Effects of controlled physical training in patients with heart failure

Heart failure (HF) is a clinical syndrome characterized by cardiac symptoms (e.g.,breathlessness, ankle swelling, and fatigue), which may be accompanied by signs (e.g., elevated jugular venous pressure, pulmonary crackles, and peripheral edema). Patients with HF often experience frequent hospitalizations, impaired quality of life, and shortened life expectancy. They also have decreased exercise capacity, primarily due to impaired hemodynamics within the active skeletal muscles. Patients with HF should undergo a cardiopulmonary exercise test to assess their activity level and type, as well as to perform risk stratification. The initial step should include evaluating the patient’s current exercise capacity and needs, then creating a personalized exercise program that details the types of exercises, their intensity, repetitions, duration in minutes per session, and the number of days per week allocated for training. Cycling (either on a stationary or regular bicycle) and walking are recommended because they are aerobic, dynamic forms of exercise. Aerobic training should be performed 3–5 times a week (30–60 minutes per session), with emphasis on interval training. This type of training enhances skeletal muscle strength and endurance, leading to increased muscle mass. In patients with heart failure and cachexia, resistance training is advised, combining both isotonic and isometric exercises. This type of training should be performed twice a week for 12 to 20 minutes per session. Resistance training also enhances skeletal muscle strength and endurance and encourages muscle growth. Physical training enhances skeletal muscle mass, fiber diameter, strength, endurance, and exercise capacity.

INTRODUCTION

Heart failure (HF) is a clinical syndrome characterized by cardiac symptoms (e.g., shortness of breath, leg swelling, and fatigue), which may be accompanied by signs (e.g., elevated jugular venous pressure, pulmonary crackles, and peripheral edema). HF occurs due to structural and/or functional abnormalities of the heart, leading to increased intracardiac pressures and/or inadequate cardiac output at rest and during exertion. Identifying the etiology of cardiac dysfunction is essential for diagnosing HF and guiding further treatment. Most often, HF results from myocardial dysfunction, which can be systolic, diastolic, or both [1].

HF remains a leading global cause of mortality, morbidity, and poor quality of life, with high resource utilization and healthcare costs. Although the incidence of HF has slightly decreased over time, its prevalence continues to increase due to improved HF treatments and increased life expectancy in the general population [2]. In European countries, the median incidence of HF is 3.20 cases per 1000 people, while the median prevalence is 17.20 cases per 1000 individuals [1],[3].

Although ischemic heart disease remains one of the most common causes of HF, advances in treating acute myocardial infarction (AMI) and secondary prevention have lowered the risk of HF hospitalization after a first AMI. The prevalence of heart failure increases with age, and among patients under 75 years old, the most common cause is coronary artery disease [1],[4],[5],[6].

Patients with HF often have multiple other comorbidities. Comorbidities are generally classified into cardiovascular and non-cardiovascular conditions. Among cardiovascular comorbidities, the most common are arterial hypertension, coronary artery disease, and atrial fibrillation [7],[8]. For non-cardiovascular comorbidities, the most frequent include diabetes mellitus, renal insufficiency, chronic obstructive pulmonary disease, and anemia [9],[10].

According to left ventricular ejection fraction (LVEF), heart failure is classified into preserved, mildly reduced, and reduced ejection fraction. Reduced LVEF is defined as ≤40%, indicating a significant decrease in left ventricular systolic function, known as heart failure with reduced ejection fraction (HFrEF). Patients with LVEF between 41% and 49% have mildly reduced systolic function, called heart failure with mildly reduced ejection fraction (HFmrEF). Heart failure with preserved ejection fraction (HFpEF) refers to an LVEF of 50% or higher. To diagnose HF with preserved or mildly reduced LVEF, symptoms and signs must be present along with elevated natriuretic peptide levels and at least one of the following: relevant structural heart disease (such as left ventricular hypertrophy or left atrial enlargement) and/or left ventricular diastolic dysfunction [1],[11],[12],[13].

Heart failure can also result from right ventricular dysfunction. Right ventricular mechanics and function may be affected by pressure or volume overload. The primary cause of chronic right ventricular failure is pulmonary hypertension due to left ventricular dysfunction, although many other causes exist [1],[14].

