Abstract
Skeletal Muscle O2 Diffusion and the Limitation of Aerobic Capacity in Heart Failure: A Clarification.
Highlights
The capacity to convey oxygen (O2) from the atmosphere in to mitochondria essentially determines maximal aerobic metabolism in humans [1,2,3,4,5,6]
While classic empirical studies in heart failure (HF) patients support the primary role of impaired cardiac pumping capacity in the limitation of VO2peak [14, 15], a recent paradigm based on theoretical assumptions attribute the main importance to skeletal muscle abnormalities in O2 diffusion from capillaries in to mitochondria [16]
DMO2 is portrayed as the ratio of skeletal muscle O2 consumption (VO2) and O2 pressure gradient between microvessels and mitochondria [21, 23, 24]
Summary
The capacity to convey oxygen (O2) from the atmosphere in to mitochondria essentially determines maximal aerobic metabolism in humans [1,2,3,4,5,6]. While classic empirical studies in HF patients support the primary role of impaired cardiac pumping capacity in the limitation of VO2peak [14, 15], a recent paradigm based on theoretical assumptions attribute the main importance to skeletal muscle abnormalities in O2 diffusion from capillaries in to mitochondria [16].
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