To study the role of muscle mass and muscle activity on lactate and energy kinetics during exercise, whole body and limb lactate, glucose, and fatty acid fluxes were determined in six elite cross-country skiers during roller-skiing for 40 min with the diagonal stride (Continuous Arm ϩ Leg) followed by 10 min of double poling and diagonal stride at 72-76% maximal O2 uptake. A high lactate appearance rate (Ra, 184 Ϯ 17 mol ⅐ kg Ϫ1 ⅐ min Ϫ1 ) but a low arterial lactate concentration (ϳ2.5 mmol/l) were observed during Continuous Arm ϩ Leg despite a substantial net lactate release by the arm of ϳ2.1 mmol/min, which was balanced by a similar net lactate uptake by the leg. Whole body and limb lactate oxidation during Continuous Arm ϩ Leg was ϳ45% at rest and ϳ95% of disappearance rate and limb lactate uptake, respectively. Limb lactate kinetics changed multiple times when exercise mode was changed. Whole body glucose and glycerol turnover was unchanged during the different skiing modes; however, limb net glucose uptake changed severalfold. In conclusion, the arterial lactate concentration can be maintained at a relatively low level despite high lactate Ra during exercise with a large muscle mass because of the large capacity of active skeletal muscle to take up lactate, which is tightly correlated with lactate delivery. The limb lactate uptake during exercise is oxidized at rates far above resting oxygen consumption, implying that lactate uptake and subsequent oxidation are also dependent on an elevated metabolic rate. The relative contribution of whole body and limb lactate oxidation is between 20 and 30% of total carbohydrate oxidation at rest and during exercise under the various conditions. Skeletal muscle can change its limb net glucose uptake severalfold within minutes, causing a redistribution of the available glucose because whole body glucose turnover was unchanged. lactate dehydrogenase; cross-country skiing; tracers AS EARLY AS 1907, Fletcher and Hopkins (11) not only provided definitive evidence of the relation between muscle activity and production of lactic acid in the amphibian skeletal muscle, but they also concluded that skeletal muscles possess the requisite chemical mechanisms for the removal of lactic acid once formed. Despite this early finding, lactate was long considered a metabolic end product, that is, lactate produced during muscle contraction and released into the circulation for subsequent uptake by the liver for recycling via gluconeogenesis. The importance of skeletal muscle in lactate clearance in humans became clear from experiments starting in the late 1950s. It was shown that, during exercise, lactate was taken up by nonactive skeletal muscles (1,7,12). Furthermore, when the arterial lactate concentration was also elevated, active skeletal muscles cleared lactate (12,26,30), and when two-legged cycle ergometer exercise was performed with one leg having a normal and the other a low glycogen content, the leg with the normal glycogen content released lactate, whereas lactate was taken up ...