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[Exercise is Medicine]

Congestive Heart Failure: Training for a Better Life

James R. Clark, MD, with Carl Sherman

Series Editor: Nicholas A. DiNubile, MD

THE PHYSICIAN AND SPORTSMEDICINE - VOL 26 - NO. 8 - AUGUST 2021


In Brief: Congestive heart failure (CHF) patients who exercise regularly can increase exercise tolerance, decrease dyspnea and fatigue, reduce the risk of arrhythmias, and improve quality of life. Initial stress testing is important for assessing a patient's physiologic response to exercise and for establishing a target heart rate for an individualized exercise program. Patients may need to begin aerobic exercise with interval training and progress slowly. Strength exercise is also useful. Exercise used along with the customarily prescribed CHF medications improves symptoms more than either modality alone.

The incidence of congestive heart failure (CHF) and the resulting death rate (1) have risen significantly in recent decades, partially because of the aging of the population. Over 4 million Americans now suffer from the disorder, which, broadly defined, is an inability of the heart to pump enough blood to meet the body's metabolic needs. The causes are many, but the vast majority of cases involve left ventricular dysfunction related to coronary artery disease, hypertension, or idiopathic dilated cardiomyopathy (2).

CHF patients were traditionally counseled to rest and avoid exercise in order to delay disease progression and to promote diuresis induced by bed rest (3). However, CHF theory and clinical practice have changed radically, especially in the last decade, as research has demonstrated that exercise offers much gain at little risk (3-9). Indeed, most CHF patients who exercise can markedly improve their functional status and quality of life (3,5-8). In addition, exercise may reduce the risk of death for CHF patients, just as it does for patients who have coronary artery disease (10).

Causes of Exercise Intolerance

Such gains are not surprising. Exercise intolerance and fatigue, hallmarks of CHF and principal sources of disability (11), are the result of the central hemodynamic abnormality and other pathophysiologic and compensatory events associated with the disease (10).

The heart's impaired pumping efficiency results in decreased blood flow to the muscles. However, left ventricular dysfunction alone does not correlate well with declines in exercise capacity (12). Pulmonary congestion—and ultimately fibrosis—is also involved, since it interferes with alveolar gas transport, causing dyspnea and reducing the oxygen available for delivery to the muscles. Weakened respiratory muscles impair ventilation still further.

Hormonally, CHF is associated with elevated levels of catecholamines, which increase vascular resistance and further reduce muscle oxygenation. Increased renin output leads to peripheral and pulmonary edema, which contribute to dyspnea that limits exercise capacity.

Perhaps the largest effect on exercise capacity comes from changes in the muscles themselves. Muscle atrophy often occurs early in the disease (13), probably as a result of decreased activity and reduced blood flow. There is an increased proportion of type 2 (fast-twitch) muscle fibers, which produce more lactate at lower workloads and thus fatigue more easily than type 1 fibers. Declines in mitochondrial volume in CHF patients have been noted and related to the duration of the disease (14).

Demonstrated Exercise Benefits

Studies documenting the benefits of exercise for CHF patients are fewer than those demonstrating its benefits for coronary artery disease patients. (Earlier cardiac studies, in fact, systematically excluded patients who had severe left ventricular dysfunction.) However, in the past decade, researchers have produced increasing evidence that training can reverse some of the physiologic changes responsible for poor exercise tolerance and, more strikingly, effect significant improvements in functional capacity and quality of life (3,5-9).

Exercise tolerance. Generally, these studies have shown that exercise tolerance—defined as time to exhaustion at submaximal intensity—increases in the range of 26% to 37%.(8) Individuals report less fatigue, more energy, and more endurance after training programs. The improvement in exercise tolerance is double that seen with angiotensin-converting enzyme (ACE) inhibitors or digoxin (8).

Quality of life. Research (3,5-9) has also shown that exercise can produce significant and lasting changes in patients' quality of life. One investigator (5) found that 50% of patients returned to work after exercise training. Three years after the study, 92% were still physically active, 31% were asymptomatic during activity, and 46% reported minimal impairment in daily life.

Functional improvements. Most of the studies have involved patients who had New York Heart Association (NYHA) class 1 to 3 CHF and were doing aerobic exercise at 40% to 80% of maximum heart rate. One controlled trial (15) engaged class 3 patients in 52 weeks of progressive, supervised aerobic walking. Fifteen of 21 patients completed the training program. Improvements in walking speed became apparent by the fourth week of the trial and rose to a mean of 18% over baseline by the end of the trial. Peak oxygen uptake, resting heart rate, peak power output, and ventilatory threshold also improved significantly, while fatigue decreased significantly. Patients in a control group showed virtually no changes in these variables.

