Influence of endurance training and catecholamines on exercise VO₂ response

For constant-load, heavy exercise (i.e., above the lactate threshold (T_Lac)), 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 Reductions in exercise VO₂ have been reported after 7-8 wk of training; unpublished observations suggest that the VO₂ slow component may be attenuated after just 2 wk of training.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 T_Lac resulted in similar reductions in exercise VO₂ as did training above T_Lac. 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 β-adrenergic blockade diminish the magnitude of the slow component of VO₂.