Exercise intolerance in patients with heart failure is driven by both central and peripheral factors, with peripheral impairments playing a relatively greater role in limiting exercise performance in those with preserved ejection fraction.
What are the mechanisms of exercise intolerance in patients with HFrEF and HFpEF?
Exercise intolerance in HFpEF may be more heavily driven by peripheral vascular and skeletal muscle impairments compared to HFrEF, highlighting potential therapeutic targets.
This mini-review summarizes the literature regarding the mechanisms of exercise intolerance in patients with heart failure and reduced or preserved ejection fraction (HFREF and HFPEF, respectively). Evidence to date suggests that the reduced peak pulmonary oxygen uptake (pulm V̇o₂) in patients with HFREF compared with healthy controls is due to both central (reduced convective O₂ transport) and peripheral factors (impaired skeletal muscle blood flow, decreased diffusive O₂ transport coupled with abnormal skeletal morphology, and metabolism). Although central and peripheral impairments also limit peak pulm V̇o₂ in HFPEF patients compared with healthy controls, emerging data suggest that the latter may play a relatively greater role in limiting exercise performance in these patients. Unlike HFREF, currently there is limited evidence-based therapies that improve exercise capacity in HFPEF patients, therefore future studies are required to determine whether interventions targeted to improve peripheral vascular and skeletal muscle function result in favorable improvements in peak pulm and leg V̇o2 and their determinants in HFPEF patients.
Haykowsky et al. (Sat,) conducted a review in Heart failure with reduced or preserved ejection fraction. Exercise intolerance in patients with heart failure is driven by both central and peripheral factors, with peripheral impairments playing a relatively greater role in limiting exercise performance in those with preserved ejection fraction.