Ventilatory Anaerobic Threshold and Improves Submaximal Exercise Performance

We have recently demonstrated that exercise training can induce important hemodynamic and metabolic adaptations in patients with chronic heart failure due to severe left ventricular dysfunction. This study examines the accompanying changes in submaximal exercise performance and the ventilatory response to exercise in these patients. Before and after 16-24 weeks of exercise training, subjects underwent two symptom-limited bicycle exercise tests, one with an incremental graded workload, and one vwith a constant workload that represented 79±11% of the pretraining peak oxygen consumption. Breath-by-breath expired gas analysis was performed continuously during each test, and central hemodynamic, leg blood flow, and blood lactate measurements were obtained during the incremental protocol. The ventilatory anaerobic threshold was determined during the incremental exercise study from coplotted breathby-breath ventilatory data with standard criteria by observers who were unaware of patient identity or training status. As previously reported, exercise training increased peak oxygen consumption by 23% from 16.8±3.8 to 20.6±4.7 ml/kg/min and reduced blood lactate levels during submaximal exercise. The training-induced decrease in lactate accumulation was accompanied by a decrease in carbon dioxide production, respiratory exchange ratio, and ventilation during submaximal exercise. The ventilatory anaerobic threshold was delayed from 284±43 to 352+±91 seconds of exercise (p=0.02), and it occurred at an increased oxygen consumption (10.1+1.2 vs. 12.1+2.6 ml/kg/mmn, p=0.01). Exercise duration during the constant workload protocol increased from 938+±410 to 1,429±691 seconds (p<0.01). Thus, exercise training improved submaximal and maximal exercise performance in patients with chronic heart failure. The present study provides further evidence of a close physiologic link between the ventilatory and metabolic responses to exercise in patients with chronic heart failure, which is similar to that previously described in normal subjects, and demonstrates that an intervention that causes a significant delay in lactate accumulation during exercise can be accompanied by an appropriate change in the ventilatory anaerobic threshold. (Circulation 1989;79:324-329)