In another trial (16,17), patients who had class 1 to 3 CHF and a mean ejection fraction of 24% did graded bicycle exercise 4 hours per week for 4 to 6 months. Their average NYHA classification improved from 2.4 before the beginning of the study to 1.3 afterward. Peak oxygen consumption increased, and heart rate was reduced at rest and at submaximal exercise. Single-leg blood flow and oxygen delivery increased significantly after training, and lactate concentrations were "markedly reduced" during submaximal exercise. (It should be noted that 3 of 16 patients in this trial had adverse outcomes, including 1 sudden death that was unrelated to exercise, 1 case of progressive heart failure, and 1 of prolonged fatigue (16).)

Cellular changes. A number of investigators have observed a reversal of the decline in mitochondria and peripheral oxidative capacity associated with CHF. For example, in a 6-month study (11) of patients who exercised 40 minutes daily, volume density of cytochrome c oxidase-positive mitochondria increased by 41%, and the change was significantly associated with oxygen uptake at the ventilatory threshold and with peak oxygen uptake.

Exercise intensity and mode. Although most studies have used aerobic programs in which patients aimed at achieving 50% to 75% of maximum heart rate with exercise, less demanding protocols are beneficial as well. In one controlled trial (18), 27 patients who had mild, chronic CHF were randomly assigned to 8 weeks of low-intensity aerobic training (performed at 40% of peak oxygen uptake, 3 times per week) or no training. Significant increases in peak oxygen uptake, volume density of mitochondria, lactic acidosis threshold, and peak workload occurred in the training group but not in controls.

Another trial (7) tested the effects of graded resistance training on CHF patients. By using a protocol that works one muscle group at a time, researchers hoped to achieve positive results while putting less demand on the cardiovascular system, relative to other methods of strength training. After 90 days, the patients' scores on a multidimensional quality-of-life survey increased 63%, and 80% wanted to continue the program.

In addition to its positive impact on the disease itself, regular exercise is beneficial for a host of other medical and nonmedical problems to which CHF patients are prone. Seventy percent of CHF cases are related to coronary heart disease and hypertension, and exercise has a documented value for both. Exercise also improves lipid profiles and reduces the risk of diabetes. Most CHF patients are over 65, and exercise has been shown to help prevent and ameliorate osteoporosis(19) and the decreased mobility of aging (20).

The Exercise Prescription

In my clinical experience, CHF patients have much to gain from exercise, so I include it in my prescription for treatment. However, because most CHF patients have been sedentary and comorbidity is common, low-level, symptom-limited stress testing should precede the start of the exercise program. Such testing should monitor blood pressure and chest pain and include an electrocardiogram (EKG), all of which are invaluable in calculating a safe, optimum heart rate for patients' exercise programs. Of course, exercise is clearly contraindicated for some. For a discussion of safety issues, see "When Is Exercise Contraindicated?" below.

Target heart rate. Research has shown that the greatest aerobic gains occur when CHF patients exercise at 60% to 80% of their maximum heart rate. Traditionally, this rate has been calculated by subtracting a person's age from 220 and multiplying by 0.6 to 0.8. This age-based formula is unsuitable for CHF patients for two reasons. At a given age, individuals vary markedly in exercise capacity; one 50-year-old may be unable to walk a mile, while another can run marathons. Furthermore, many CHF patients have a high resting heart rate, which should be considered when calculating the target heart rate.

Therefore, the patient's target heart rate should be derived from the results of the symptom-limited stress test. To calculate a safe, maximally effective target heart rate for the patient's exercise prescription, subtract the resting heart rate from the maximum heart rate on the test, multiply by 0.6 to 0.8, and add back the resting pulse (21).

A gradual approach. Long warm-ups are important to promote vasodilation before the demands of exertion. A protocol of at least 10 minutes of stretching, slow walking, or other exercise can increase blood flow to muscles without raising the pulse above 40% to 50% of maximum heart rate.

Ideally, patients should exercise—walk or ride a stationary bicycle—at their prescribed heart rate for 20 to 40 minutes three to five times a week. (See "A Guide to Exercise for Congestive Heart Failure Patients.") For many, this can be best achieved, at least in the early stages of the program, with interval training. Alternating activity with rest closely resembles the demands of daily life—climbing stairs or crossing the room to get a newspaper—and has been shown to elicit the same cardiovascular responses as continuous training if the total exercise time is the same (22).

Patients should generally start interval training with 2 to 4 minutes of exercise followed by a minute of rest, until they can do 10 to 15 minutes of exercise. They should then work up to 5 minutes of exercise followed by 2 minutes of rest for a total of 20 to 40 minutes of exercise per session. Patients should progress gradually until they can sustain continuous exercise for the entire session.

