Background: Reduced heart pump function and skeletal muscle abnormalities are considered important determinants for the low physical exercise capacity in chronic heart failure. Because of reduced ventricular function, traditional physical rehabilitation may cause underperfusion and low local work intensity, thereby producing suboptimal conditions for skeletal muscle training.
Hypothesis: The study was undertaken to determine the effects of local exercise training, designed as one- or two-legged knee extensor training, on exercise capacity in patients with moderate chronic heart failure. Because such exercise models use only about one quarter to half the muscle mass used in cycle ergometer training, the influence of a restricted circulatory capacity should therefore be limited. Further, we aimed to determine whether or not chronic heart failure skeletal musculature abnormalities are counteracted with such training.
Methods: Fourteen patients with chronic heart failure [age 58 +/- 3 years, ejection fraction (EF) 28 +/- 4%] were randomized to two different training protocols three times a week for 8 weeks and compared with a nontraining control group (n = 7, age 62 +/- 3, EF 27 +/- 3%). Group 2L (n = 7) underwent simultaneous two-legged knee extensor training (about 4 kg working muscle) for 15 min at 65-75% of VO2 max of the two-legged kick. Group 1L (n = 7) trained each leg at a time for 15 min of continuous one-legged dynamic knee extensor work with the same training load per muscle mass, that is, at 35% of VO2 max of the two-legged kick (about 2 kg working muscle). Peak VO2 of two-legged knee extensor exercise (l/min), two-legged endurance (W), and strength (Nm) were determined before and after the training period. The activity of citrate synthase (CS) was estimated in tissue samples from the quadriceps femoris muscle.
Results: Peak VO2 did not change with training. Two-legged knee extensor endurance exercise capacity increased by an average of 40-50% (p < 0.01) in all training patients in both the 2L and 1L groups, while no change was observed in the control group. Depressed skeletal muscle CS activity increased by 25-35% in both training groups (p < 0.01). Strength increased by 16% in the 2L group after training (p < 0.05), while no change was seen in the 1L and control groups.
Conclusions: Skeletal muscle changes in stable moderate chronic heart failure are not entirely irreversible. A major factor contributing to these changes and to exercise limitation is deconditioning. Local muscle training is efficient and can at least partially improve skeletal muscle function in these patients. Different degrees of local activation, that is, one- or two-legged knee extensor exercise, do not seem to differ in terms of their effect on exercise capacity. Depressed skeletal muscle oxidative capacity adapts to such physical training with increased activity to an extent not different from that for healthy volunteers.