This paper: 1) Reviews evidence for the location of the slow component of VO2 kinetics either within the exercising limbs or alternatively at some site in the rest of the body, e.g., ventilatory, cardiac or accessory muscles. 2) Presents evidence in support of both the fast and slow components (i.e., < 3 min and > 3 min from exercise onset, respectively) of the exercise VO2 response residing predominantly in the exercising muscle. For a pulmonary VO2 slow component in excess of 600 ml O2.min-1, more than 80% could be attributed to an augmented VO2 across the exercising limbs. 3) Assesses the potential for the lactate ion per se to exert a metabolic stimulatory effect in exercising muscle in the absence of the potentially confounding influences of changes in muscle temperature, H+, blood flow or O2 delivery. Within the surgically isolated, electrically stimulated canine gastrocnemius, square wave infusions that increased arterial blood [lactate] by approximately 10 mM and intramuscular [lactate] to in excess of 9 mM did not increase muscle VO2. In summary, these investigations demonstrate that the exercising muscle is the predominant site of the VO2 slow component. However, despite the close temporal association between changes in blood lactate and VO2 during intense exercise, lactate itself does not mandate an additional VO2 demand in exercising dog muscle.