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Exercise for Those With Chronic Heart Failure

Matching Programs to Patients

Randy W. Braith, PhD

Exercise and Sports Cardiology Series
Editor: Paul D. Thompson, MD

THE PHYSICIAN AND SPORTSMEDICINE - VOL 30 - NO. 9 - SEPTEMBER 2002


In Brief: Exercise training increases functional capacity and improves symptoms in selected patients with chronic heart failure and moderate-to-severe left ventricular systolic dysfunction. Patients should be assessed before they start an exercise program. Initial programs should be supervised, and the duration increased as tolerated. The most consistent benefits occur with exercise done at least three times per week for 12 or more weeks. Aerobic sessions can vary from 20 to 40 minutes, at 50% to 85% of peak heart rate on graded exercise tests or 40% to 70% of peak oxygen consumption. Low-risk patients who have completed at least 6 to 12 weeks of exercise without adverse effects may incorporate light-to-moderate resistance training.

Chronic heart failure (CHF) in the United States is now pandemic. Approximately 500,000 new cases are diagnosed each year, and 70,000 of these qualify for heart transplantation. It is extremely important, therefore, to focus on interventions that may significantly reduce morbidity and mortality in these populations. The growing clinical consensus suggests that stable, compensated CHF patients respond favorably to exercise training. Patients who exercise not only have diminished symptoms but also may actually alter the clinical course of the disease.

Chronic Heart Failure

Patients with CHF uniformly report fatigue and activity intolerance. Exercise tolerance, as assessed by peak oxygen consumption (Vo2max), is a powerful predictor of survival in these patients (figure 1).1 Before the 1980s, CHF patients were excluded from exercise rehabilitation programs because of concerns for their safety. Previous strategies touted rest as first-line therapy for all CHF patients. Patients were advised to restrict physical activity to reduce circulatory demands, but prolonged rest is neither necessary nor beneficial. In fact, deterioration of physical fitness may actually contribute to the secondary manifestations of CHF.

Exercise rehabilitation has been used increasingly in recent years in conjunction with contemporary vasodilator drugs to attain functional and symptomatic improvement in CHF. Aerobic exercise appears safe once CHF patients have achieved clinical compensation. The risk of myocardial infarction (MI) or life-threatening arrhythmia in selected patients with CHF is probably not significantly higher with exercise than is the background level of risk in CHF.

Contributors to Exercise Intolerance

Impaired left ventricular systolic function. Central hemodynamic abnormalities are, by definition, the primary pathophysiologic features of CHF. Exercise tolerance, however, is not directly related to the degree of cardiac dysfunction. Left ventricular ejection fraction (LVEF) is important in assessing the extent of myocardial systolic dysfunction but offers little value for predicting a patient's ability to exercise.1

Impaired left ventricular diastolic function. CHF patients with preserved left ventricular (LV) systolic function also have significant exercise intolerance. Abnormalities in LV diastolic function prevent augmentation of stroke volume, producing diminished cardiac output and severe exercise intolerance.

Baroreflex desensitization and sympathetic activation. In the acute phase of low-output CHF, arterial and cardiopulmonary baroreflexes are activated to help maintain systemic blood pressure. However, sensitivity of both arterial and cardiopulmonary baroreceptors becomes diminished in CHF. In addition, dramatically increased levels of muscle sympathetic nerve activity occur both at rest and during exercise.

Abnormal neurohormonal stimulation. Neurohormonal mechanisms play a central role in CHF progression.2,3 In acute heart failure, neurohormonal activation is a desirable compensatory mechanism, but sustained neurohormonal arousal further complicates heart failure syndrome and is associated with poor long-term prognosis in CHF.

Impaired vasodilatory capacity. Sympathetic stimulation and neurohormonal activation are potent sources of vasoconstriction in CHF. However, peripheral alpha-adrenergic blockade and angiotensin-converting enzyme (ACE) inhibitor therapy do not immediately restore vasodilating capacity, indicating that intrinsic vascular abnormalities such as endothelial dysfunction possibly contribute to impaired vasodilatory capacity.

Skeletal muscle abnormalities. Reduced blood flow, muscle mass, and aerobic enzyme activity, and an increased percentage of fast-twitch, type 2b fibers (more glycolytic, less fatigue-resistant) act together in skeletal muscle to induce early anaerobic metabolism during exercise.4 Early onset of anaerobic metabolism, in turn, limits exercise tolerance in patients with CHF,5 findings confirmed with 31P magnetic resonance spectroscopy (31P MRS).4,6

Pulmonary abnormalities. Exertional dyspnea is a prominent symptom in CHF, and various pulmonary function abnormalities are believed to be exacerbated by CHF. Dyspnea in nonedematous CHF patients, however, may be as much or more related to deconditioning and metabolic abnormalities in muscle than to pulmonary congestion.7

Responses to Exercise Training

Chronic exercise induces several favorable clinical effects,2,6,8 but long-term data are still lacking about the effects in CHF on mortality or morbidity.

