Mitochondrial oxygen affinity increases after sprint interval training and is related to the improvement in peak oxygen uptake, 2020, Larsen et al

[Andy]

Aims

The body responds to exercise training by profound adaptations throughout the cardiorespiratory and muscular systems, which may result in improvements in maximal oxygen consumption (VO2peak) 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 (p50mito) at physiological oxygen levels.

Methods
In this study, we examined the p50mito 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 p50mito were compared to changes in whole‐body VO2peak.

Results
We here show that p50mito 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 VO2peak modelled from changes in p50mito was correlated to actual measured changes in VO2peak (R2 = .41, P = .002).

Conclusion
Together with mitochondrial respiratory capacity, p50mito 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.

Open access, https://onlinelibrary.wiley.com/doi/full/10.1111/apha.13463

 

[Snow Leopard]

Note that a lower p50mito means the mitochondria have greater oxygen affinity, which reflects excess respiration capacity.

Unless the participant has a severe disease, VO2Max is always limited by the vascular system, namely the amount of oxygen that can be delivered to the muscle. Mitochondrial capacity is normally in excess of this.

But this begs the question, what happens during exercise training, how is this mitochondrial capacity regulated and how is this related to oxygen affinity?

The study results suggest that mitochondrial respiratory capacity is well regulated and remains in excess of the VO2Peak capacity after sprint training. Although the correlation between change in p50mito and VO2Peak was only moderate (R^2=0.41).