1. To determine if the recovery period after exercise is abnormal in chronic cardiac failure, we studied 15 patients with stable chronic cardiac failure, and 14 normal subjects during and after symptom-limited maximal treadmill exercise. 2. In patients, O 2 consumption fell exponentially from 16.8 (13.7-20.0) ml min −1 kg −1 at peak exercise to 6.0 (5.2-6.7) ml min −1 kg −1 at 3 min of recovery and in control subjects it fell from 30.2 (27.0-33.5) ml min −1 kg −1 to 6.7 (5.9-7.4) ml min −1 kg −1 (mean and 95% confidence intervals). The associated decay constants were slower in patients [0.70 (0.58-0.83) min −1 versus 0.93 (0.81-1.05) min −1 in control subjects ( P < 0.01, t -test)]. 3. CO 2 consumption kinetics displayed similar abnormalities [( k : 0.55 (0.41-0.69) min −1 versus 0.71 (0.59-0.83) min −1 , P < 0.05)] and heart rate kinetics showed a similar trend [( k : 0.53 (0.33-0.74) min −1 versus 0.76 (0.62-0.89) min −1 , P = 0.08]. 4. We conclude that patients with cardiac failure recover more slowly from exercise than normal subjects, and that this may further impair their ability to perform exercise, with consequent effect on quality of life.
1. Resting energy expenditure has previously been shown to be elevated in the acute phase of heart failure, but the situation in the compensated state of chronic cardiac failure is unclear. Resting energy expenditure was assessed in 14 patients with stable chronic cardiac failure and 14 matched control subjects by using indirect calorimetry. 2. Resting energy expenditure was significantly elevated in the patients with chronic cardiac failure (112.6 ± 18.1 versus 87.1 ± 12.2 kJ day −1 kg −1 total body weight, P < 0.0002; mean ± sd ) as were resting O 2 consumption (3.88 ± 0.64 versus 3.00 ± 0.43 ml min −1 kg −1 , P < 0.0002), ventilation (164 ± 40.3 versus 104 ± 16.2 ml min −1 kg −1 , P < 0.0001) and heart rate (85.8 ± 16.9 versus 66.6 ± 6.9 beats/min, P < 0.001). Both the resting plasma concentration of noradrenaline (4.48 ± 1.52 versus 2.28 ± 0.96 nmol/l, P < 0.0001) and the serum concentration of free fatty acids (0.78 ± 0.21 versus 0.57 ± 0.27 mmol/l, P < 0.03) were greater in the patients with chronic cardiac failure. Analysis of covariance indicated that most of the difference in resting energy expenditure could be accounted for by the elevated ventilation in the patients with chronic cardiac failure. Arm muscle area, an index of wasting, was lower in the patients with chronic cardiac failure (39.1 ± 13.1 versus 50.5 ± 9.4 cm 2 , P < 0.02) and resting energy expenditure was found to account for some of this difference. 3. We conclude that an elevated basal metabolism occurs in chronic cardiac failure. It is associated with excess ventilation, and could be an aetiological factor in the development of cardiac cachexia.
1. Skeletal muscle metabolism in chronic cardiac failure may be influenced by the many circulatory and neurohumoral adaptations in the condition. We investigated aerobic metabolism during exercise using indirect calorimetry in 15 patients with chronic cardiac failure and in 14 control subjects. Subjects exercised on a treadmill for 20 min at a steady-state submaximal workload. 2. Venous lactate levels were relatively constant throughout the exercise, although they were slightly greater in the patients with chronic cardiac failure than in the control subjects. The respiratory exchange ratio was lower in patients with chronic cardiac failure (0.777 ± 0.021 vs 0.833 ± 0.037, means ± sd; P < 0.0002, Mann-Whitney U -test). Relative fat utilization, expressed as a percentage of total energy expenditure, was therefore greater in patients with chronic cardiac failure (71.8 ± 7.0 vs 54.1 ± 12.3%, P < 0.0005) and this was mirrored in a lower carbohydrate utilization (24.7 ± 6.5 vs 43.3 ± 12.1%, P < 0.0002). Levels of free fatty acids, glycerol and noradrenaline were greater in patients with chronic cardiac failure. 3. We conclude that there is an increased reliance on fat, as opposed to carbohydrate, metabolism during exercise in chronic cardiac failure, and that this may relate to the elevated catecholamine and free fatty acid levels present. This may be a compensatory mechanism to preserve muscle glycogen stores, but as fat utilization is less efficient in terms of oxygen consumed, this shift may further impair exercise capacity.
1. To examine the importance of angiotensin II formation in the production of frusemide's acute peripheral venous and arterial responses, the effect of pretreatment with captopril was studied. 2. Captopril abolished the acute increases in venous capacitance and blood pressure and attenuated the increases in forearm vascular resistance produced by intravenous frusemide. 3. The study provides evidence that angiotensin II formation performs an essential role in the production of the acute vascular effects of frusemide in man.