Exercise Training in Heart Failure: How?

Abstract

Patients with congestive heart failure (CHF) reach a lower peak oxygen uptake (peak VO2) than that attained by ageand sex-matched healthy subjects [1,2]. In CHF patients, there has been no relationship observed between left ventricular ejection fraction (LVEF) and peak exercise performance [1,2]. Furthermore, peak VO2 is not related to the change in LVEF from rest to peak exercise. Also, acute improvements of central hemodynamics have not been found to acutely improve exercise performance, while longterm improvements do result in a signi~cant increase in peak VO2 [1,2]. These ~ndings suggest that the reduction in exercise capacity experienced by CHF patients may be more signi~cantly in_uenced by factors other than poor ventricular function. Patients with CHF have been found to have reduced maximum muscle strength compared to healthy individuals, greater fatigue at a given workload, and a lower peak VO2. Skeletal muscle atrophy has been observed and can occur early in the course of the disease [1,2]. Furthermore, signi~cant positive linear relationships have been found between peak VO2 and measures of skeletal muscle mass, suggesting that muscle atrophy contributes to effort intolerance. Muscle atrophy is not the only factor responsible for reduced performance since the results from a number of studies would suggest that the impairment of skeletal muscle blood _ow may also play at least a partial role. A number of potential mechanisms underlie the reduction in vasodilatory capacity, including a reduction in endothelium-derived relaxing factor, salt retention, and increases in various vasoconstrictive neurohormones such as endothelin, norepinephrine, renin, angiotensin II, and vasopressin [1,2]. Abnormalities in skeletal muscle metabolism have been observed in CHF patients that could impair exercise capacity. The abnormalities of metabolism are independent of the effects of muscle atrophy and reductions in blood _ow observed in these patients. Finally, abnormalities of skeletal muscle histology and biochemistry have been observed that could contribute to the impairment of exercise capacity found in CHF patients [1,2]. These ~ndings in the skeletal muscle have led to the development of the skeletal muscle hypothesis to explain exercise intolerance in CHF patients [3]. This theory suggests that left ventricular dysfunction sets in motion a series of events that leads to abnormalities of skeletal muscle metabolism, function, and atrophy. In response to these changes, the patient experiences both muscle fatigue and dyspnea, as well as excessive vasoconstrictor drive to nonexercising vascular beds. The theory suggests that after instituting treatment to correct hemodynamics, there will be a delay in the improvement of exercise capacity until there has been resolution of the skeletal muscle abnormalities. Exercise training would potentially speci~cally reverse the changes found in the skeletal muscles of CHF patients. Standardized guidelines for exercise training of CHF patients have not been established, although some recommendations have been made for this patient population [4]. These recommendations have been based on the results of previous studies or on experience from rehabilitation of coronary patients without CHF and have been modi~ed for the CHF population [1,4]. Furthermore, these recommendations have not taken into consideration the results of more recent studies outlining alternative strategies for exercise training of CHF patients. Any recommendations for exercise training should be based on the underlying pathophysiology found in CHF patients. Accordingly, the documented pathophysiology would support the use of an exercise training program designed to improve the aerobic and strength capacities of these patients. The purpose of this article is to review training techniques used in CHF patients and to provide direction as to the type of exercise training program that could be used by these individuals.