Haemodynamic responses to small muscle mass exercise before and after lung transplantation in end-stage chronic obstructive pulmonary disease.

Cardiovascular control during exercise is impaired in chronic obstructive pulmonary disease (COPD). The central cardiopulmonary pathologies in COPD might drive the local muscle vascular abnormalities. We hypothesised that contracting muscle perfusion and O2 utilisation improve after lung transplantation (LTx) in COPD. Ten patients with end-stage COPD were tested on the LTx waiting list (pre-LTx) and again 6 months after LTx (post-LTx). We measured leg blood flow ( Q ̇ leg , main outcome) during submaximal one-leg knee-extensor exercise (KEE), and femoral arterial-venous blood samples were obtained for the determination of O2 kinetics across the leg and vasoactive compounds. Cardiac output and stroke volume in response to KEE peak workload (WLpeak), walking distance and physical activity (triaxial accelerometry) were also assessed. Lung function (one single and nine double LTx), walking distance and physical activity increased post-LTx, whereas leg lean mass and WLpeak remained unchanged. Arterial oxygen partial pressure decreased in response to KEE pre-LTx but was maintained at resting levels post-LTx. Working muscle capillary O2 tension and saturation were also higher post-LTx, with no difference in muscle O2 conductance or extraction. We found no changes in Q ̇ leg during submaximal KEE (pre-LTx: 1026 ± 278 vs. post-LTx: 941 ± 186 mL min-1, P = 0.49); mean arterial pressure and circulating pro-brain natriuretic peptide levels were lower post-LTx and cardiac output higher. Cardiac output (pre-LTx: 6.1 ± 0.4 vs. post-LTx: 8.3 ± 0.5 L min-1, P = 0.0001) and stroke volume responses to WLpeak were also higher post-LTx. LTx did not affect muscle blood flow regulation during moderate-intensity KEE in end-stage COPD and seemed to be disconnected from the augmented cardiac output responses to exercise.