Peak oxygen consumption. Training-induced improvements in Vo2max are consistent in patients with CHF and range from 1.4 to 7 mL/kg/min. CHF patients who had less than 40% LVEF and anginal symptoms on a treadmill test may not achieve exercise-induced improvements in Vo2max, because the low anginal threshold could limit exercise intensity. However, patients whose LVEF is less than 40% after a severe MI, but who remain free of anginal symptoms, can safely engage in an exercise program and increase their Vo2max.

Myocardial remodeling. The influence of exercise training on myocardial wall thinning and the "remodeling" process in MI patients generates considerable debate. Although initial animal studies9 and a study in CHF patients10 demonstrated remodeling, subsequent studies have not confirmed those findings.11,12 It appears that selected CHF patients without clinical complications can benefit from exercise training without experiencing negative effects on supine resting LV volume, function, or wall thickness.

Baroreflex and sympathetic activation. Markers of autonomic nervous system function in patients with CHF show a significant shift away from sympathetic activity toward greater dominance of vagal parasympathetic tone after exercise training, although specific mechanisms have not been identified. One study13 found a 30% improvement in baroreflex sensitivity in CHF patients after an exercise program. The clinical implication is that improved baroreflex function and vagal tone could diminish susceptibility to life-threatening arrhythmias in CHF patients. Baroreflex sensitivity, exercise capacity, and survival rate are all improved in CHF patients by ACE inhibitor therapy.14-16

Neurohormonal regulatory systems. A study at the University of Florida2 was the first randomized controlled trial of intermediate-term exercise training to measure fluid regulatory hormone levels in patients with CHF. At study entry, neurohormonal levels did not differ between groups, but after 4 months of training all resting levels of neurohormones were significantly reduced (about 30%) in the exercise group but not in the controls. Diminished neurohormonal activity could be interpreted as a marker for improved cardiac pump function. However, results from previous CHF training studies7,11,17 do not demonstrate increased cardiac output.

Vasodilatory capacity. The vascular endothelium must be considered a therapeutic target to reduce CHF symptoms.8,18-20 Hornig et al8 were the first to suggest exercise enhancement of vasodilatory capacity. Exercise training restored flow-dependent vasodilatory capacity in CHF patients, but enhanced vasodilation was specific to the region trained and was lost after 6 weeks of cessation of training. Their data suggested that exercise induced release of endothelial nitric oxide.

Skeletal muscle metabolism. Studies6,21 employing 31P MRS and in-magnet exercise protocols revealed significant improvement in muscle endurance, limb blood flow, and cardiac output following training. Improved exercise tolerance was attributed to a reduced depletion of phosphocreatine (PCr), higher muscle pH at submaximal workloads, and more rapid resynthesis of PCr.21

Favorable Outcomes With Exercise

Both home-based22 and hospital-based11,17 studies have demonstrated that chronic exercise induces favorable clinical effects by significantly increasing Vo2max, reducing sympathetic drive, improving endothelial function,8 enhancing skeletal muscle metabolism,6 and suppressing neurohormonal overactivity.2 However, these studies have included only about 500 to 600 patients with CHF, and valuable long-term follow-up data are lacking. What is desperately needed is a definitive answer to whether exercise training decreases mortality or morbidity.

Belardinelli et al23 provided the first longitudinal data that support the notion that long-term exercise training imparts favorable clinical outcomes. Vo2max improved 18%, and the thallium activity score improved 24% (P <0.001). Exercise was associated with both lower total all-cause mortality (9 vs 20 deaths; risk reduction 63%; P <0.01), and hospital readmission for heart failure (5 vs 14 admissions; risk reduction 71%; P <0.02). Although it does not prove that exercise reduces mortality, these results do implicate exercise as beneficial.

Designing an Exercise Program

Risk stratification and patient screening. The American Heart Association (AHA), American College of Sports Medicine, American Association for Cardiovascular and Pulmonary Rehabilitation, and the Centers for Disease Control and Prevention have all published updated guidelines on exercise in clinical populations.24 These organizations encourage stratifying patients into risk categories before they start an exercise program. The AHA recommends that medically stable patients with CHF participate in exercise programs (table 1). Most stable CHF patients will be classified as class C patients, but a significant number of patients with mild heart failure may be classified as class B and be qualified to participate in comprehensive rehabilitation programs, including light-to-moderate resistance training. Regardless of the classification, the exercise program should be individualized and medical supervision provided until safety is established.

