Exercise capacity in patients with heart failure with preserved ejection fraction (HFpEF) is undermined by multiple defects, including reductions in cardiac output and skeletal muscle diffusion capacity, a recent study found. The mechanism of exercise intolerance in each of 134 patients (n= 79 with HFpEF; n=55 controls) was examined. Cardiopulmonary exercise testing (CPET) with invasive monitoring was performed to measure hemodynamics, blood gases, and gas exchange during exercise in order to quantify 6 steps of oxygen transport and utilization and to identify the defective steps that hinder exercise capacity (peak V_O2). Researchers found:

• Peak V_O2 was reduced by 34%±2% in HFpEF compared with controls of comparable age, gender, and body mass index (BMI).
• 97% of HFpEF patients concealed defects at multiple steps of the O₂ pathway.
• Cardiac output and skeletal muscle O₂ diffusion were impaired relative to controls by an average of 27±3% and 36±2%, respectively.
• Correcting a patient’s cardiac output led to a 7±0.5% predicted improvement in exercise intolerance.
• At the individual level, the impact of any given O₂ pathway defect on a patient’s exercise capacity was strongly influenced by comorbid defects.