in a Pulmonary Rehabilitation Program in Patients With Airflow Obstruction: Exercise tolerance

In contrast to the improvements in exercise tolerance seen within the training cohort, peak values for WR, Ve, and V02 within the nontraining control group were largely unchanged when reassessed after 12 weeks (Table 2; Fig 2). We are aware however, that a major limitation of this study was the lack of prospective randomization into the training and nontraining control groups. Allowing for the disparity in numbers, the two groups nevertheless were well matched, although the nontraining control cohort were younger (Table 1), with the implicit acceptance that age may be an important factor in disease progression. Furthermore, although the nontraining control group that was used may have been biased by patients who declined rehabilitation because of lack of motivation, the principal reason for the failure to participate was time constraint. Despite these limitations, we have included comparative data from the nontraining control cohort (Table 2), recognizing that statistical and clinical interpretation may be difficult. read

Further evidence of training effects that were induced by the present exercise program can be seen from the physiologic responses to a given level of exercise. At an identical WR during the incremental exercise test, Ve, VC02, Ve/Vo2, and HR were all significantly lower after 12 weeks of training (Table 3). Moreover, we observed increases in the AT after training, implying that the training program might have induced functional changes in the exercising muscles, most notably allowing them to increase their capacity for aerobic work and forestall the onset of lactic acidosis. Indeed, recent evidence obtained by comparable exercise programs has demonstrated that training improved cellular bioenergetics and resulted in increased levels of aerobic enzymes within the leg muscles of patients with severe COPD; these adaptations were associated with reduced exercise-induced lactic acidosis. Reduced lactic acidosis could benefit patients with COPD by removing, at least in part, some of the acid stimulus to breathe, thereby lowering the ventilatory requirement at a given exercise level. The reduction in Ve (13%) is in a good agreement with two previous studies of Casaburi et al- (12% and 9%, respectively), and is considerably greater than in two further comparative studies by Maltais et al> (5% and 6%, respectively). Reductions in V02 at identical levels of exercise seen in this study were also comparable (8%) to previously reported data.