Premium
Improving exercise capacity, 6 wk training tends to reduce circulating endothelin after heart transplantation
Author(s) -
Doutreleau Stèphane,
Piquard François,
Lonsdorfer Evelyne,
Rouyer Olivier,
Lampert Eliane,
Mettauer Bertrand,
Richard Ruddy,
Geny Bernard
Publication year - 2004
Publication title -
clinical transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 76
eISSN - 1399-0012
pISSN - 0902-0063
DOI - 10.1111/j.1399-0012.2004.00265.x
Subject(s) - medicine , heart transplantation , endurance training , transplantation , heart rate , vo2 max , cardiology , aerobic exercise , endothelin 1 , physical exercise , physical therapy , blood pressure , receptor
Short‐term survival is no longer the pivotal issue after heart transplantation but, most heart‐transplant (Htx) patients still present with increased circulating endothelin‐1 (ET) and reduced exercise capacity. ET‐1 limits both exercise‐induced vasodilation and blood flow redistribution toward acting muscles and might be accessible to training. This study was performed to investigate the effect of training on ET‐1 and whether an eventual training‐induced improvement in exercise capacity may be related to reduced baseline or exercise circulating ET‐1 in Htx patients. Five Htx patients performed a maximal bicycle exercise test and an endurance exercise test before and after a training program of 18 exercises sessions during 6 wk. ET‐1 was determined by radioimmunoassay at rest, end endurance exercise and 30 min recovery, before and after training. Training improved significantly Htx's maximal oxygen uptake (+13.1 ± 4.8%; p < 0.05) and also reduced significantly the endurance exercise‐induced heart rate increase. Resting ET‐1 was increased in Htx (5.98 ± 1.88 vs. 1.61 ± 0.25 pmol/L in controls; p < 0.01) but although ET‐1 modulation might participate in training‐induced beneficial effects, training failed to modulate either resting or exercise ET‐1 plasma level. Training‐induced improvement in exercise capacity might not mainly due to decreased ET‐1 after heart transplantation. Further supporting the usefulness of training, these preliminary data suggest that improved exercise capacity may not be mainly due to decreased ET‐1 in Htx patients. Further, larger scale studies will be needed to investigate whether an impaired nitric oxide pathway stimulation might explain such results and whether a longer training program can reduce local ET‐1, arising from working muscles after heart transplantation.