Congestive Heart Failure (CHF) accounts for about a quarter of a million deaths a year, and currently its prevalence among the U.S. population is 4.8 million (1). CHF occurs when the heart cannot meet the demands of the body. The symptoms are breathlessness and fatigue due to a build up of fluid in and around the lungs. The failing heart inflates like a water balloon and, over time, gets stretched out to the point where it becomes a flimsy sac saturated with blood. If this sac is agitated with vigorous exercise it can, in some cases, fail. Thus whether a CHF patient should exercise is now a controversial issue. Cardiologists are often times reluctant to prescribe exercise to CHF patients because of the possibility that their failing hearts may have a negative response to the increased workload and stress of exercise (2). The negative short-term responses to exercise may include a decrease in ejection fraction (fraction of blood pumped out of the heart), arrhythmias (arrhythmic beating of the heart), and a drop in oxygen saturation of the blood. CHF patients struggle on a daily basis to perform simple tasks such as walking up stairs or even dribbling a basketball in extreme cases; this results in a drastically compromised quality of life. On the other hand, exercise may allow optimal cardiac output and other secondary therapeutic effects. The purpose of this review is to provide an overview of the positive and negative effects of cardiovascular exercise on ejection fraction, the onset of arrhythmias and dyspnea (shortness of breath), and functional capacity in congestive heart failure patients.
Cardiac muscle works similarly to skeletal muscle in that they both follow the Frank-Starling length-tension curve. This curve indicates that the contractility (force of contraction) of the heart increases with increased venous return. Venous return is the amount of blood that returns from the body to the heart in order to be pumped back out again into the lungs for oxygenation and, eventually, to the rest of the body. As venous return increases, the heart is stretched further and produces more contractile force; this happens in a healthy heart during exercise due to the increase in demands of the active skeletal muscle. However, the Frank-Starling curve is U-shaped and there is a point beyond which increased stretching leads to decreased contractile force. This is the level that CHF patients reach while performing simple tasks such as walking up a flight of stairs. Therefore, further stressing their hearts with vigorous cardiovascular exercise can result in decreased contractility, thus a decreased ejection fraction. “It (ejection fraction) is commonly expressed as a percentage and normally ranges from 55% to 80% (mean 67%) under resting conditions. Ejection fractions of less than 55% indicate depressed myocardial contractility” (3). With a depressed ejection fraction, the heart of a CHF patient inflates like a saggy water-balloon during exercise as fluid builds up. Syncope (fainting) and Arrhythmias are common results of poor tolerance to physical exertion in CHF patients. Therefore, the short-term effects of exercise can be detrimental to someone with Congestive Heart Failure.
However, there have been studies that show that long-term effects of exercise can significantly improve cardiac function. When sedentary men aged 60-70 with normal ejection fractions were put on a 12-month cardiovascular training program their ejection fractions improved by 7% and stroke volumes improved by 22mL. Exercise has the same effect on subjects with impaired ejection fractions such as those with CHF. “In a randomized study of patients with CHF, involving 2 weeks of inhospital ergometer exercise for 10 minutes 4 to 6 times per day, followed by 6 months of home-based ergometer exercise training for 20 minutes per day at 70% of peak oxygen uptake, patients in the exercise training group showed not only improvements in New York Heart Association functional class, maximal ventilation, exercise time, exercise capacity, and decreased resting heart rate, but also a 14-mL increment of stroke volume at rest, with an increase in mean resting LV” left ventricular “ejection fraction from 30% to 35%” (4). Along with the increase in strength of the heart muscle, exercise causes an increase in blood plasma volume, which causes the blood to become less viscous. The increase in blood volume can assist in a larger venous return, which in turn can cause an increase in contractility of the heart (assuming it does not pass the maximum level of contractility using the principle from the Frank-Starling length-tension curve).
“The initial response to heart failure and the incomplete filling of the arterial system leads to increased discharge of the sympathetic nervous system and increased secretion of renin and aldosterone, so that Na + and water are retained. These responses are initially compensatory, but eventually the failure worsens and the ventricles dilate” (5). When the heart of CHF patients becomes distended like a balloon, the myocardium (heart muscle) becomes irritable and can cause deadly arrhythmias such as ventricular fibrillation to occur. Ventricular fibrillation is an asynchronous contraction of the ventricles (chambers) of the heart and if a patient stays in ventricular fibrillation, death will occur due to the lack of blood flow to the brain and the rest of the body. Arrhythmias are defects in the electrical conduction pathways of the heart. If the electrical signal is disrupted or altered, the heart will not contract properly (each chamber will contract at the wrong time or the chamber itself will not contract as one unit but will essentially vibrate); the result is an inefficient pumping of blood.
