Mechanisms of the Improvement in Peak VO₂ With Exercise Training in Heart Failure With Reduced or Preserved Ejection Fraction

Heart failure (HF) is a major health care burden associated with high morbidity and mortality. Approximately 50% of HF patients have reduced ejection fraction (HFrEF) while the remainder of patients have preserved ejection fraction (HFpEF). A hallmark of both HF phenotypes is dyspnoea upon exertion and severe exercise intolerance secondary to impaired oxygen delivery and/or use by exercising skeletal muscle. Exercise training is a safe and effective intervention to improve peak oxygen uptake (VO_2peak) and quality of life in clinically stable HF patients, however, evidence to date suggests that the mechanism of this improvement appears to be related to underlying HF phenotype. The purpose of this review is to discuss the role of exercise training to improve VO_2peak, and how the central and peripheral adaptations that mediate the improvements in exercise tolerance may be similar or differ by HF phenotype (HFrEF or HFpEF).