EXERCISE CAPACITY AFTER HEART-TRANSPLANTA TION

Independently of phenomena related to rejection, atherosclerosis of th e grafted heart or high blood pressure, there exists a qualitative and quantitative degradation of response to exercise in heart transplant recipients, Maximal oxygen consumption is generally reduced to 40 to 6 0% of normal levels. There are several interactive mechanisms. Paradox ically, the transplanted heart is a clear demonstration of the Pact th at several other elements are involved in the organisms response to ex ercise. Indeed, ventilation, exercise load, peripheral circulation, mu scle metabolism and neurohormonal response also play a role, Vasoactiv ity of the peripheral arteries limits distribution and extraction of o xygen during exercise. Noradrenaline, renin, atrial natriuretic factor , vasopressin and endothelin levels are normal at rest, but an overrea ction occurs during exercise. The percentage of type I (oxidative) fib res is reduced in muscles. Cyclosporine has also been shown to have a toxic effect on mitochondria in muscles. The deinnervated transplanted heart is thus called upon to work in coordination with peripheral ele ments which have also undergone alterations. Consequently, response to exercise cannot be significantly increased above the level reached be fore transplantation. Usually patients are not greatly hindered in the ir daily activities and rarely complain of breathlessness. Nevertheles s, an improvement would be appreciated, A coherent physical rehabilita tion programme can increase maximal oxygen consumption by 25 to 30% in these patients, essentially via improvement in peripheral anomalies. It is more difficult to modify cardiac response.