An assessment of DmO 2 is essential to help resolve the mechanistic basis for the deficits in ΔAV o 2 seen in patients with HFpEF. Thus, DmO 2 is a purer reflection of skeletal muscle properties than ΔAV o 2, incorporating features such as capillarity, fiber size, and fiber composition into its determination. In contrast, skeletal muscle diffusional conductance for oxygen (DmO 2) is a lumped parameter that summarizes all impediments to the transfer of oxygen from red blood cells into mitochondria, accounting for differences in blood flow. Because slower blood flow through the capillary can lead to greater oxygen extraction because of longer capillary transit time, ΔAV o 2 is not dependent solely on skeletal muscle properties ( 7). However, ΔAV o 2 is a complex metric, as the movement of oxygen out of skeletal muscle capillaries and into mitochondria is governed both by its delivery to the skeletal muscle capillary network (“convective transport”) and by factors that drive oxygen out of red blood cells and ultimately into skeletal muscle mitochondria (“diffusive transport”) ( 8). Several studies have focused on the arteriovenous oxygen content difference (ΔAV o 2), noting its reduction at peak exercise in subjects with HFpEF ( 5–7) and suggesting that this reflects impairments within the skeletal muscle itself. In addition to myocardial abnormalities ( 4), increasing evidence suggests that abnormalities outside the heart exist, giving rise to the possibility of “peripheral” contributors to exercise intolerance in patients with HFpEF. The heterogeneity of the condition, in addition to its incompletely understood pathophysiologic mechanisms, has led to a dearth of effective therapeutic options for these patients ( 3). An increasing number of patients have heart failure with preserved ejection fraction (HFpEF) ( 1), leading to hospitalizations and decreased quality of life ( 2).
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