Improving exercise capacity, 6 wk training tends to reduce circulating endothelin after heart transplantation

Authors: Doutreleau, Stèphane; Piquard, François; Lonsdorfer, Evelyne; Rouyer, Olivier; Lampert, Eliane; Mettauer, Bertrand; Richard, Ruddy; Geny, Bernard

Source: Clinical Transplantation, Volume 18, Number 6, December 2004 , pp. 672-675(4)

Publisher: Blackwell Publishing

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Abstract:

Doutreleau S, Piquard F, Lonsdorfer E, Rouyer O, Lampert E, Mettauer B, Richard R, Geny B. Improving exercise capacity, 6 wk training tends to reduce circulating endothelin after heart transplantation.

Clin Transplant 2004 DOI: “10.1111/j.1399-0012.2004.00265.x”

© Blackwell Munksgaard, 2004 Abstract: 

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.

Keywords: endothelin-1; exercise; heart transplantation; training

Document Type: Research article

DOI: 10.1111/j.1399-0012.2004.00265.x

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