Objective-To assess energy depletion in skeletal muscle in patients with congestive heart failure by measuring blood purine metabolites during exercise and, at the same time, determine the implications of the ammonia response to exercise in these patients. Setting-Tottori University Hospital, Yonago, Japan. Patients-49 heart failure patients (New York Heart Association (NYHA) grades I-III) and 16 normal subjects. Main outcome measures-Blood lactate, ammonia, and hypoxanthine levels were measured during exercise with expired gas analysis. Results-In normal exercising subjects as well as in each heart failure subgroup, the ammonia threshold was significandy higher than both the lactate threshold [control: 218 (SD 5.3) v 17-4 (3.3) ml/kg/min; NYHA class I: 18-9 (3.8) v 15*5 (2.6); class II: 14*8 (2.5) v 12-7 (2.4); class III: 13*5 (2.6) v 11-8 (2.5)] and the ventilatory threshold (P < 0-01). The difference between the ammonia and lactate thresholds was noted in all normal subjects and in all heart failure patients. The ammonia threshold, however, was significantly lower in heart failure patients than in normal subjects and it decreased with increasing NYHA class (P < 0.01). Maximum ammonia levels were lower in the heart failure group and decreased further with higher NYHA classifications [control: 198 (52)
These results suggest that treatment with alacepril may cause a reduction of sympathetic activation during orthostatic stress and may enhance arterial baroreflex function in patients with mild to moderate heart failure.
We assessed blood pressure and neurohumoral factors at rest and during exercise in 10 patients with essential hypertension before and after treatment with the new angiotensin converting enzyme inhibitor, alacepril (25-50 mg day-'). Alacepril significantly lowered mean blood pressure at rest and at the same exercise load as before treatment without affecting heart rate response. The response of plasma renin activity, plasma aldosterone, and plasma adrenaline were not changed by alacepril, but increase of plasma angiotensin II and plasma noradrenaline during exercise were significantly attenuated after alacepril treatment (ANOVA, P = 0.04, both). The change in mean blood pressure during exercise was positively correlated with the decrease in plasma angiotensin II (r = 0.65, P < 0.05). These results demonstrated that alacepril was effective in essential hypertension both at rest and during exercise, suggesting that the antihypertensive effect during exercise might be related to the decrease in pressor hormones, especially in plasma angiotensin II.
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