TABLE 1. American Heart Association (AHA) Risk Stratification Criteria


AHA Class and Description
NYHA
Class
Exercise
Capacity
Angina, Ischemia, and
Clinical Traits

ECG Monitoring

A. Apparently healthy None >6 METs <40 yr old, without symptoms,
no major risk factors, and
normal GXT
No supervision or
monitoring required

B. Known stable coronary
artery disease, low risk for
vigorous exercise
1 or 2 5-6 METs No ischemia or angina at rest
or on GXT, EF = 40%-60%
Monitored and supervised
during prescribed sessions
(6-12); light resistance
training may be included in
a comprehensive program

C. Stable CV disease with low
risk for vigorous exercise but
unable to self-regulate activity
1 or 2 5-6 METs Same as class B, but without
ability to self-monitor exercise
Medical supervision and
ECG monitoring during
prescribed sessions;
nonmedical supervision of
other exercise sessions

D. Moderate-to-high risk for
cardiac complications
during exercise
3 <6 METs Ischemia (4.0-mm ST
depression) or angina during
exercise; >2 previous MIs;
EF <30%
Continuous ECG monitoring
during rehabilitation until
safety is established; medical
supervision for all exercise
until safety is established

E. Unstable disease with
activity restriction
3 <6 METs Unstable angina;
uncompensated heart failure;
uncontrollable arrhythmias
No activity for conditioning
efforts; effort should focus
on restoring patient to
class D or above

NYHA = New York Heart Association; ECG = electrocardiogram; MET = metabolic equivalent; GXT = graded exercise test; EF = ejection fraction; CV = cardiovascular; MI = myocardial infarction

Adapted with permission from Braith RW: Exercise for chronic heart failure and heart transplant patients, in Thompson PD (ed): Exercise and Sports Cardiology, New York City, McGraw-Hill Medical Publishing, pp 317-353.

Before starting an exercise program, patients must be in stable condition, and their fluid volume status should be controlled (figure 2). CHF patients with an LVEF of less than 30% should be carefully screened for ischemia. Pretraining evaluation with a symptom-limited bicycle or treadmill graded exercise test is essential. Only patients free of unstable or exercise-induced ventricular arrhythmias should be considered for exercise. In addition, echocardiographic assessment of ventricular function and expired gas analysis for assessment of Vo2max are helpful in preparing prescription guidelines about exercise frequency, intensity, duration, mode, and progression.

Initial intensity. The initial exercise intensity should be customized for each patient. Because many patients with CHF have marked exercise intolerance, an interval training approach may be needed. For example, we have employed initial training regimens that consisted of 2 to 6 minutes of low-level activities alternated with 1 to 2 minutes of rest.2 Training frequency may be as often as two to three times a day during the early stages of the program, with symptoms and general fatigue serving as guidelines for determining frequency. Warm-up and cooldown periods should be longer than normal to watch for possible arrhythmias. Appropriate exercise intensity should be based on Vo2max rather than peak heart rate because the chronotropic response to exercise is frequently abnormal.

Initially, intensity should be 40% to 60% of Vo2max, or 10 beats/min less than that experienced with any significant symptoms including angina, exertional hypotension, dysrhythmias, and dyspnea. Continuous supervision may be necessary during the early stages, and frequent monitoring of blood pressure and echocardiographic responses should be used in patients at higher risk (AHA class C). Rating of perceived exertion should range from 11 to 14 ("light" to "somewhat hard") on the Borg scale. Anginal symptoms should not exceed 2+ on the 0 to 4 angina scale ("moderate to bothersome"), and exertional dyspnea should not exceed 2+ on the dyspnea scale ("mild, some difficulty").24 Full resuscitation equipment should be available during phase 2 rehabilitation but may not be essential in maintenance programs.

Exercise progression. Duration should be increased gradually to 30 minutes, as tolerated at about 70% to 85% of peak heart rate or 40% to 60% of Vo2max. The most consistent benefits occur with exercise training at least three times per week for 12 or more weeks. In selected patients, after 6 to 12 weeks of supervised exercise without evidence of adverse events or arrhythmia, submaximal exercise may continue unsupervised (eg, a home program). Exercise should include activities that are predominantly cardiovascular in nature, such as walking or cycling.

Current guidelines by the AHA and other organizations do not include recommendations for resistance training for CHF patients. However, light-to-moderate resistance training could be integrated as part of a comprehensive rehabilitation program for low-risk (AHA class B) patients who have successfully completed at least 6 to 12 weeks of cardiovascular exercise training without adverse events.

