Muscle mass and inspired oxygen influence oxygen extraction at maximal exercise: Role of mitochondrial oxygen...

We examined the Fick components together with mitochondrial O₂ affinity (p50_mito ) in defining O₂ extraction and O₂ uptake during exercise with large and small muscle mass during normoxia (NORM) and hyperoxia (HYPER).

Seven individuals performed 2 incremental exercise tests to exhaustion on a bicycle ergometer (BIKE) and 2 on a 1-legged knee extension ergometer (KE) in NORM or HYPER. Leg blood flow and VO₂ were determined by thermodilution and the Fick method. Maximal ADP-stimulated mitochondrial respiration (OXPHOS) and p50_mito were measured ex vivo in isolated mitochondria. Mitochondrial excess capacity in the leg was determined from OXPHOS in permeabilized fibres and muscle mass measured with magnetic resonance imaging in relation to peak leg O₂ delivery.

The ex vivo p50_mito increased from 0.06 ± 0.02 to 0.17 ± 0.04 kPa with varying substrate supply and O₂ flux rates from 9.84 ± 2.91 to 16.34 ± 4.07 pmol O₂ ·s^-1 ·μg^-1 respectively. O₂ extraction decreased from 83% in BIKE to 67% in KE as a function of a higher O₂ delivery and lower mitochondrial excess capacity. There was a significant relationship between O₂ extraction and mitochondrial excess capacity and p50_mito that was unrelated to blood flow and mean transit time.

O₂ extraction varies with mitochondrial respiration rate, p50_mito and O₂ delivery. Mitochondrial excess capacity maintains a low p50_mito which enhances O₂ diffusion from microvessels to mitochondria during exercise.