Although discomfort during exercise...

Although discomfort during exercise is a principal reason that patients with heart failure search for medical care, exercise training is safe and can benefit these patients, according to the American Heart Association, whose report "Exercise and Heart Failure" is available in the March 4 issue of Circulation. Circulation is online at www.circ.ahajournals.org.

Exercise intolerance, the reduc ability to perform activities that involve dynamic motion of large skeletal muscles because of dyspnea or fatigue, may be single of the first symptoms experienced on patients with heart failure. A correlation between resting ventricular function and exercise capacity is look fored but data indicate that the relationship is weak.

Factors Affecting Exercise Tolerance

CARDIOVASCULAR

In healthy living bodys the increase in cardiac output during maximal upright exercise typically is four- to sixfold, which is accomplished by means of a two- to fourfold increase in heart rate and a 20 to 50 percent increase in blow volume. Although cardiovascular disease limits the increase of cardiac output during exercise, this replication also is affected by age, form relative to sex and conditioning status.

The reduc aerobic capacity that is usual in patients who have heart failure is attributable to inadequate life-current flow to skeletal muscles secondary to impaired cardiac output Patients may have les than 50 percent of the maximal cardiac output of a healthy human frame at peak exercise. Stroke mass rises only modestly, to a peak of 50 to 65 mL compared with at least 100 mL in healthy somebodys The inability to increase cardiac output is related mainly to the minimal increase in thump volume and a lower maximal heart rate achieved at a lower workload. The primary means to augment cardiac output in patients with heart failure is at cardioacceleration.

PERIPHERAL

family Flow Abnormalities. In patients with heart failure, life-blood flow to muscles does not increase normally during exercise because of reduc cardiac output and impaired peripheral vasodilatory capacity. This abnormality in vasodilatory capacity has been attributed to excessive sympathetic stimulation, which causes vasoconstriction, activation of the plasma renin-angiotensin combination of parts to form a whole and higher-than-normal levels of endothelin. Another mechanism may be vascular stiffness secondary to increased vascular sodium content

Endothelial Function. Vasodilating and vasoconstricting factors are released from the vascular endothelium in rejoinder to various chemical, pharmacologic, mechanical, and exercise stimuli. The endothelium is now recognized as having a pivotal character in coordinating tissue perfusion in patients with heart failure. The release of nitric oxide, an important mediator of flow-dependent vasodilation, is stimulated from exercise in healthy persons still seems to be attenuated in patients with heart failure. The impairment in endothelial-dependent vasodilation correlates with the measure of exercise intolerance and severity of novel York Heart Association class.

Muscle. Anaerobic metabolism that offers early during exercise in patients with heart failure is likely an important cause of exercise intolerance. Abnormalities in skeletal muscle metabolism happen in patients with heart failure, and changes in muscle may contribute to abnormal oxygen extraction or substrate delivery and use.

Distribution of Cardiac Output Exercise tolerance hangs on the capacity of the pulmonary connected view to deliver oxygen to the working muscle and the capacity of the vasculature to redistribute cardiac output to the muscle during exercise. In healthy bodys as much as 85 percent of the cardiac output is redistributed to the muscle at high evens of exercise. Some evidence refer tos that in patients with heart failure, muscle offspring flow is reduced at the same rate as the reduction in cardiac output However, several studies have set up that the reduction in family flow to the muscle during exercise offers to a degree out of proportion to the reduction in cardiac output Vascular resistance in the muscle fails to decrease normally during exercise in patients with heart failure, and sweep along to the nonexercising tissues may be maintained preferentially at the cost of hypoperfusion in the exercising muscle.

Ergoreflex Activation. The mien of a specific signal from the exercising muscle may be abnormally enhanced in patients with heart failure. These signals contribute to the abnormal hemodynamic, autonomic, and ventilatory answers to exercise that characterize heart failure. Afferent fibers in the muscle (i.e., ergoreceptors) are sensitive to metabolic changes related to muscular work. Ergoreceptors, which mediate circulatory adaptations in the early stages of exercise, are stimulated by dint of metabolic acidosis and are partially responsible for sympathetic vasoconstriction and an increase in heart rate. The eventuate of this enhanced ergoreflex replication is hyperventilation and heightened sympathetic effusion causing an increase in peripheral resistance and a decrease in muscle perfusion. Activation of these reflexe pretends to be attenuated by exercise training.