In clinical practice, the severity of HF is usually assessed using the New York Heart Association (NYHA) classification and the American College of Cardiology/ American Heart Association (ACC/AHA) classification [1].

The NYHA functional classification is based on symptom severity and physical activity:

• Class I: No restrictions on physical activity; regular physical activity does not lead to fatigue, dyspnea, or palpitations.
  • Class II: Slight restriction in physical activity; comfortable at rest, but normal activity causes fatigue, dyspnea, or palpitations.
  • Class III: Significant restriction of physical activity; comfortable at rest, but less-than-normal activity causes symptoms.
  • Class IV: Symptoms of heart failure are present at rest; any physical activity leads to increased discomfort.

ACC/AHA Classification of Heart Failure Severity:

• Stage A: High risk of developing heart failure but without structural heart disease or heart failure symptoms.
  • Stage B: Structural heart disease present but without signs or symptoms of HF.
  • Stage C: Structural heart disease presenting with symptoms of heart failure.
  • Stage D: Refractory heart failure requiring specialized interventions.

HEMODYNAMIC CHANGES IN HEART FAILURE

In patients with HF, physical exercise capacity is limited. This limitation mainly results from hemodynamic changes in active skeletal muscle (secondary to reduced cardiac output), so these patients can achieve a lower maximal cardiac output than healthy individuals. Inadequate blood flow hemodynamics in active skeletal muscle also stem from endothelial dysfunction, leading to insufficient vasodilation during physical activity. Stroke volume at rest, which is significantly reduced in systolic HF, increases only slightly during exercise due to impaired ability to enhance left ventricular preload and LVEF [15]. The reduced capacity to increase left ventricular end-diastolic volume results from the dilated left ventricle already operating near its maximum volume, exhausting its preload reserve [4],[16].

In patients with HF, peak oxygen consumption (peak VO2) and VO2 at the ventilatory anaerobic threshold are usually diminished compared to healthy individuals, in proportion to the severity of HF symptoms. The ventilatory anaerobic threshold is based on the idea that, at a certain workload, oxygen delivery to the muscles no longer meets their metabolic needs. This imbalance increases reliance on anaerobic glycolysis for energy production, with lactate as the end product. Lactic acid is then buffered by bicarbonate, releasing excess CO₂. The rise in CO₂ levels stimulates increased ventilation by activating chemoreceptors in the carotid sinuses, aiming to eliminate excess CO₂.

When expressed relative to measured peak VO₂, the ventilatory anaerobic threshold generally occurs at about 40%–60% of peak VO₂ in most cardiac patients, with a tendency toward a higher proportion of peak VO₂ in patients with chronic HF [16].

PHYSICAL TRAINING / EXERCISE – GENERAL CONSIDERATIONS

The term “exercise” is defined as “activity that requires physical effort and is performed to maintain or improve health and fitness” or as “physical exertion undertaken to develop and maintain physical fitness.” Numerous similar definitions exist, all emphasizing that exercise is an active process during which an individual consciously exerts extra effort (compared with rest), involving a certain degree of physical load. A review of medical history shows that exercise has been recommended for health maintenance and therapeutic purposes since ancient times. One of the most frequently cited quotes attributed to Hippocrates states: “If we could give every individual the right amount of nourishment and exercise, not too little and not too much, we would have found the safest way to health.” However, in the past decade, the concept “Exercise is Medicine” has become a global health initiative, aiming to make physical activity assessment and the promotion of exercise a standard part of clinical practice, connecting healthcare with evidence-based physical activity and exercise. This approach is based on the idea that physical activity and exercise promote optimal health and should be essential for preventing and treating many medical conditions. This strategy encourages physicians and other healthcare providers to include exercise in treatment plans and refer patients to evidence-based exercise programs and qualified exercise professionals. The role of exercise in preventing and managing chronic diseases is relatively well understood [17]. It is believed that, alongside exercise, proper dietary modification can also reduce the risk of nearly all chronic diseases [18]. Systematic reviews and meta-analyses show that exercise is as effective as pharmacological treatments for several chronic conditions, providing scientific support for the “Exercise is Medicine” concept [19],[20].