New Thoughts About CHF and Exercise

New standards and guidelines have been directed toward physicians and other health professionals who are involved in regular exercise testing and exercise training. For primary care physicians, who are increasingly using exercise testing, clinical competency requirements are available.25

Rehabilitation personnel must watch for symptoms of cardiac decompensation during exercise, including cough or dyspnea, hypotension, light-headedness, cyanosis, angina, and arrhythmias. The patient's body weight should be recorded before exercise, and daily pulmonary auscultation for rales and shortness of breath is recommended. Patients should avoid exercise immediately after eating or taking a vasodilator. Fluid and electrolyte balance is vital. Patients who have potassium or magnesium deficiency should take supplements to replenish electrolytes before exercising.

References

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  2. Braith RW, Welsch MA, Feigenbaum MS, et al: Neuroendocrine activation in heart failure is modified by endurance exercise training. J Am Coll Cardiol 1999;34(4):1170-1175
  3. Cohn JN, Levine TB, Olivari MT, et al: Plasma norepinephrine as a guide to prognosis in patients with chronic congestive heart failure. N Engl J Med 1984;311(13):819-823
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  7. Sullivan MJ, Higginbotham MB, Cobb FR: Exercise training in patients with chronic heart failure delays ventilatory anaerobic threshold and improves submaximal exercise performance. Circulation 1989;79(2):324-329
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  10. Jugdutt BI, Michorowski BL, Kappagoda CT: Exercise training after anterior Q wave myocardial infarction: importance of regional left ventricular function and topography. J Am Coll Cardiol 1988;12(2):362-372
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  12. Giannuzzi P, Tavazzi L, Temporelli PL, et al: Long-term physical training and left ventricular remodeling after anterior myocardial infarction: results of the Exercise in Anterior Myocardial Infarction (EAMI) trial. EAMI Study Group. J Am Coll Cardiol 1993;22(7):1821-1829
  13. La Rovere MT, Mortara A, Specchia G, et al: Myocardial infarction and baroreflex sensitivity: clincal studies. J Ital Cardiol 1992;22(5):639-645
  14. Grassi G, Cattaneo BM, Seravalle G, et al: Effects of chronic ACE inhibition on sympathetic nerve traffic and baroreflex control of the circulation in heart failure. Circulation 1997;96(4):1173-1179
  15. The CONSENSUS Trial Study Group: Effects of enalapril on mortality in severe congestive heart failure: results of the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS). N Engl J Med 1987;316(23):1429-1435
  16. The SOLVD Investigators: Effect of enalapril on survival in patients with reduced left ventricular ejection fractions and congestive heart failure. N Engl J Med 1991;325(5):293-302
  17. Sullivan MJ, Cobb FR: Central hemodynamic response to exercise in patients with chronic heart failure. Chest 1992;101(5 suppl):340S-346S
  18. Hambrecht R, Fiehn E, Weigl C, et al: Regular physical exercise corrects endothelial dysfunction and improves exercise capacity in patients with chronic heart failure. Circulation 1998;98(24):2709-2715
  19. Smith CJ, Sun D, Hoegler C, et al: Reduced gene expression of vascular endothelial NO synthase and cyclooxygenase-1 in heart failure. Circ Res 1996;78(1):58-64
  20. Rieder MJ, Carmona R, Krieger JE, et al: Suppression of angiotensin-converting enzyme expression and activity by shear stress. Circ Res 1997;80(3):312-319
  21. Stratton JR, Dunn JF, Adamopoulos S, et al: Training partially reverses skeletal muscle metabolic abnormalities during exercise in heart failure. J Appl Physiol 1994;76(4):1575-1582
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  23. Belardinelli R, Georgiou D, Cianci G, et al: Randomized, controlled trial of long-term moderate exercise training in chronic heart failure: effects on functional capacity, quality of life, and clinical outcome. Circulation 1999;99(9):1173-1182
  24. ACSM Guidelines for Exercise Testing and Prescription, ed 5. Baltimore, Williams & Wilkins, 1995, pp 98-100
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This article was adapted from the recently published book: Thompson PD (ed): Exercise and Sports Cardiology, New York City, McGraw-Hill Medical Publishing, 2001 (to order: 1-800-262-4729 [ISBN:0-07-134773-9]).

Dr Braith is associate professor of exercise physiology and director of clinical exercise physiology at the University of Florida College of Medicine in Gainesville. Address correspondence to Randy W. Braith, PhD, Director, Clinical Exercise Physiology, College of Health and Human Performance, University of Florida, PO Box 118206, Rm 25 Florida Gym, Stadium Rd, Gainesville, FL 32611; e-mail to [email protected].

Disclosure information: Dr Braith discloses no significant relationship with any manufacturer of any commercial product mentioned in this article. No drug is mentioned in this article for an unlabeled use.


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