Exercise intolerance in HFpEF is multifactorial, involving both cardiac and skeletal muscle defects, which supports the use of broad interventions like exercise training rather than targeting single defects.
Systematic analysis of the O2 pathway in HFpEF showed that exercise capacity was undermined by multiple defects, including reductions in cardiac output and skeletal muscle diffusion capacity. An important source of disease heterogeneity stemmed from variation in each patient's personal profile of defects. Personalized O2 pathway analysis could identify patients most likely to benefit from treating a specific defect; however, the system properties of O2 transport favor treating multiple defects at once, as with exercise training.
Houstis et al. (Mon,) studied this question.