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 Reductions in exercise VO2 have been reported after 7-8 wk of training; unpublished observations suggest that the VO2 slow component may be attenuated after just 2 wk of training.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 beta-adrenergic blockade diminish the magnitude of the slow component of VO2.