[Effects of aerobic training in patients with moderate chronic heart failure]

To evaluate the effects of a program of moderate intensity in patients (pts) with clinically stable chronic heart failure (CHF), we studied 20 pts (18M, 2F, mean age 61 years) with dilated cardiomyopathy, Weber Class B, ejection fraction (EF) < 40% and aerobic capacity of 16 +/- 2 ml/kg/min on cardiopulmonary exercise testing. We randomly assigned pts to 2 groups, a training group (T, 10 pts) and a control group (C, 10 pts), similar for anatomical and clinical characteristics, group T underwent a thrice weekly, 8 week-long ambulatory program of aerobic activity, beginning at 40% of maximal oxygen uptake. At the end, in Group T we observed a significant increase of exercise tolerance (+45%; p < 0.005), peak oxygen uptake (VO2 max) (+20%; p < 0.001), anaerobic ventilatory threshold (AT) (+37%; p < 0.005), lactate threshold (+36%; p < 0.005), peak heart rate (< 10%; p < 0.01) and of peak systolic pressure (+12%; p < 0.007); and a significant reduction in resting heart rate (-17%; p < 0.005), resting diastolic pressure (-11%; p < 0.005), plasma lactate (LA) at rest (-26%; p < 0.01), at peak (-21%; p < 0.005) and at recovery (-22%; p < 0.005), plasma norepinephrine (NE) both at rest (-38%; p < 0.005) and at peak (-13%; p < 0.005) and of plasma epinephrine (E) (-38%; p < 0.005; -32%, p < 0.001, respectively). We observed no change in EF at the end in both groups nor any untoward cardiac effects during training. We didn't note any correlation between AT and venous oxygen saturation (r = 0.15; p = 0.65) changes at the end. The increase in peak VO2 after training was not correlated to any AT increase (r = 0.12; p = 0.72). We observed, however, a significant correlation between lactate threshold and AT changes after training (r = 0.81; p = 0.005) and between LA and resting, submaximal and peak NE (r = 0.89; p = 0.005) and E (r = 0.78; p = 0.007) changes at the end of training.

a) in pts with clinically stable CHF a program of aerobic activity well tolerated in terms of frequency, intensity and duration may determine a significant increase in exercise tolerance, aerobic capacity, AT and LA threshold, and a significant decrease in plasma LA, NE and E at rest, submaximal and peak levels; b) in our opinion, such modifications are partly determined by a delay in lactate accumulation and partly by sympathetic tone lowering, and permit us to underline the concept that physical inactivity may provoke important peripheral changes that, in turn, may reduce exercise tolerance and aerobic capacity, by creating a vicious circle difficult to break by medical therapy alone.