This study was undertaken to quantitatively account for the metabolic disposal of lactate in skeletal muscle exposed to an elevated lactate concentration during rest and mild-intensity contractions. The gastrocnemius plantaris muscle group (GP) was isolated in situ in seven anesthetized dogs. In two experiments, the muscles were perfused with an artificial perfusate with a blood lactate concentration of ~9 mM while normal blood gas/pH status was maintained with [U-¹⁴C]lactate included to follow lactate metabolism. Lactate uptake and metabolic disposal were measured during two consecutive 40-min periods, during which the muscles rested or contracted at 1.25 Hz. Oxygen consumption averaged 10.1 ± 2.0 µmol · 100 g¹ · min¹ (2.26 ± 0.45 ml · kg¹ · min¹) at rest and 143.3 ± 16.2 µmol · 100 g¹ · min¹ (32.1 ± 3.63 ml · kg¹ · min¹) during contractions. Lactate uptake was positive during both conditions, increasing from 10.5 µmol · 100 g¹ · min¹ at rest to 25.0 µmol · 100 g¹ · min¹ during contractions. Oxidation and glycogen synthesis represented minor pathways for lactate disposal during rest at only 6 and 15%, respectively, of the [¹⁴C]lactate removed by the muscle. The majority of the [¹⁴C]lactate removed by the muscle at rest was recovered in the muscle extracts, suggesting that quiescent muscle serves as a site of passive storage for lactate carbon during high-lactate conditions. During contractions, oxidation was the dominant means for lactate disposal at >80% of the [¹⁴C]lactate removed by the muscle. These results suggest that oxidation is a limited means for lactate disposal in resting canine GP exposed to elevated lactate concentrations due to the muscle's low resting metabolic rate.