Exercise Limitations in Heart Failure with Reduced and Preserved Ejection Fraction

The hallmark symptom of chronic heart failure (CHF) syndrome is severe exercise intolerance. Impaired perfusive and diffusive O₂ transport are two of the major determinants of reduced physical capacity and lowered maximal O₂ uptake (VO₂max) in CHF patients. It has now become evident that this syndrome manifests two different phenotypic variations: heart failure with preserved or reduced ejection fraction (HFpEF and HFrEF, respectively). Unlike HFrEF, however, there is currently limited understanding of HFpEF pathophysiology leading to a lack of effective pharmacological treatments for this subpopulation. This brief review focuses on the disturbances within the O₂ transport pathway resulting in limited exercise capacity in both HFpEF and HFrEF. Evidence from human and animal research reveals CHF-induced impairments in both perfusive and diffusive O₂ conductances identifying potential targets for clinical intervention. Specifically, utilization of different experimental approaches in humans (e.g., small vs. large muscle mass exercise) and animals (e.g., intravital microscopy and phosphorescence quenching) has provided important clues to elucidating these pathophysiological mechanisms. Adaptations within the skeletal muscle O₂ delivery-utilization system following established and emerging therapies (e.g., exercise training and inorganic nitrate supplementation, respectively) are discussed. Clarifying the underlying mechanisms of skeletal muscle dysfunction and exercise intolerance is necessary for the development and refinement of treatments for CHF patients.

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