Heart failure (HF) is a complex clinical syndrome characterized by a constellation of signs and symptoms involving various organ systems. Structural and/or functional cardiac abnormalities form a cornerstone to the pathophysiology of HF. However, extracardiac dysfunction plays an equally important role in its development and progression.1Approximately 50% or more of HF patients have HF with preserved left ventricular ejection fraction (HFPEF), and the proportion is higher among women and the elderly.2,3The main symptoms of this entity – similar to HF with reduced ejection fraction (HFREF) – are related to exercise intolerance4–9(dyspnea and fatigue) as well as reduced quality of life.5However, the pathophysiology of exercise intolerance in this group of patients is not well understood. There is scarcity in HFPEF mechanistic clinical studies and relatively few data regarding its treatment.10Exercise intolerance can be objectively expressed by reduced peak exercise oxygen consumption (VO2) measured by expired gas analysis, a technique that is valid and reproducible in patients with HFPEF.11,12According to Fick's equation, reduced peak VO2 results from either reduced cardiac output (CO), peripheral arterial-venous oxygen difference (A-VO2 Diff), or both.Many studies have reported that endurance exercise training (EET) improves peak VO2 in patients with HFREF,13,14and that this improvement results from favorable changes in cardiac,13,15–17peripheral vascular,15and skeletal muscle function.16,18–20These changes increase oxygen delivery to, and utilization by, the active muscles (i.e., increased A-VO2 Diff). In contrast, there are only four studies of such kind in patients with HFPEF21–24and the mechanisms of exercise training effects in this group are not known yet.
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