For the patient with heart failure, fatigue and dyspnea are the exercise-limiting factors. The pathophysiologist tends to subsume these factors in the peak oxygen consumption (VO, max), obtained by cardiopulmonary testing. In normal individuals, V02 max ranges from 30 to 40 mL’1-min’1-kg’1; some patients with heart failure do not exceed 10 mL’1-min’1-kg’1. Although there is some correlation between clinical symptoms and peak V02, the correlation between peakV02 and most hemodynamic indicators measured at rest is poor. Two reasons may explain this discrepancy:
Hemodynamic parameters at rest do not explore cardiac contractile reserve during exercise. Only when cardiac output and chronotropic reserve are measured during exercise do they correlate with V02. Peak cardiac output correlates with peak exercise capacity.
Cardiac hemodynamic parameters at rest ignore peripheral (circulation and muscle) factors.
The various determinants of peak V02 must therefore be taken into account when considering exercise capacity in heart failure (Table).
Cardiac factors limiting exercise capacity Heart rate response
Tachycardia increases cardiac output and is thus a favorable and necessary adaptive mechanism during exercise. An impaired heart rate response limits exercise capacity by decreasing total cardiac output. In the failing heart chronotropic reserve is impaired for a variety of reasons. Patients often have resting tachycardia, with correspondingly less margin available for exertion. Neurohumoral mechanisms, such as (3-receptor desensitization and the reduced rise of norepinephrine levels during exercise, also contribute to the blunted heart rate and contractile responses to exertion.
Stroke volume response
In the normal heart during exercise, a slight increase in end-diastolic volume is accompanied by a decreased end-systolic volume, resulting in an increased left ventricular contractile response, and hence an increased stroke volume. In the failing heart, the volumes tend to be markedly increased, since the heart is usually dilated. As in the normal heart, end-diastolic volume (EDV) increases during exertion with the increase in pressure gradient, but due to the impaired contractile response, end-systolic volume remains markedly increased and stroke volume correspondingly decreased. There are also diastolic changes: elevated end-systolic pressures and increased wall stiffness shorten the filling time. Although tachycardia intervenes as a reflex compensatory mechanism, it further shortens diastole and thus compounds the hemodynamics. In summary, exercise capacity is limited in heart failure because systolic and diastolic dysfunction both contribute to inadequate cardiac output.
Peripheral factors limiting exercise capacity
Peripheral vascular response to exercise
Much evidence suggests that systemic vascular resistance during exercise is higher in heart failure patients than in normal subjects and thus limits exercise capacity by decreasing the blood flow to muscle. Various observations support the concept of muscle blood flow modulation by intrinsic vascular changes that determine the capacity for vasodilatation. It has been observed that patients… can increase their peak oxygen consumption during exercise when arm exercise is added to leg exercise, suggesting that the periphery plays a fundamental role in determining exercise capacity.
In the neurohumoral hyperstimulation that characterizes heart failure, vasoconstrictor antinatriuretic systems predominate over vasodilatory natriuretic systems (natriuretic peptides, prostaglandins). Vasoconstrictor agents such as endothelin, prostaglandins, and angiotensin II are all overproduced in heart failure, causing a rise in peripheral resistance. Abnormalities in endothelium-mediated vasodilatation have also been identified. Thus, acetylcholine-mediated nitric oxide release and nitric oxide synthase gene expression are both impaired in heart failure.
Chronic exposure to the modified neurohumoral environment induces vascular remodeling, consisting of adaptive functional and morphological changes. There is experimental evidence that exposing the vessel wall to components such as angiotensin II and a sodium concentrated environment induces vascular structural abnormalities. Angiotensin II, for example, induces smooth muscle cell hypertrophy.
Peripheral muscle response
In heart failure, due to malnutrition, deconditioning, and the toxic effects of circulating cytokines such as tumor necrosis factor (TNF), muscle is typically atrophic. The wasting syndrome, or cardiac cachexia, has a number of histological features. Infiltration by fatty tissue decreases functional muscle mass. Type lib fast-glycolytic muscle fibers replace type I slow-oxidative fibers. Mitochondria become fewer and smaller. Coupled with the decrease in Krebs cycle enzymes, these changes explain why heart failure patients work in anaerobiosis during exercise. The decreased energy yielded by anaerobic metabolism can only in turn decrease exercise capacity.
Both cardiac and peripheral factors limit exercise capacity in heart failure. Although much data are still preliminary, advances in the understanding of the multifactorial determinants of exercise capacity have suggested ways of enhancing exercise capacity. Abnormal neurohumoral activation plays an important role. Thus, inhibition of the detrimental effects of a specific neurohumoral system can increase exercise capacity. Long-term angiotensin-converting enzyme inhibition augments peripheral blood flow. Furthermore, rehabilitation programs reverse the morphological and enzymatic changes in deconditioned peripheral muscle. These are just two examples of the practical implications of our improved understanding of the factors limiting exercise capacity.
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