This study determined and compared rates and mechanisms of lactate transport in red blood cells (RBCs) of persons with: 1) sickle cell disease (HbSS), 2) sickle cell trait (HbAS) and; 3) a control group (HbAA). Blood samples were drawn from 30 African American volunteers (10 HbSS, 10 HbAS, 10 HbAA). Lactate influx into RBCs was measured by using ¹⁴C-lactate at six (2, 5, 10, 15, 25, and 40 mM) unlabeled lactate concentrations ([La^-]s). The monocarboxylate transporter (MCT) pathway was blocked by PCMBS to determine its percentage contribution to total lactate influx. Generally, total lactate influx into RBCs from the HbSS group was significantly greater than influx into RBCs from HbAS or HbAA with no difference between HbAS and HbAA. Faster influx into HbSS RBCs was attributed to increased MCT activity (increased apparent V_max = V_max'). V_max' (4.7 ± 0.6 µmol^.ml^-1.min^-1) for HbSS RBCs was significantly greater than V_max' of HbAS RBCs (2.9 ± 1.5) and HbAA RBCs (2.0 ± 0.5). K_m (42.8 ± 8 mM) for HbSS RBCs was significantly greater than K_m (27 ± 12 mM) for HbAA RBCs. We suspect that elevated erythropoietin (EPO) levels in response to chronic anemia and/or pharmacological treatment (EPO injections, hydroxyurea ingestion) is the underlying mechanism for increased lactate transport capacity in HbSS RBCs.