Decreased vagal activity (parasympathetic stimulation via the vagus nerve), which decreases HRV (heart rate variability) in between beats, is associated with a high mortality rate due to arrhythmias. “The ‘UK-Heart’ study which examined 433 patients with moderate or severe heart failure, showed that those with depressed HRV had an annual mortality rate of 51.4% compared to 5.5% in those with nearly normal values” (6). One long-term effect of exercise, however, is a decrease in sympathetic nervous activation to the heart and an increase in vagal activity (7). The decrease in sympathetic tone will not only decrease the occurrence of arrhythmias, but will lower heart rate both at rest and during exercise. Therefore, along with an increase in ejection fraction, an endurance-trained heart operates at a lower heart rate, demanding less oxygen. The result is a heart muscle with a higher capacity that is better adapted to handle the rigors of life. It is the equivalent of putting a bigger engine in the same car; you simply increase the horsepower of the heart.
The shortness of breath that CHF causes is very debilitating; it deters exercise and makes it un-enjoyable. In a healthy individual, the lungs are well adapted and are never the limiting factor during maximal exercise. However, in a CHF patient, the fluid buildup in the lungs severely impairs breathing and limits the patient’s exercise ability. Additionally, because the heart is so stretched out in CHF patients, it has an impaired cardiac output and struggles to pump adequate blood to the lungs for oxygenation. As a result, O 2 saturation of the blood drops.
Exercise training has shown to improve the strength and endurance of the muscles of respiration, relieving dispnea during exercise and even during rest. Another effect of cardiovascular training is the increased capacity of both the heart (to pump blood) and skeletal muscle (to extract and utilize oxygen). “The mechanism responsible for this favorable effect” in the skeletal muscle “involves an increase in mitochondrial density, which reflects an improvement in oxidative capacity of trained skeletal muscles” (8). The resulting effect is that the lungs are relieved of their burden of ventilation and the patient feels less of an urge to breathe at a given level of exertion, thus relieving dyspnea (shortness of breath).
A three-month training protocol involving breathing exercises such as repeated bouts of resistive breathing showed that patients improved their maximum sustainable ventilatory capacity and maximum voluntary ventilation. As a result of the previous mentioned areas of pulmonary functional improvement, submaximal and maximal exercise capacity as well as V02 max was significantly improved (9).
In spite of risks like syncope, ventricular fibrillation or even death, cardiovascular exercise improves ejection fraction, reduces the onset of dyspnea, and increases the oxidative capacity of the skeletal muscles. A study published in The American Journal of Cardiology reported findings that six minute walking distance, workload and exercise time on a cycle ergometer test, and quality of life improved in CHF patients who exercised. All of these variables were measured in the experimental and control group of 40 individuals each. The experimental group consisted of CHF patients who were prescribed exercise while the control group consisted of CHF patients who did not exercise. Six-minute walking distance improved in the experimental group by 58 meters, quality of life in the Minnesota Living with Heart Failure Questionnaire improved by 10 points, and exercise time improved by 53 seconds in exercising CHF patients within 4 months after enrollment in the study. Thus, aerobic interval training improved long-term functional capacity and quality of life in CHF patients (10).
Other studies have shown similar results. A considerably larger study was conducted where one treatment group (701 patients) with CHF received exercise training while the control group (651 patients) with CHF received standard medical treatment. The results of this study showed that the treatment group improved in the following areas: peak VO 2, maximal power output, and 6 minute walking distance (10). Exercise capacities are measured using maximum oxygen consumption (VO 2 max). People with high VO 2 maxes (high levels of cardio-respiratory fitness) have a reduced risk of cardiovascular morbidity and mortality (12).
Thus, exercise training improves sub-maximal and maximal exercise performance in patients with CHF (13). Simply put, exercise trains the heart and skeletal muscles to operate more effectively at any given workload, even in a flimsy CHF heart; therefore, exercise trained CHF patients fatigue at higher workloads compared to sedentary CHF patients.
