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

AIM

We examined the Fick components together with mitochondrial O affinity (p50 ) in defining O extraction and O uptake during exercise with large and small muscle mass during normoxia (NORM) and hyperoxia (HYPER).

METHODS

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 VO were determined by thermodilution and the Fick method. Maximal ADP-stimulated mitochondrial respiration (OXPHOS) and p50 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 O delivery.

RESULTS

The ex vivo p50 increased from 0.06 ± 0.02 to 0.17 ± 0.04 kPa with varying substrate supply and O flux rates from 9.84 ± 2.91 to 16.34 ± 4.07 pmol O ·s ·μg respectively. O extraction decreased from 83% in BIKE to 67% in KE as a function of a higher O delivery and lower mitochondrial excess capacity. There was a significant relationship between O extraction and mitochondrial excess capacity and p50 that was unrelated to blood flow and mean transit time.

CONCLUSION

O extraction varies with mitochondrial respiration rate, p50 and O delivery. Mitochondrial excess capacity maintains a low p50 which enhances O diffusion from microvessels to mitochondria during exercise.