Exercise In Chronic Heart Failure Research Articles

Altered skeletal muscle metabolic response to exercise in chronic heart failure. Relation to skeletal muscle aerobic enzyme activity.

Exertional fatigue, which frequently limits exercise in patients with chronic heart failure, is associated with early anaerobic metabolism in skeletal muscle. The present study was designed to examine the skeletal muscle metabolic response to exercise in this disorder and determine the relation of reduced muscle blood flow and skeletal muscle biochemistry and histology to the early onset of anaerobic metabolism in patients. We evaluated leg blood flow, blood lactate, and skeletal muscle metabolic responses (by vastus lateralis biopsies) during upright bicycle exercise in 11 patients with chronic heart failure (ejection fraction 21 +/- 8%) and nine normal subjects. In patients compared to normal subjects, peak exercise oxygen consumption was decreased (13.0 +/- 3.3 ml/kg/min versus 30.2 +/- 8.6 ml/kg/min, p less than 0.01), whereas peak respiratory exchange ratio and femoral venous oxygen content were not different (both p greater than 0.25), indicating comparable exercise end points. At rest in patients versus normals, there was a reduction in the activity of hexokinase (p = 0.08), citrate synthetase (p less than 0.02), succinate dehydrogenase (p = 0.0007), and 3-hydroxyacyl CoA dehydrogenase (p = 0.04). In patients, leg blood flow was decreased at rest, submaximal, and maximal exercise when compared to normal subjects (all p less than 0.05), and blood lactate accumulation was accelerated. In patients, during submaximal exercise blood lactate levels were not closely related to leg blood flow but were inversely related to rest citrate synthetase activity in skeletal muscle (r = -0.74, p less than 0.05). At peak exercise there were no intergroup differences in skeletal muscle glycolytic intermediates, adenosine nucleotides, or glycogen, whereas in patients compared to normal subjects less lactate accumulation and phosphocreatine depletion were noted (both p less than 0.05), suggesting that factors other than the magnitude of phosphocreatine depletion or lactate accumulation may influence skeletal muscle fatigue in this disorder. The results of the present study suggest that in patients with chronic heart failure reduced aerobic activity in skeletal muscle plays an important role in mediating the early onset of anaerobic metabolism during exercise. Our findings are consistent with the concept that reduced aerobic enzyme activity in skeletal muscle is, in part, responsible for determining exercise tolerance and possibly the response to chronic intervention in patients with chronic heart failure.

Multicentre study of the determination of peak oxygen uptake and ventilatory threshold during bicycle exercise in chronic heart failure

Assessment of the ventilatory threshold (VT) has been proposed to assess exercise tolerance more objectively, particularly in clinical trials, but reproducibility, interobserver variability and feasibility of the graphical methods for determination of VT have not been properly studied in patients with chronic heart failure (CHF). Fifty-one patients with mild to moderate CHF (mean peak oxygen uptake (VO2): 20.5 ml.min-1.kg-1) were assessed during two consecutive bicycle exercise tests within 8 days. Two graded exercise protocols were compared with stages of 30 W every 3 min (22 patients) or 10 W/min (29 patients). VT was determined separately by five trained physicians using five different graphical methods. The 'crossing method' (first crossing of the VCO2 and VO2 curves) yielded the highest rate of determination (88%) but tended to overestimate the mean VT. The VE method (disproportionate increase of ventilation relative to VO2) produced the best interobserver agreement (coefficient of variation = 78%). Peak VO2 was very highly reproducible in both exercise protocols (relative difference 2-test 1/test 1 = -0.32% for the 30 W 3 min protocol; +2.18% for the 10 W.min-1 protocol). The reproducibility of VT was slightly lower regardless of the graphical method used to determine it (relative differences varied from -3.3% to +7.3%). Therefore, peak VO2 appears more suitable than VT for assessment of exercise tolerance in CHF.

Respiratory and circulatory analysis of CO2 output during exercise in chronic heart failure.

