The relationship between maximal expiratory flow and increases of maximal exercise capacity with exercise training

We previously reported that patients with mild to moderate airflow limitation have a lower exercise capacity than age-matched controls with normal lung function, but the mechanism of this reduction remains unclear (1). Although the reduced exercise capacity appeared consistent with deconditioning, the patients had altered breathing mechanics during exercise, which raised the possibility that the reduced exercise capacity and the altered breathing mechanics may have been causally related. Reversal of reduced exercise capacity by an adequate exercise training program is generally accepted as evidence of deconditioning as the cause of the reduced exercise capacity. We studied 11 asymptomatic volunteer subjects (58 ± 8 yr of age [mean ± SD]) selected to have a range of lung function (FEV₁ from 61 to 114% predicted, with a mean of 90 ± 18% predicted). Only one subject had an FEV₁ of less than 70% predicted. Gas exchange and lung mechanics were measured during both steady-state and maximal exercise before and after training for 30 min/d on 3 d/wk for 10 wk, beginning at the steady-state workload previously determined to be the maximum steady-state exercise level that subjects could sustain for 30 min without exceeding 90% of their observed maximal heart rate (HR). The training workload was increased if the subject's HR decreased during the training period. After 10 wk, subjects performed another steady-state exercise test at the initial pretraining level, and another maximal exercise test. HR decreased significantly between the first and second steady-state exercise tests (p < 0.05), and maximal oxygen uptake (V̇O(2max)) and ventilation increased significantly (p < 0.05) during the incremental test, indicating a training effect. However, the training effect did not occur in all subjects. Relationships between exercise parameters and lung function were examined by regression against FEV₁ expressed as percent predicted. There was a significant positive correlation between V̇O(2max) percent predicted and FEV₁ percent predicted (p < 0.02), and a negative correlation between FEV₁ and end-expiratory lung volume (EELV) at maximal exercise (p < 0.03). There was no significant correlation between FEV₁ and maximal HR achieved during exercise; moreover, all subjects achieved a maximal HR in excess of 80% predicted, suggesting a cardiovascular limitation to exercise. These data do not support the hypothesis that the lower initial V̇O(2max) in the subjects with a reduced FEV₁ was due to deconditioning. Although increased EELV at maximal exercise, reduced V̇O(2max), and a reduced V̇O(2max) response with training are all statistically associated with a reduced FEV₁ there is no direct evidence of causality.