The body responds to exercise training by profound adaptations throughout the cardiorespiratory and muscular systems, which may result in improvements in maximal oxygen consumption (VO ₂ peak) and mitochondrial capacity. By convenience, mitochondrial respiration is often measured at supra-physiological oxygen levels, an approach that ignores any potential regulatory role of mitochondrial affinity for oxygen (p50 _mito ) at physiological oxygen levels.
In this study, we examined the p50 _mito of mitochondria isolated from the Vastus lateralis and Triceps brachii in 12 healthy volunteers before and after a training intervention with seven sessions of sprint interval training using both leg cycling and arm cranking. The changes in p50 _mito were compared to changes in whole-body VO ₂ peak.
We here show that p50 _mito is similar in isolated mitochondria from the Vastus (40 ± 3.8 Pa) compared to Triceps (39 ± 3.3) but decreases (mitochondrial oxygen affinity increases) after seven sessions of sprint interval training (to 26 ± 2.2 Pa in Vastus and 22 ± 2.7 Pa in Triceps, both P < .01). The change in VO ₂ peak modelled from changes in p50 _mito was correlated to actual measured changes in VO ₂ peak (R ² = .41, P = .002).
Together with mitochondrial respiratory capacity, p50 _mito is a critical factor when measuring mitochondrial function, it can decrease with sprint interval training and should be considered in the integrative analysis of the oxygen cascade from lung to mitochondria.