For constant-load, heavy exercise (i.e., above the lactate threshold (TLac)), a slow component of oxygen uptake (VO2) is observed. Endurance training reduces the magnitude of the slow component and, hence, end-exercise VO2. Reductions in exercise VO2 have been reported after 7-8 wk of training; unpublished observations suggest that the VO2 slow component may be attenuated after just 2 wk of training. A minimum training intensity for eliciting reductions in constant-load exercise VO2 has not been established; however, in the elderly, training at an intensity below TLac resulted in similar reductions in exercise VO2 as did training above TLac. Mechanisms responsible for the reduced slow component of VO2 after training remain to be firmly established. Evidence both for and against blood lactate concentration ([L-]) as a mediator of the slow component has been published; high correlations between [L-] and the slow component, and between the training-induced reductions in these variables, appear to be more coincidental than causal. Decreased pulmonary ventilation after training may account for between 14% and 30% of the reduction in the slow component of VO2. Epinephrine infusion does not augment exercise VO2, nor does beta-adrenergic blockade diminish the magnitude of the slow component of VO2.