Despite many advances in the management of heart failure, it remains a life threatening condition. Symptomatic heart failure continues to confer a worse prognosis than the majority of cancers in the United States, with 1-year mortality averaging 45%. Thus, physicians must work toward widespread implementation of exercise prescription to decrease morbidity and mortality of congestive heart failure. The long-term effects of exercise have proven to strengthen cardiac muscle causing an increase in the ejection fraction of the heart. Additionally, exercise reduces the occurrence of deadly arrhythmias in CHF patients. Furthermore, through exercise training, CHF patients experience a decrease in the severity of shortness of breath because their respiratory muscles and heart work together more effectively. All of these physiological changes result in an increased functional capacity that directly correlates to the quality of life that a CHF patient experiences.
Although exercise is proven to lessen the severity of symptoms of CHF, it can be more effectively and safely used as a primary preventative measure. The broad range of benefits of exercise warrant additional support and funding to invest in cardiac rehabilitation programs where cardiac patients such as those with CHF can train in a supervised environment. Over half of the deaths in the U.S. result from different forms of cardiovascular disease, and there is one factor that can delay the onset of or even prevent the occurrence of these diseases—that factor is exercise. Thus far, there has been no single medication that provides the wide array of benefits that cardiovascular exercise does. Primary preventative measures can save our national health care system millions of dollars. Ultimately we should hope that exercise training is a more widely implemented measure against heart disease in the United States.
Advertising revenue contributes to the work of Kappa Omicron Nu. Advertisers are not affilifiated with or endorsed by KON.
1. Health Grades, Inc. All rights reserved. Last Update: 4 October, 2008. http://www.wrongdiagnosis.com/c/congestive_heart_failure/stats.htm
2. Steve E Selig , David L Hare. British Journal of Sports Medicine; 41:407-408. 2007
3. Mohrman DE, Heller LJ, Cardiovascular Physiology, 6th Edition.” Chapter 3. The Heart Pump". http://www.accessmedicine.com/content.aspx?aID=2372865
4. Zhi You Fang, Thomas H. Marwick. Mechanisms of exercise training in patients with heart failure American Heart Journal, Volume 145, Issue 5, Pages 904-911. 2003
5. Ganong WF, "Chapter 33. Cardiovascular Homeostasis in Health & Disease" (Chapter). Ganong WF: Review of Medical Physiology, 22nd Edition: http://www.accessmedicine.com/content.aspx?aID=706250
6. Nolan, J., Batin, P. D., Andrews, R., Lindsay, S. J., Brooksby, P., Mullen, M., W., Flapan, A. D., Cowley, A., Prescott, R. J., Neilson, J. M. & Fox, K.A. Prospective study of heart rate variability and mortality in chronic heart failure: Results of United Kingdom Heart Failure evaluation and assessment of risk trial (UK-heart). Circulation 98, 1510-1516. 1998
7.Lehmann, M. Sympatho-vagal changes induced by physical training in cardiac patients. European Heart Journal [0195-668X] vol: 9 Suppl F pg: 55 -61. 1988
8. MD Romualdo Belardinelli, MD Demetrios Georgiou, MD Vito Scocco, PhD Thomas J. Barstow, MD Augusto Purcaro. Low intensity exercise training in patients with chronic heart failure. 1995
9. Mancini D.M., Henson D., La Manca J., Donchez L., Levine S. Benefit of selective respiratory muscle training on exercise capacity in patients with chronic congestive heart failure Circulation, 91 (2), pp. 320-329. 1995
10. Ferreira, I. Twisk, J.W.R. Stehouwer, C.D.A. van Mechelen, W. Kemper, H.C.G. Longitudinal changes in VO2max: associations with carotid IMT and arterial stiffness. Medicine & Science in Sports & Exercise: Vol. 35 Issue 10. p. 1670-1678. Oct 2003
11. Sullivan M.J., Higginbotham M.B., Cobb F.R. Exercise training in patients with chronic heart failure delays ventilatory anaerobic threshold and improves submaximal exercise performance (1989) Circulation, 79 (2), pp. 324-329. 1995
12. Benno A.F. van Tol, Rosalie J. Huijsmans, Dineke W. Kroon, Maaike Schothorst, Gert Kwakkel. Effects of exercise training on cardiac performance, exercise capacity and quality of life in patients with heart failure: A meta-analysis
European Journal of Heart Failure, Volume 8, Issue 8, Pages 841-850. 2006
13. Nilsson BB, Westheim A, Risberg MA. Long-term effects of a group-based high-intensity aerobic interval-training program in patients with chronic heart failure. American Journal of Cardiology. 102(9): 1220-4. 2008