The output of carbon dioxide (VCO2) is controlled by both hemodynamics and ventilation. To understand VCO2 in patients who have chronic heart failure (CHF), we studied 14 patients who had New York Heart Association functional class III failure by measurements of hemodynamics, ventilation, and arterial and venous blood gases at rest and at 50 W of cycle ergometry exercise. Fick principle analysis of VCO2 showed that because of a limited increase in cardiac output, CHF patients widened their venoarterial CO2 content difference from 4.9 +/- 3.5 ml/dl at rest to 11.1 +/- 4.0 ml/dl with exercise (p less than 0.05). This increase in CO2 content difference was achieved with no change in venous CO2 content (from 54.3 +/- 3.3 ml/dl at rest to 54.5 +/- 4.8 ml/dl at exercise, p = NS); however, there was a decrease of arterial CO2 content (from 49.4 +/- 3.7 ml/dl at rest to 43.4 +/- 2.3 ml/dl with exercise, p less than 0.05). Modeling of the CO2 tension-content relation showed that there would have been a small, nonproportional increase of venous CO2 content as venous CO2 tension increased from 43.2 +/- 1.8 mm Hg at rest to 55.3 +/- 4.2 mm Hg during exercise (p less than 0.05); however, the development of metabolic acidosis during exercise entirely blunted the increase of CO2 content. In contrast, both the shape of the tension-content relation and the acidosis of exercise further influenced the decrease of arterial CO2 content as arterial CO2 tension decreased from 37.0 +/- 2.9 mm Hg at rest to 32.0 +/- 3.4 mm Hg during exercise (p less than 0.05) as a result of excess ventilation. In CHF patients during exercise, the circulatory limitations imposed by a low cardiac output on VCO2 are compensated by a widened venoarterial CO2 content difference. The content difference is not widened through an increase of venous CO2 content but rather by a decrease of arterial CO2 content caused by arterial hypocapnia and metabolic acidosis.

The role of oxygen extraction in peripheral tissues in exercise capacity in chronic heart failure.

To elucidate the role of oxygen extraction during exercise in chronic heart failure (CHF), 26 patients underwent the symptom-limited maximal exercise. Hemodynamics, oxygen uptake (VO2) and blood gas were examined during exercise. Group I (n = 16, VO2max less than 20 ml/min/kg) showed severe cardiac dysfunction during exercise compared with group II (n = 10, VO2max greater than or equal to 20 ml/min/kg). Though VO2 was similar in both groups at rest and with a 25-watt load, oxygen extraction was significantly higher in group I than in group II. At the maximal work load, VO2max was significantly lower in group I, whereas there was no significant difference in oxygen extraction between the two groups. With a 25-watt load, mixed venous partial oxygen tension was similar, however, oxygen saturation was significantly lower in group I. It was concluded that oxygen extraction during exercise rapidly increased in group I, and this may play an important role in the maintenance of exercise capacity during mild physical activity in CHF.

Dynamics of Dyspnoea during Exercise in Chronic Heart Failure

Dynamics of Dyspnoea during Exercise in Chronic Heart Failure

Discrepancy between first—dose converting enzyme inhibition at rest and subsequent inhibition during exercise in chronic heart failure

Low-dose angiotensin-converting enzyme inhibition is thought to completely block the renin-angiotensin system. This study examined the hemodynamic and hormonal responses to initial low- and higher dose converting-enzyme inhibitor (lisinopril or captopril) at rest compared with the response during subsequent chronic therapy while treadmill exercise testing was performed in nine patients with chronic heart failure. At rest, similar changes in systemic arterial pressure, plasma renin activity, and plasma aldosterone concentration were found with initial low and higher doses. However, after at least 4 weeks of therapy, dose-dependent increases in plasma renin activity and decreases in plasma aldosterone concentration were noted during exercise without significant differences in exercise systemic arterial pressure or heart rate. This discrepancy suggests that initial low-dose converting enzyme inhibition does completely block the enzyme, but higher dose therapy is required for complete blockade during subsequent exercise in chronic heart failure.

Regulation of active Na+-K+ transport in skeletal muscle.

Regulation of active Na+-K+ transport in skeletal muscle.

Haemodynamics, Distribution of Blood Flow and Lactate Concentrations at Rest and during Treadmill Exercise in Chronic Heart Failure: Effects of Oral Pirbuterol

Haemodynamics, Distribution of Blood Flow and Lactate Concentrations at Rest and during Treadmill Exercise in Chronic Heart Failure: Effects of Oral Pirbuterol

Paradox of improved exercise but not resting hemodynamics with short-term prazosin in chronic heart failure

In patients with chronic heart failure exercise allows the simultaneous observation of the cardiovascular pathophysiology and the symptoms of these patients. We administered short-term, oral prazosin to 10 patients with severe chronic heart failure. Prazosin increased cardiac output and stroke volume significantly during exercise (both P < 0.05) but not at rest (both P > 0.10). Prazosin decreased the arteriovenous oxygen difference and left ventricular filling pressure significantly during exercise (both P < 0.05) but not at rest (both P > 0.10). There was no significant correlation between prazosin-induced changes at rest and during exercise in cardiac output ( r = 0.12), stroke volume ( r = 0.02), arteriovenous oxygen difference ( r = 0.33) or left ventricular filling pressure ( r = 0.43). Prazosin predominantly affects hemodynamics during exercise because its pharmacologic activity as an alpha-adrenergic blocking agent is most prominent during exercise. The full evaluation of prazosin-induced changes in the hemodynamics of patients with chronic heart failure requires evaluation during exercise.