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LETTER TO THE EDITOR
In fact, the relative role of central and peripheral impairments on exercise limitation after heart transplantation greatly depends on multiple factors: interactions between pulmonary, cardiac, neurohormonal, vascular and skeletal muscle functions, and type of exercise (submaximal vs. maximal and small vs. large muscular mass involvement).
We agree that a reduced cardiac output increase during exercise, related to an impaired heart rate reserve and/or to an impaired stroke volume reserve might result in an inadequate O2 transport toward exercising muscles. However, assuming that inotropic and lusitropic cardiac properties and pulmonary exchanges remain in the normal range, an enhanced stroke volume increase might counterbalance the reduced heart rate increase. This should allow the cardiac output to match the blood convection needed. Accordingly, despite either normal peak muscle blood flow or normal peak heart rate and normal heart rate kinetic related with functional heart reinnervation, a decreased peak oxygen consumption was observed in heart transplant recipients (Htx) during submaximal exercise (4). Similarly, during small muscle mass exercise, peripheral limitations might play a greater role compared with large muscle mass aerobic exercise (3). Furthermore, increased systemic vascular resistance (SVR) and therefore reduced SVR reserve likely participated in the reduced cardiac output (3). Thus, besides cardiac diastolic dysfunction, these data likely explain why the increase in the vasodilatory cardiac hormone brain natriuretic peptide secretion was related to flow-mediated artery dilatation during exercise after heart transplantation (5).
Should we therefore state that a decreased heart rate reserve always plays a minor role in exercise capacity limitation after heart transplantation?
Probably not. Indeed, although the main driving mechanism of the cardiac response to exercise relies on peripheral metabolic demand and although a reduced muscular energetic need secondary to muscular alterations might participate importantly in Htx exercise limitation, patients' skeletal muscle mitochondrial oxidative dysfunction might be, at least partly, reversed by both pharmaceutical and physical therapies. Similarly, the degree of endothelial dysfunction might vary after heart transplantation, depending on the duration of heart failure before transplantation and on the intensity and duration of postoperative treatment-induced deleterious effects on conduit vessels and microcirculation (1, 2, 4). Thus one might propose that when vascular and muscular functions are only slightly impaired, allowing an important muscular metabolic demand to be made, Htx exercise capacity might be limited by central factors, including chronotropic incompetence secondary to the surgical cardiac denervation. This is particularly true, in well being and well trained patients, who achieve very high level of maximal exercise capacity.
In summary, both central and peripheral factors can participate in exercise capacity limitation after heart transplantation. The quantitative role of each factor is difficult to determine precisely because of their interactions but it is likely that peripheral factors play a main role in a majority of patients during submaximal exercise. Cardiac denervation should play a much greater role when Htx perform exercise of very high intensity or duration.
REFERENCES
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