Editorial: Exercise and heart failure

Heart failure (HF) is a complex disease that plagues public health with a still very high degree of mortality regardless of ejection fraction: reduced (HFrEF) or preserved (HFpEF) (Owan et al., 2006). The study of exercise physiology is of crucial importance to define the functional status of HF patients, to estimate prognosis, to guide therapy as well as to plan a possible rehabilitation program. In fact, exercise limitation is one of the cardinal symptoms of the patient with HF, not only in the case of maximal exertion, but also with regard to activities of daily living whose limitation negatively affects quality of life (Wilson and Mancini, 1993; Mapelli et al., 2020). The driver of exercise is the metabolic cost coupled by the hemodynamic and respiratory response, so that the jamming of one of the “gears” participating in this complex mechanism is actually the main cause of the disease. The most important parameter for measuring exercise capacity is oxygen uptake (VO2), which, according to Fick’s law, depends on cardiac output and arteriovenous oxygen content difference. Therefore, at a first glance exercise limitation is basically due to insufficient or delayed supply of O2 to the muscle, and in particular to the mitochondria. The proper delivery of oxygen to exercising muscles mitochondria basically depends on three variables: O2 delivery, pO2 reduction from arteries to capillaries, and O2 diffusion from capillaries to the mitochondrion (Wagner, 1992; Wagner, 1996; Rovai et al., 2021). The complex adjustment of these three factors is exemplified by Wagner’s diagram (Wagner, 1996; Rovai et al., 2021) (Figure 1), which shows: