Failure to augment maximal limb blood flow in response to one-leg versus two-leg exercise in patients with severe heart failure.

Abstract

Lower limb blood flow, oxygen uptake, and femoral vein 02 content were measured at rest and during maximal bicycle exercise, performed with two legs and one leg, in four normal subjects and in five patients with severe congestive heart failure. While in normal subjects femoral vein blood flow and lower limb vascular conductance were significantly greater during one-leg exercise than during two-leg exercise (6084 + 745 vs 5370 + 803 ml/min, p < .05, and 52.3 8.0 vs 45.1 + 8.2 U x 1o3, p < .05, respectively), in patients with severe congestive heart failure these values were similar during the two forms of exercise (1082 ± 459 vs 1053 ± 479 m/min and 9.6 ± 3.7 vs 9.4 + 3.5 U x 103, respectively). In five additional patients, one-leg maximal bicycle exercise was performed before and after administration of phentolamine into the femoral artery of the active leg. Regional a-adrenergic blockade with phentolamine did not alter maximal oxygen uptake attained during one-leg bicycle exercise (9.8 ± 1.5 vs 10.3 ± 1.9 ml/kg). Lower limb blood flow and femoral vein 02 content attained during maximal one-leg exercise were also similar before and after phentolamine. Thus, in contrast with normal subjects, patients with severe congestive heart failure were unable to further increase limb blood flow during one-leg bicycle exercise. Moreover, local a-adrenergic blockade does not augment blood flow to the active limb during maximal one-leg bicycle exercise. This suggests that the ability of the muscular vasculature to vasodilate during exercise is impaired and may be a limiting factor to maximal exercise capacity in such patients. Circulation 74, No. 2, 245-251, 1986. PATIENTS with congestive heart failure, when compared with normal subjects, have a reduced metabolic arteriolar vasodilative response after restoration of flow to an ischemic limb.1 They also do not have an adequate increase in forearm blood flow in response to rhythmic handgrip exercise of increasing intensity.2 Thus, an inability of the peripheral muscle vasculature to dilate appropriately during dynamic exercise may be a limiting factor to maximal exercise capacity in patients with severe congestive heart failure.In normal subjects, during graded exercise involving 40% or more of the total muscle mass, such as bicycling with two legs, maximal functional capacity, i.e., oxygen uptake, is limited by the ability of the heart to increase its output. In contrast, when graded exercise involves a smaller percentage of the total mus- Received Jan. 9, 1986; revision accepted May 5, 1986. cle mass, such as bicycling with one leg, maximal exercise capacity is attained before maximal cardiac output or V02 max is reached, suggesting that a lack of output by the heart is no longer the limiting factor. Of interest, when the effects of one-leg vs two-leg bicycle exercise are compared in normal subjects, the maximal workload per leg is greater during one-leg exercise than during two-leg exercise, suggesting that peak blood flow to the active limb during two-leg exer...

Cutaneous Arteriolar Thioredoxin Expression in Patients With Heart Failure.

“…Most investigators have studied the reduced blood flow response in the arm and during exercise in patients with CHF. 9 On the other hand, completely normal vasodilator capacity and vascular resistance have also been demonstrated in CHF, 10,11 and some of this discrepancy could be related to differences in the duration or severity of the CHF in the patients studied.…”

“…7 In addition, it has been demonstrated that TRX is induced in the myocardium by inflammatory or oxidative stress stimuli. 9 There is a definite correlation between oxidative stress and ventricular dysfunction, and the ventricular remodeling and progressive dilation leading to endstage heart failure may be mediated by oxygen-derived free radicals. We have already demonstrated that serum concentrations of TRX are increased in patients with heart failure, 7 suggesting excessive oxidative stress in this condition.…”

Alterations of skeletal muscle in chronic heart failure.

“…The normal subjects had a normal physical examination, ECG, chest x-ray, M-mode and two-dimensional echocardiographic evaluation, and a normal peak oxygen consumption (peak Vo2 >25 ml/min/kg). All 3.3'-diaminobenzidine-tetra HCl in 10 ml TrisHCl buffer at pH 7.2. The sections were incubated at 37°C in a water bath for 180 minutes.…”

Cardiac Output Response to Exercise in Chronic Cardiac Failure Patients

“…1,2) Because oxygen uptake (V ・ O 2 ) is the product of cardiac output (CO) and the arterio-venous oxygen content difference [C(a-v)O 2 ], a decrease in peak V ・ O 2 may be due to a decrease in either CO and/or C(a-v)O 2 at peak exercise. The CO response of patients with CHF during exercise is attenuated compared to that in normals.…”