Exercise training in patients with severe congestive heart failure: Enhancing peak aerobic capacity while minimizing the increase in ventricular wall stress

Objectives. The aims of the study were to 1) assess the effects of 12 weeks of exercise training at low work loads (i.e., corresponding to less than or equal to 50% of peak oxygen consumption [VO2]) on peak VO2 and hyperemic calf blood flow in patients with severe congestive heart failure; and 2) evaluate left ventricular diastolic pressure and wall stress during exercise performed at work loads corresponding to less than or equal to 50% and 70% to 80% of peak VO2. Background. Whether the benefits of exercise training can be achieved at work loads that result in lower left ventricular diastolic wall stress than those associated with conventional work loads is unknown in patients with severe congestive heart failure. Methods. Sixteen patients with severe congestive heart failure trained at low work loads for 1 h/day, four times a week, for 12 weeks. Peak VO2 and calf and forearm reactive hyperemia were measured before and during training, Nine of the 16 patients underwent right heart catheterization and echocardiography during bicycle exercise at low and conventional work loads (i.e., 50% and 70% to 80% of peak VO2, respectively). Results. The increase in left ventricular diastolic wall stress was substantially lower during exercise at low work loads than during exercise at conventional work loads, (i.e., [mean +/- SEM] 23.3 +/- 7.4 vs. 69.6 +/- 8.1 dynes/cm(2) (p < 0.001). After 6 and 12 weeks of training, peak VO2 increased from 11.5 +/- 0.4 to 14.0 +/- 0.5 and 15.0 +/- 0.5 ml/kg per min, respectively (p < 0.0001 vs. baseline for both). Peak reactive hyperemia significantly increased in the calf but not in the forearm. The increases in peak VO2 and calf peak reactive hyperemia correlated closely (r = 0.61, p < 0.02). Conclusions. In patients with severe congestive heart failure, peak VO2 is enhanced by exercise training at work loads that result in smaller increases in left ventricular diastolic wall stress than those observed at conventional work loads. (C) 1997 by the American College of Cardiology.