Patients may receive a comprehensive assessment and a personalized exercise “prescription” in the clinical module. Based on this, exercise should be implemented within the community module. Advances in active health technology enable patients to exercise more effectively. Developments in exercise equipment allow individuals to gain a better exercise experience and reduce the likelihood of injuries. Recent progress in technology, including rehabilitation robotics, wearable devices, virtual reality, artificial intelligence, and innovative telemedicine, provides patients with real-time feedback and continuous support in meeting their exercise goals [21].

Individualization involves choosing the intensity and duration of exercise based on personal abilities. It is not advisable to completely follow other people’s exercise routines. Progressiveness means gradually increasing the intensity and duration. Sudden high-intensity or long-duration exercise can cause harm rather than health benefits. The principle of persistence emphasizes that individuals should see exercise as part of daily life and develop consistent habits. Not following these principles decreases the chances of reaching desired results. Selecting the type, intensity, duration, and frequency of exercise is a complex task [22],[23].

PHYSICAL TRAINING IN CARDIOVASCULAR PATIENTS

Current World Health Organization guidelines on physical activity and sedentary behavior stress that all adults should accumulate 150–300 minutes of moderate-intensity physical activity each week [24]. This can be replaced with high-intensity exercise or a combination of moderate- and high-intensity aerobic activities totaling 75–150 minutes weekly. Physical inactivity has serious consequences for global health and is a key risk factor for cardiovascular disease and all-cause mortality, while regular physical activity has the opposite effect [25]. One of the most extensive studies, involving 116,221 participants, showed that cardiovascular risk factors and all-cause mortality decrease by 19%–25% when the minimum weekly physical activity guidelines are followed, and by 15%–31% when both duration and high-intensity criteria are met [26].

Cardiovascular diseases are, at least in part, caused by poor or unhealthy diets and other lifestyle habits, which can be summarized as maladaptive dietary and lifestyle factors. A key aspect of lifestyle is physical activity and exercise [27]. Achieving and maintaining the recommended levels of physical activity is associated with lower risks of myocardial infarction, stroke, and cardiovascular death [28],[29]. Exercise likely protects against coronary heart disease by lowering risk factors such as hypertension, obesity, hyperlipidemia, and insulin resistance. Additionally, exercise has positive effects on myocardial remodeling [5]. Regular moderate-intensity exercise (about 60–75 minutes daily) reduces the risk of mortality linked to prolonged sitting [30]. Engaging in higher-intensity exercise and reducing sedentary time further decreases overall mortality risk [31]. Meta-analytic findings indicate that meeting recommended physical activity levels lowers the risk of adverse cardiovascular events by 17%, cardiovascular mortality by 23%, and the incidence of type 2 diabetes mellitus by 26% [32]. These findings were supported by Kivimäki et al. [33], who reported that physical inactivity was linked to a 24% higher risk of coronary heart disease, a 16% increased risk of stroke, and a 42% higher risk of type 2 diabetes mellitus. Recent meta-analytic data show a 17% lower risk of cardiovascular mortality when this type of activity is performed for 40–60 minutes weekly [34]. A combination of moderate- and high-intensity physical activity produces the most significant improvements in cardiovascular health and mortality reduction [35],[36],[37]. Secondary prevention of cardiovascular diseases ideally includes personalized exercise programs along with lifestyle changes (reducing sedentary behavior, quitting smoking, dietary planning) [38],[39]. A five-year study showed a 32% reduction in mortality among patients with cardiovascular disease (previous myocardial infarction, cardiothoracic surgery, angina pectoris) who participated in cardiac rehabilitation programs compared to those who did not [40]. Authors of a study involving 23,430 cardiovascular patients concluded that exercise-based cardiac rehabilitation leads to decreased mortality and better quality of life [41].

Exercise should be regarded as an intervention that must be tailored and continuously adjusted to match the characteristics and preferences of the individuals it’s prescribed for. Ideally, a maximal exercise test with direct measurement of maximal oxygen consumption (VO2 max) should be conducted for accurate risk assessment and to determine exercise zones before developing a program [42]. Exercise, especially high-intensity exercise, is contraindicated in certain situations, such as the first two days after acute coronary syndrome or in conditions like uncontrolled arrhythmia, active endocarditis, myocarditis, or pericarditis, severe symptomatic aortic stenosis, decompensated heart failure, acute pulmonary embolism, deep vein thrombosis, or acute aortic dissection [42],[43].

