Exercise and dyspnoea in COPD

Abstract

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 COPD allow 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.

Inspiratory High Frequency Airway Oscillation Attenuates Resistive Loaded Dyspnea and Modulates Respiratory Function in Young Healthy Individuals

“…COPD is specifically associated with increased respiratory work (41) and skeletal neuromuscular weakness [13] . Such mechanisms can perpetuate a viscous cycle of functional decline (for review see [14] ). Experimental elevation of the perception of breathing effort/work can be reproduced via external resistive or elastic loads [15] by volitional hyperpnoea [16] , or neuromuscular blockade [17] .…”

The Impact of Exercise-Induced Bronchoconstriction on Athletic Performance: A Systematic Review

“…Whilst it is accepted that limitations exist in the current methodology and techniques available to evaluate the impact of in-exercise airflow limitation [34], it seems possible that changes in maximum expiratory flow volume during exercise may influence airflow and the perception of dyspnoea experienced by athletes with EIB, as they adopt ventilatory strategies to overcome this constraint.…”

Home parasternal electromyography tracks patient-reported and physiological measures of recovery from severe COPD exacerbation

“…Generalisability of our data is limited by the small sample, comprised predominantly of patients with very severe COPD who were willing to accept daily home-based assessments. Physiological evaluation of exacerbation recovery is notoriously challenging to conduct due to patient reluctance to attend repeated clinical assessments and perform forced respiratory manoeuvres during recovery [ 19 ]. Unlike previous studies, which have missing data and comparable sample sizes [ 13 , 14 ], we mitigated loss to follow-up by using home-based assessments and achieved 100% adherence to EMG para measurement.…”