Abstract des Autors

In summary, several lines of evidence suggest that the heart-transplanted patient differs from a 'mildly insufficient heart failure patient' and that his exercise limitation results from a defective oxidative capacity of the skeletal muscle having a multifactorial origin rather than from a central defective delivery of oxygen to the periphery. Physical exercise disrupts molecular and cellular adaptation of muscles, but we have shown that training is safe and stimulates the main peripheral factors. Thus, the observed improvement of exercise tolerance and the shifted disruption towards a higher work rate confirm the usefulness of exercise training as a standard therapy after heart transplantation. Verf.-Referat