Heart Failure is a relatively common condition, with around 5 million Americans currently living with it. And about 550,000 more people are diagnosed with Heart Failure with Reduced Ejection Fraction (HFrEF) each year. It disproportionately affects older individuals, with over 5% of the population aged 60-69 having the condition. Heart failure is responsible for about 11 million physician visits each year and is the most common diagnosis in hospitals for patients aged 65 and older. Lastly, slightly more that half of the people who develop Heart Failure will die within 5 years of their diagnosis.
Heart failure may be defined as the inability of the heart to meet the demands of the various tissues of the body and universally will result in symptoms of exercise intolerance. Exercise intolerance can be described as the reduced ability to perform activities of daily life that involve the dynamic movement of skeletal muscles because symptoms of fatigue or shortness of breath. To relate this feeling to athletes, this would be similar to when you have deconditioned in your off-season and have shortness of breath when starting activity again, only to a greater degree. These symptoms tend to make the patients hesitant about being active, as they believe that this means their heart may not be able to handle the stress or take these feelings as a worsening of their disease.
Although many years ago the medical community discouraged exercise training in patients with heart failure for fears of worsening symptoms and the overall condition; evidence now supports a role of exercise training as a way to improve the functional status, quality of life, and clinical outcomes of patients with heart failure. It has been proven that exercise training has both clinical and physiologic benefits. Training can improve left ventricular function, making the heart beat better, and reduce total peripheral resistance so the heart doesn’t have to work as hard. Training improves exercise tolerance and health-related quality of life, as well as reducing symptoms of depression. Importantly, it has been shown to be safe regardless of age or cause of heart failure.
So how does exercise training in people diagnosed with HFrEF help to improve their clinical status? In years past it was previously thought that exercise intolerance in HFrEF was caused by hemodynamic derangements, meaning that blood was not pumped through the body in an effective and efficient manner. It seemed then that various medications would be able to circumvent these changes and improve function. However, it has been demonstrated that there are also changes in the skeletal muscles that can contribute to the symptoms of heart failure.
Exercise capacity, which can be defined as “the maximum ability of the cardiovascular system to deliver oxygen to exercising skeletal muscle and of the exercising muscle to extract oxygen from the blood,” is reduced in patients with HFrEF. This decrease is due to two factors: (1) a reduction in the cardiac output of the heart secondary to impaired ability to pump blood throughout the body, and (2) the skeletal muscles being unable to effectively use the oxygen in the blood.
HFrEF is characterized by a decrease in function of the left ventricle of the heart as measured by the left ventricular ejection fraction (LVEF), which is how well the ventricle pushes blood into the body. This will cause other problems in the body, like high blood pressure as the body attempts to ensure blood is pushed to all corners of the body. Exercise training has demonstrated significant improvements in LVEF and subsequently an increase in cardiac output. Training has also demonstrated changes in the hemodynamics of the body by lowering the sympathetic nervous system activation and increasing the parasympathetic nervous system. These changes have been associated with a lower resting heart rate and a decrease in the resistance of the blood vessels, which allows the heart to pump with less effort.
There are also changes in the skeletal muscles of HFrEF patients. This dysfunction is believed to be due to the muscles being chronically hypoperfused (not enough blood going to the muscles), which may lead to an interference with the way the muscles use oxygen from the blood and may then lead to muscle wasting. Additionally, it is believed that physical deconditioning from inactivity may contribute to the dysfunction. Exercise training has been shown to improve muscle energetics and allows the muscles to use the oxygen in blood more efficiently. Training can also induce changes in the blood vessels and allow them to form more molecules of nitric oxide that allows the vessels to dilate and deliver more blood to the muscles.
The bottom line is that exercise training in patients with Heart Failure with Reduced Ejection Fraction have demonstrated an improvement in their functional capacity and quality of life. Although there is debate if exercise training can decrease the one-year mortality of these patients, it has been shown to decrease the rate of hospitalizations due to the condition. Therefore, exercise training is a safe and effective way to improve the functional state of a patient with HFrEF.
Chase King, MS-IV
David Carfagno, D.O., C.A.Q.S.M
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