These patients should be supervised, at least in the early stages of training, to ensure their safety. However, if the stress test has revealed no evidence of exercise-induced hypertension, no significant EKG changes or arrhythmias, and the patient has been properly instructed, the program can usually be done at home.

Strength training. While aerobic training is the cornerstone of the exercise program, exercises to strengthen ventilatory muscles of the diaphragm and abdomen have been shown to reduce dyspnea, improve quality of life, and boost exercise tolerance (23). Resistance training using dumbbells and ankle weights or strength training machines can be added to redress the muscle fatigue that often limits activity in CHF. Using low weight and high repetitions prevents straining and breath holding, which place greater demands on the heart. The focus should be on the major muscles of the upper and lower body and torso. One to two sets with 12 to 15 repetitions per set provides an adequate training stimulus.

Cautions for patients. Patients must be taught the signs of decompensation—angina, worsening breathlessness, weight gain, or leg swelling—and counseled to discontinue exercise and seek medical attention if they occur. Exacerbations are common in CHF and are usually unrelated to exercise, but patients should refrain from activity until the condition has been controlled.

Medication

Other treatments for CHF are compatible with and, in fact, complement exercise. These treatments include ACE inhibitors and diuretics, the first-line medications for the disease; ACE inhibitors dilate blood vessels and decrease sympathetic tone, and diuretics decrease blood volume. Hydralazine and nitrates, which also reduce vascular resistance, may be prescribed for symptomatic relief. Digoxin increases the contractility of the left ventricle, raising the amount of blood pumped by the heart. Low-dose beta-blockers may be prescribed to reduce the toxic effects of sympathetic overactivity.

Vasodilators, such as ACE inhibitors and hydralazine, and digoxin have been shown to improve exercise capacity, but to a lesser extent than exercise training. The combination of these drugs and exercise appears to be more effective than either alone in this regard (24).

Some cautions. Vasodilators can cause a drop in blood pressure, dizziness, and even loss of consciousness in those who exercise. To minimize the risk of such problems, these medications should be taken and training done at different times of day. Complications with digoxin therapy are possible with a disrupted electrolyte balance, which is a theoretical risk in patients who perspire substantially during exercise. This reaction has not occured in my patients, nor is it likely at the prescribed intensity.

Other concerns. By the same token, the amount of fluid and electrolytes lost during the exercise advocated here need not interfere with the dietary management indicated for CHF. Nevertheless, patients—especially those with impaired renal function—should avoid excessive water consumption. Sodium restriction (a maximum of 2 g per day) is usually part of the strategy to minimize edema.

Given the considerable benefits of exercise, its limited risks, and its compatibility with other modes of treatment, a systematic training program should be part of the management of CHF for almost all patients.