Sudden cardiac death accounts for about 50% of mortality within the first year after myocardial infarction. Patients recovering from myocardial infarction often retain risk factors for ischemic heart disease, necessitating strict management to lower the risk of further complications and death. In addition to medication, exercise plays a crucial role in managing risk factors [44]. Poor diet and physical inactivity contribute to atherosclerosis [45].

Patients after coronary artery bypass grafting (CABG) remain at risk for new cardiovascular events, arrhythmias, and sudden cardiac death [46]. Additionally, the postoperative period is characterized by prolonged physical inactivity due to mostly lying in bed, which leads to skeletal muscle hypotrophy, impaired peripheral circulation, and autonomic dysfunction. Clinically, this manifests as significantly reduced exercise tolerance, postural hypotension, resting tachycardia, and psychological issues, most commonly depression or anxiety. The degree of reduced exercise tolerance mainly depends on the duration of bed rest and the severity of left ventricular dysfunction [47]. Therefore, strict management of risk factors is essential for secondary prevention of coronary disease. Data show that among patients who do not engage in physical activity, approximately 15% experience restenosis within one year, and 88% face adverse cardiovascular events, including myocardial infarction, stroke, revascularization procedures, or hospitalization for angina pectoris [48].

New findings could create opportunities to improve exercise outcomes through more efficient or targeted methods. Although this goal may seem futuristic, its potential advantages should encourage further research in this area. Meanwhile, the benefits that are already well-supported by evidence should be prioritized and implemented as critical initiatives [27],[49].

It must always be emphasized that exercise programs should be safe and free from harmful effects, and that health benefits partly depend on the proper dose. The best approach is to view exercise as a therapeutic tool for cardiovascular disease. Healthcare professionals, primarily physicians, should play a role in encouraging, guiding, and promoting appropriate exercise habits in patients. The phrase “Exercise is Medicine” should go beyond simply telling patients to “exercise” or “exercise a few times per week,” and instead mean that “exercise be prescribed to patients similarly to medication” [50],[51]. This process begins with assessing the patient’s current abilities and exercise needs, then developing an initial program that specifies the type of exercise, intensity, repetitions, daily duration in minutes, and weekly sessions. Additional strategies should be employed to motivate and support the patient throughout the program. Involving qualified professionals is the most effective way to ensure proper implementation and monitoring. A structured approach can be developed by updating medical education curricula at both undergraduate and specialty-training levels, incorporating courses focused on the importance and application of exercise in disease prevention and treatment.

PHYSICAL TRAINING IN HEART FAILURE

The positions and recommendations of leading international cardiology societies have changed significantly over the past fifty years. A clear example is the major shift in how patients with heart failure are treated. Before the 1980s, stopping physical activity was considered a key treatment strategy for these patients [52]. The common belief was that exercise could be harmful and might lead to left ventricular dilatation, decompensation, dangerous arrhythmias, sudden cardiac death, and increased overall mortality. However, about twenty years later, studies not only challenged the idea that exercise was harmful but also demonstrated many health benefits [53],[54]. Today, treating patients with heart failure involves multiple options, with exercise being one of the main components. Although intense physical activity is not recommended for heart failure patients, controlled physical training is beneficial for those with NYHA class I–III (HF-ACTION) [55]. Patients with heart failure should undergo a cardiopulmonary exercise test to assess their level and type of physical activity that will be prescribed, and risk stratification is essential. In patients with heart failure, physical training does not cause significant ischemia or arrhythmias; instead, it improves exercise capacity and alleviates symptoms. Cycling (stationary or regular) and walking are recommended as aerobic, dynamic forms of exercise. For patients with NYHA class II, an exercise intensity of 70%–80% of peak VO₂ is advised, while for NYHA class III patients, the recommended intensity is 50%–65% of peak VO₂, with interval training being preferred. Aerobic exercise should be performed 3–5 times per week (30–60 minutes per session), prioritizing interval training [56].

