The purpose of this study was to determine lactate transport kinetics in single isolated rat ventricular cardiac myocytes after 1) 8 wk of myocardial volume overload (MVO) and 2) congestive heart failure (CHF). Twenty male Sprague-Dawley rats were assigned to one of four groups: myocardial hypertrophy (MH), MH sham (MHS), CHF, or CHF sham (CHFS). A chronic MVO was induced in the MH and CHF groups by an infrarenal arteriovenous fistula. Postdeath heart and lung weights were significantly greater (P < 0.05) for the MH and CHF groups compared with controls. Isolated cardiac myocytes were loaded with BCECF to determine intracellular pH (pH_i) changes after the addition of lactate to the extracellular superfusate. Alterations in pH_i with the addition of varied lactate concentrations were attenuated 72-89% by 5.0 mM -cyano-4-hydroxycinnamate. Significant differences (P < 0.05) were found in estimated maximal lactate transport rates between the experimental and sham groups (MH = 19.4 ± 1.1 nmol · µl¹ · min¹ vs. MHS = 15.1 ± 1.1 nmol · µl¹ · min¹; CHF = 20.2 ± 2.0 nmol · µl¹ · min¹ vs. CHFS = 14.0 ± 0.9 nmol · µl¹ · min¹). Western blot analysis confirmed a 270% increase in monocarboxylate symport protein 1 (MCT1) protein content in CHF compared with CHFS rats. The results of this study suggest that MH and CHF induced by MVO engender a greater maximal lactate transport capacity across the cardiac myocyte sarcolemma along with an increase in MCT1 protein content. These alterations would likely benefit the cell by attenuating intracellular acidification during a period of increased myocardial load.