Before training, our patients were severely symptomatic, as evidenced by a mean baseline peak Vo2 of 11.5 ± 0.4 ml/min per kg. After 6 and 12 weeks of training, peak Vo2 increased by 22% and 30%, respectively. The effects of exercise training at a conventional work load have been assessed by several investigators in patients with moderate congestive heart failure ([1–4]). Coats et al. ([3]) reported an 18% increase in peak Vo2 after 8 weeks of conventional training, whereas Sullivan et al. ([1]) and Hambrecht et al. ([4]) observed 23% and 31% increases in peak Vo2, respectively, after 24 weeks of training. Overall, the magnitude of the increase in peak Vo2 documented in our patients with low work load exercise training is comparable to that attained with training at conventional work loads. Recently, Bellardinelli et al. ([10]) documented a 17% increase in peak Vo2 with low intensity training for 8 weeks in patients with moderate congestive heart failure. Our data extend the benefits of training to patients with severe congestive heart failure. Our data also point out the dissimilar effects of exercising at low and conventional work loads on left ventricular diastolic wall stress. Although training at low work loads increases peak Vo2 to a similar extent as that of training at conventional work loads, the increase in left ventricular diastolic wall stress is significantly less. Finally, our data suggest that low work load training may increase peak Vo2 by enhancing maximal vasodilation in the trained limb, as evidenced by an increase in calf peak reactive hyperemia.