References

  1. American Heart Association: 1997 Heart and Stroke Statistical Update. Dallas, American Heart Association, 1996
  2. Sullivan MJ: Congestive heart failure: trends in epidemiology and therapy, in Kennedy G, Crawford M (eds): Congestive Heart Failure: Current Clinical Issues, ed 1. New York City, Futura Pub Co, 1994, pp 1-15
  3. Sullivan MJ, Hawthorne MH: Nonpharmacologic interventions in the treatment of heart failure. J Cardiovasc Nurs 1996;10(2):47-57
  4. Sullivan MJ, Hawthorne MH: Exercise intolerance in patients with chronic heart failure. Prog Cardiovasc Dis 1995;38(1):1-22
  5. Squires TK, Lavie CJ, Brandt TR, et al: Cardiac rehabilitation in patients with severe ischemic left ventricular dysfunction. Mayo Clin Proc 120217;62:997
  6. Kao W, Jessup M: Exercise testing and exercise training in patients with congestive heart failure. J Heart Lung Transplant 1994;13(4):S117-S121
  7. Koch M, Douard H, Broustet JP: The benefit of graded physical exercise in chronic heart failure. Chest 1992;101(5 suppl):231S-235S
  8. Keteyian SJ, Brawner CA, Schairer JR: Exercise testing and training of patients with heart failure due to left ventricular systolic dysfunction. J Cardiopulm Rehabil 1997;17(1):19-28
  9. Coats AJ, Adamopoulos S, Meyer TE, et al: Effects of physical training in chronic heart failure. Lancet 1990;335(8681):63-66
  10. McKelvie RS, Teo KK, McCartney N, et al: Effects of exercise training in patients with congestive heart failure: critical review. J Am Coll Cardiol 1995;25(3):789-796
  11. Hambrecht R, Niebauer J, Fiehn E, et al: Physical training in patients with stable chronic heart failure: effects on cardiorespiratory fitness and ultrastructural abnormalities of leg muscles. J Am Coll Cardiol 1995;25(6):1239-1249
  12. Franciosa JA, Park M, Levine TB: Lack of correlation between exercise capacity and indexes of resting left ventricular performance in heart failure. Am J Cardiol 120211;47(1):33-39
  13. Lipkin DP, Jones DA, Round JM, et al: Abnormalities of skeletal muscle in patients with chronic congestive heart failure. Int J Cardiol 120218;18(2):187-195
  14. Drexler H, Riede U, Munzel T, et al: Alterations of skeletal muscle in chronic heart failure. Circulation 1992;85(5):1751-1759
  15. Kavanaugh T, Myers MG, Baigrie RS, et al: Quality of life and cardiorespiratory function in chronic heart failure: effects of 12 months' aerobic training. Heart 1996;76(1):42-49
  16. Sullivan MJ, Higginbotham MB, Cobb FR: Exercise training in patients with severe left ventricular dysfunction: hemodynamic and metabolic effects. Circulation 120218;78(3):506-515
  17. Sullivan MJ, Higginbotham MB, Cobb FR: Exercise training in patients with chronic heart failure delays ventilatory anaerobic threshold and improves submaximal exercise performance. Circulation 120219;79(2):324-329
  18. Belardinelli R, Georgiou D, Scocco V, et al: Low intensity training in patients with chronic heart failure. J Am Coll Cardiol 1995;26(4):975-20212
  19. Katz A, Sherman C: Osteoporosis: the role of exercise in optimal management. Phys Sportsmed 192021;26(2):33-43
  20. Buckwalter JA: Decreased mobility in the elderly: the exercise antidote. Phys Sportsmed 1997;25(9):127-136
  21. Durstine JL, King AC, et al, (eds): Resource Manual for Guidelines for Exercise Testing and Prescription, ed 2. Philadelphia, Lea and Febiger, 1993
  22. Meyer K, Samek L, Schwaibold M, et al: Interval training in patients with severe chronic heart failure: analysis and recommendations for exercise procedures. Med Sci Sports Exerc 1997;29(3):306-312
  23. Mancini DM, Henson D, La Manca J, et al: Benefit of selective respiratory muscle training on exercise capacity in patients with chronic congestive heart failure. Circulation 1995;91(2):320-329
  24. Coats AJS: Exercise rehabilitation in chronic heart failure. J Am Coll Cardiol 1993;22(4 suppl A):172A-177A


When Is Exercise Contraindicated?

Concerns about the risk of exercise-related arrhythmias in patients who have congestive heart failure have not been borne out. In fact, no significant ischemic or arrhythmic complications have been reported in any major trials. (However, patients who have persistent ischemia, poorly controlled arrhythmias, or decompensated heart failure are generally excluded from these studies (1). In fact, exercise training may actually reduce the risk of arrhythmias by improving autonomic function. Studies have shown that training is associated with significant declines in plasma catecholamines at rest and at submaximal exercise (2), and with reductions in sympathetic activity and enhanced vagal tone (3).

Exercise, however, can be contraindicated. If heart failure is secondary to obstructive valvular disease, severe aortic stenosis, or viral or autoimmune myocarditis, physical activity is contraindicated. Similarly, patients who have exercise-induced arrhythmias should not engage in exercise training. Unstable angina or uncompensated heart failure must be addressed and corrected before a patient can begin a training program.

References

  1. Kao W, Jessup M: Exercise testing and exercise training in patients with congestive heart failure. J Heart Lung Transplant 1994;13(4):S117-S121
  2. Hambrecht R, Niebauer J, Fiehn E, et al: Physical training in patients with stable chronic heart failure: effects on cardiorespiratory fitness and ultrastructural abnormalities of leg muscles. J Am Coll Cardiol 1995;25(6):1239-1249
  3. Coats AJ, Adamopoulos S, Radaelli A, et al: Controlled trial of physical training in chronic heart failure: exercise performance, hemodynamics, ventilation and autonomic function. Circulation 1992;85(6):2119-2131


Dr Clark is a board-certified internist and medical director of Medical Fitness in Charlottesville, Virginia. He is fellowship trained in primary care sports medicine and is a member of the American College of Sports Medicine. Mr Sherman is a freelance writer in New York City. Dr DiNubile is an orthopedic surgeon in private practice in Havertown, Pennsylvania, specializing in sports medicine and arthroscopy. He is the director of Sports Medicine and Wellness at the Crozer-Keystone Healthplex in Springfield, Pennsylvania; a clinical assistant professor in the department of orthopedic surgery at the University of Pennsylvania in Philadelphia; the orthopedic consultant to the Philadelphia 76ers basketball team and the Pennsylvania Ballet; and a member of the editorial board of The Physician and Sportsmedicine. Address correspondence to James R. Clark, MD, Internal Medicine/Sports Medicine, 3010 Berkmar Dr, Charlottesville, VA 22901.


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