The concentration of lactate in the blood is the result of (1) those processes which produce lactate and contribute to its appearance in the blood and (2) those processes which catabolize lactate after its removal from the blood. Consequently, the concentration of lactate in the blood provides minimal information about the rate of lactate production in muscle. The accumulation of lactate beyond the lactate threshold [T(lact)] does provide an indication that the mechanisms of lactate removal fail to keep pace with lactate production. Lactate is produced in skeletal muscle as a direct result of increased metabolic rate and glycolytic carbon flow. Factors which influence lactate production in muscle include: the Vmax of lactic dehydrogenase (LDH), which is several times greater than the combined activities of enzymes which provide alternative pathways of pyruvate metabolism; the kM of LDH for pyruvate, which is sufficiently low to assure maximal stimulation of LDH in the conversion of pyruvate to lactate; and the K'eq of pyruvate to lactate conversion, which exceeds 1000. Recent studies on dog gracilis muscle in situ clearly indicate that lactate production occurs in contracting pure red muscle for reasons other than an O2 limitation on mitochondrial ATP production. In addition to failure of the essential assumption of the anaerobic threshold [T(an)] hypothesis that there exist limitations on O2 availability in muscles of healthy individuals during submaximal exercise, several groups of investigators have produced results which indicate that parameters associated with changes in pulmonary minute ventilation [i.e., the ventilatory threshold, T(vent)] do not always track changes in blood lactate concentration. Therefore, the T(an) hypothesis fails on the bases of theory and prediction. A series of kinetic tracer experiments to better understand lactate kinetics during exercise is proposed.