Abstract

Background Although exercise capacity is an important outcome measure in patients with COPD, its longitudinal course has not been analyzed in comparison to the change in pulmonary function. Purpose To examine how exercise capacity would deteriorate over time in patients with COPD, and what factors would contribute to it. Methods A total of 137 male outpatients with moderate-to-very-severe COPD were examined. The average age was 69.0 ± 6.6 years (± SD), and the mean postbronchodilator FEV1 was 45.9 ± 15.4% predicted. Progressive cycle ergometry and pulmonary function testing were performed at entry, and every 6 months thereafter over 5 years. Due to the presence of missing data, a mixed-effect model analysis was then used to estimate the longitudinal changes in various clinical parameters. Results Peak oxygen uptake ( V ˙ o2), peak minute ventilation ( V ˙ e), and peak tidal volume (Vt) during exercise declined significantly over time (p < 0.0001), which was no less rapid than the deterioration in FEV1. The mean decline rates for peak V ˙ o2 were 32 ± 60 mL/min/yr and 0.5 ± 1.0 mL/min/kg/yr. Multiple regression analysis revealed that the changes in peak V ˙ e, peak Vt, and peak respiratory rates were significant predictors for the change in peak V ˙ o2. Conclusion We demonstrated clear evidence of measurable and progressive deterioration in exercise capacity in COPD patients, which was no less rapid than the decline in airflow limitation. Dynamic ventilatory constraints during exercise also deteriorated over time, which most significantly contributed to this exercise capacity deterioration. In addition to pulmonary function, the longitudinal follow-up of exercise capacity is important not to miss the overall deterioration in COPD. Although exercise capacity is an important outcome measure in patients with COPD, its longitudinal course has not been analyzed in comparison to the change in pulmonary function. To examine how exercise capacity would deteriorate over time in patients with COPD, and what factors would contribute to it. A total of 137 male outpatients with moderate-to-very-severe COPD were examined. The average age was 69.0 ± 6.6 years (± SD), and the mean postbronchodilator FEV1 was 45.9 ± 15.4% predicted. Progressive cycle ergometry and pulmonary function testing were performed at entry, and every 6 months thereafter over 5 years. Due to the presence of missing data, a mixed-effect model analysis was then used to estimate the longitudinal changes in various clinical parameters. Peak oxygen uptake ( V ˙ o2), peak minute ventilation ( V ˙ e), and peak tidal volume (Vt) during exercise declined significantly over time (p < 0.0001), which was no less rapid than the deterioration in FEV1. The mean decline rates for peak V ˙ o2 were 32 ± 60 mL/min/yr and 0.5 ± 1.0 mL/min/kg/yr. Multiple regression analysis revealed that the changes in peak V ˙ e, peak Vt, and peak respiratory rates were significant predictors for the change in peak V ˙ o2. We demonstrated clear evidence of measurable and progressive deterioration in exercise capacity in COPD patients, which was no less rapid than the decline in airflow limitation. Dynamic ventilatory constraints during exercise also deteriorated over time, which most significantly contributed to this exercise capacity deterioration. In addition to pulmonary function, the longitudinal follow-up of exercise capacity is important not to miss the overall deterioration in COPD.

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