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Abstract 


Peak oxygen uptake (VO2peak) of patients with end-stage renal failure treated with hemodialysis is very low. The improvement of anemia with recombinant human erythropoietin (rHuEPO) results in a very small change in VO2peak. This change is minimal compared with the magnitude of change in hematocrit, suggesting that other factors continue to limit exercise tolerance. This article reviews the physiology of oxygen transport and the determinants of VO2peak. Anemic hemodialysis patients are limited by a reduced cardiac output response to exercise and an inability to widen the arterio-venous oxygen difference. The lack of change in cardiac output and a remaining low arterio-venous oxygen difference following improvement of anemia with rHuEPO therapy suggest an underlying muscle limitation to exercise. Evidence for this muscle limitation is presented. Exercise training may improve the ability of muscle to use oxygen, thus optimizing the effect of the increased hematocrit resulting from rHuEPO therapy.

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