Exercise and dyspnoea in COPD

Dyspnoea provoked either by exercise or during a disease exacerbation is one of the most feared symptoms of the chronic obstructive pulmonary disease (COPD) patient. It contributes to impaired quality of life and patients who are more limited by exertional dyspnoea are more likely to die. The physiological mechanisms responsible for these two outcomes vary in different settings, but in both situations, changes in the resting lung volume and increased activation of the respiratory muscles relative to their maximum capacity is the final common pathway. Although increased metabolic carbon dioxide production from weak or poorly conditioned muscles is an important cofactor, most patients limited by exertional dyspnoea exhibit dynamic hyperinflation that parallels their symptom intensity. This results from the longer respiratory time constant of the lungs in COPD and coexisting expiratory flow limitation during tidal breathing. The response of the chest wall muscles to this change in lung volume is variable: most patients with more severe COPDallow chest wall volume to increase, while others try to defend chest wall volume. The latter is not a good breathing strategy as the patient's exercise capacity is very limited. Treatment with bronchodilators reduces operating lung volumes and delays the time until tidal volume is mechanically limited by the inspiratory reserve volume. Breathing oxygen and heliox gas mixtures further increases exercise endurance and slows the rate at which end- expiratory lung volume increases. During exacerbations there is a consistent increase in end- expiratory lung volume and this parallels the reduction in forced vital capacity. This suggests that gas trapping due to airway closure is the main mechanism involved here, although changes in lung volume still track the symptomatic improvement in dyspnoea reported by patients both as the episode resolves and after nebulised bronchodilator treatment.