Background: Among the factors that contribute to limiting exercise tolerance in chronic heart failure are reduced peripheral blood flow and impaired vasodilatory capacity. Exercise training improves vasodilatory capacity in normal subjects, but controlled studies of exercise training evaluating upper and lower limb blood flow rates have not been performed in patients with reduced ventricular function. Improved vasodilatory capacity could help explain how training increases exercise capacity in these patients.
Methods: Twenty patients (mean age 55 +/- 6 years) with reduced left ventricular function (mean ejection fraction 32% +/- 6%) after a myocardial infarction were randomized to a 2-month high-intensity residential rehabilitation program or to a control group and were monitored over the subsequent year. Both groups were treated according to current practice with angiotensin-converting enzyme inhibition therapy. Training began 1 month after myocardial infarction. Baseline and postischemic flow rates were measured by plethysmography in both the upper and lower limbs 1 month, 3 months, and 1 year after the infarction. Peak oxygen uptake (VO2) and cardiac output were measured before and after training, and peak VO2 was determined again after 1 year.
Results: After 2 months of training peak VO2 increased 25%, VO2 at the lactate threshold increased 40%, and maximal cardiac output increased from 12.1 +/- 1.6 L/min to 13.9 +/- 2.4 L/min in the exercise group (all p < 0.05), whereas no differences were observed in the control group. At the 1-year follow-up no further increases in peak VO2 were noted in either group, but the higher value persisted in the trained group. However, changes in limb flow rates were poorly related to changes in both peak VO2 and maximal cardiac output. Improvements in baseline and postischemic flow rates occurred mainly in the lower limbs and were observed in the two groups to a similar degree.
Conclusion: Exercise training is highly effective in improving exercise capacity in patients with reduced ventricular function after myocardial infarction. These improvements parallel an increase in maximal cardiac output, but they are unrelated to vasodilatory capacity. In patients with reduced ventricular function after myocardial infarction, lower limb vasodilatory capacity improves gradually over the subsequent year, and these improvements occur irrespective of exercise training.