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.
Multifactorial HFpEF exercise limitation favors combined therapies; leaves open optimal single- versus multi-target strategies in trials.
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.
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Houstis et al. (2017) studied this question.
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