The purpose of this study was to determine lactate transport kinetics into single isolated rat ventricular cardiac myocytes following 1) eight weeks of myocardial volume overload (MVO) and 2) congestive heart failure. Twenty male Sprague-Dawley rats were assigned to one of four groups: myocardial hypertrophy (MH), myocardial hypertrophy sham (MHS), congestive heart failure (CHF), or congestive heart failure sham (CHFS). A chronic MVO was induced in the MH and CHF groups by an infrarenal A-V fistula. Post-sacrifice heart and lung weights were significantly greater (p<0.05) for the MH and CHF groups compared to controls. Isolated cardiac myocytes were loaded with 2', 7' Bis(carboxyethyl)-5(6)-carboxyfluorescein (BCECF) to determine intracellular pH (pH_i) changes following 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 (CHC). 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/µL/min vs MHS = 15.1 ± 1.1 nmol/µL/min; CHF = 20.2 ± 2.0 nmol/µL/min vs CHFS = 14.0 ± 0.9 nmol/µL/min. Western blot analysis confirmed a 270% increase in MCT1 protein content in CHF as compared to CHFS rats. The results of this study suggest that myocardial hypertrophy and congestive heart failure 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.