In patients with heart failure, interval training shows significantly greater improvements in left ventricular ejection fraction, along with reductions in left ventricular end-diastolic diameter and pressure, compared to continuous training. Interval training also lowers pro-B-type natriuretic peptide (pro-BNP) more effectively in patients with heart failure [57]. In the HF-ACTION study, exercise training in heart failure patients decreased all-cause mortality and hospitalizations by 11%, while cardiovascular mortality and hospitalizations were reduced by 15% [48],[56].

In patients with heart failure and cachexia, resistance training, including isotonic and isometric exercises, is recommended. This type of training should be performed twice weekly for 12 to 20 minutes. It enhances skeletal muscle strength and endurance and promotes muscle mass gain [48]. Research indicates that in chronic heart failure, exercise reduces neurohormonal activation and the production of pro-inflammatory cytokines [58]. Aerobic interval training in heart failure patients also lowers levels of natriuretic peptides, systemic vascular resistance, and oxidative stress [59]. Controlled exercise may slow the progression of heart failure by influencing its underlying mechanisms. These benefits improve symptoms, physical capacity, and quality of life. Patients who do not experience improvements in exercise capacity tend to have a poorer prognosis. Exercise intensity plays a crucial role. Sudden high-intensity exercise can increase the production of pro-inflammatory cytokines and markers of endothelial injury in heart failure patients, whereas such changes are not observed during moderate exercise [58],[59].

Endothelial abnormalities are a key feature of heart failure. Many aspects of endothelial function are impaired, including vasomotor, hemostatic, antioxidant, and inflammatory activities. The specifics of endothelial dysfunction vary depending on the cause, severity, and stability of the heart failure. It has been shown that even in healthy individuals, moderate exercise enhances acetylcholine-induced vasodilation. Improvements in flow-mediated dilation (FMD) after exercise are associated with reverse left ventricular remodeling, significant increases in LVEF, and decreases in NT-proBNP levels [59].

Exercise intensity is crucial. Sudden high-intensity activity raises the production of pro-inflammatory cytokines and markers of endothelial injury in heart failure patients, while moderate activity does not cause such changes. Besides improving vasodilation, controlled exercise encourages reverse left ventricular remodeling, significantly enhances left ventricular ejection fraction, and reduces levels of N-terminal proB-type natriuretic peptide (NT-proBNP) [38],[60]. Coronary endothelial dysfunction is independently linked to impaired left ventricular relaxation in patients with preserved LVEF who lack coronary artery disease. Additionally, based on the text, coronary endothelial dysfunction in coronary artery disease is connected with further deterioration of left ventricular diastolic dysfunction. These findings are supported by evidence that changes in nitric oxide balance contribute to myocardial ischemia caused by myocardial hypertrophy and lead to heart failure. Therefore, coronary endothelial injury may play a central role in the pathophysiology of heart failure [38].

CONCLUSION

Controlled physical training is highly beneficial for patients with heart failure. Numerous randomized, controlled trials have shown that exercise can slow the progression of heart failure’s underlying causes. In chronic heart failure, physical training reduces neurohormonal activation and pro-inflammatory cytokine production, lowers levels of natriuretic peptides and systemic vascular resistance, and decreases oxidative stress. These positive effects also enhance symptoms, exercise capacity, and quality of life. Patients who do not see improvements in exercise capacity from physical training tend to have a poorer prognosis.

The intensity and type of exercise are critically important. Exercise programs must always be safe and free of harmful effects, and the health benefits depend, to some extent, on dose. In patients with heart failure, aerobic interval training is significantly more effective than moderate continuous training. Even in healthy individuals, moderate exercise increases acetylcholine-induced vasodilation. Improved FMD after exercise leads to reverse left ventricular remodeling, increases left ventricular ejection fraction, and reduces NT-proBNP levels.

Healthcare professionals, especially physicians, should play a crucial role in encouraging, guiding, and promoting proper exercise habits in patients. The process should start with an assessment of the patient’s current exercise capacity and needs, followed by the development of an initial training program that specifies the type of exercise, intensity, repetitions, duration in minutes per day, and the number of exercise days per week. Additional strategies should be used to motivate and support patients throughout the program. Involving qualified professionals is the best way to ensure proper implementation and monitoring of the exercise program.