## 1 Introduction  
Heart failure with preserved ejection fraction (HFpEF) is a disease characterized by the inability of the heart to fill adequately with blood during diastole, despite maintaining normal systolic function [1]. In contrast to patients with heart failure with a reduced ejection fraction (HFrEF), in which systolic dysfunction is the main problem, patients with HFpEF have preserved systolic function but significant diastolic dysfunction, resulting in elevated filling pressures and impaired ventricular relaxation [2]. This dysfunction is aggravated by comorbidities such as hypertension, obesity, diabetes, and atrial fibrillation, which are common in patients with HFpEF [3]. Clinical presentation often includes exercise intolerance, fatigue, and dyspnea, and exercise capacity is an important predictor of adverse outcomes [4]. HFpEF represents a growing public health challenge due to its increasing prevalence, particularly among older adults, and its association with high morbidity and mortality rates [5]. Additionally, HFpEF represents a major clinical challenge due to its complex pathophysiology and the limited efficacy of current therapeutic strategies [6]. Therapeutic options for HFpEF are focused mainly on controlling comorbidities and improving quality of life, as there is currently no definitive treatment that addresses the underlying pathophysiology of HFpEF [7]. Common pharmacological interventions include the use of diuretics to reduce symptoms of fluid overload; beta-blockers, angiotensin-converting enzyme inhibitors (ACEIs), and angiotensin receptor antagonists (ARBs) to control blood pressure; and mineralocorticoid receptor antagonists (MRAs) to improve outcomes in selected patients [8]. In addition, sodium-glucose transport protein 2 (SGLT2) inhibitors have recently shown promise in reducing hospitalizations in patients with HFpEF [9]. Nonpharmacolied interventions, such as lifestyle modifications and structured exercise programs (referring to systematically designed exercise interventions that combine specific types of physical activity, such as aerobic and resistance training, with a defined frequency, intensity, and duration), are also crucial components of HFpEF treatment [10]. Exercise has become the cornerstone of treatment for HFpEF [11]. In contrast to pharmacological interventions, which seem to show limited success in improving HFpEF outcomes, exercise training has consistently demonstrated benefits in improving cardiovascular and musculoskeletal function [12]. Regular physical activity, particularly structured exercise programs, has been shown to improve maximal oxygen uptake (VO2 max), reduce symptoms, and improve quality of life in patients with HFpEF [13]. Aerobic exercise is the most studied modality, offering unique benefits that address the multifaceted nature of HFpEF. This involves a combination of central (cardiac) dysfunction, such as impaired diastolic function, and peripheral (vascular and muscular) abnormalities, such as endothelial dysfunction and muscle atrophy, that contribute to the general exercise intolerance observed in these patients [14]. However, modalities such as combined exercise (CE) (aerobic and strength training) and high-intensity interval training (HIIT) have shown slightly better results than aerobic exercise in patients with HFpEF [11]. These exercise interventions not only improve hemodynamic responses and ventricular distensibility, but also help mitigate peripheral abnormalities such as endothelial dysfunction and the progression of muscle atrophy, especially in the muscles of the lower extremities, including the quadriceps and calf muscles, which are crucial for locomotion in this patient population [15]. Therefore, the incorporation of exercise as a therapeutic strategy is crucial in improving functional capacity, reducing hospitalizations, and ultimately improving the prognosis of patients with HFpEF [16].