Mitochondrial affinity for oxygen was recently demonstrated to increase after sprint training and turned out to be closely associated with training‐related improvement in pulmonary peak oxygen uptake (VO₂peak) during both arm cranking and leg cycling.1 Although logically the final step of the oxygen cascade should be modulated by mitochondrial oxygen affinity with notable impact on VO₂peak, experimental evidence for such modulation is scarce. The report of Larsen and colleagues considerably strengthens this conception but also reveals the necessity of integrative considerations and current experimental limitations.

The overall research work of these authors is largely contributing to the contemporary understanding of regulatory mitochondrial function in the oxygen transport system. Their studies implicate mitochondrial oxygen affinity, among others, in the control of the basal metabolic rate (BMR) and locomotion efficiency,2 muscle mass‐related oxygen extraction3 and training‐induced improvements in aerobic capacity.1

短跑训练后，线粒体对氧气的亲和力最近得到了证明，并且与手臂弯曲和腿部骑行过程中与训练相关的肺部峰值吸氧量（VO ₂峰值）的改善密切相关。1尽管从逻辑上讲，应通过线粒体氧亲和力来调节氧级联反应的最后一步，这对VO ₂峰具有显着影响，但这种调节的实验证据很少。Larsen及其同事的报告在很大程度上强化了这一概念，但同时也揭示了综合考虑和当前实验局限性的必要性。

这些作者的整体研究工作在很大程度上促进了当代对氧气输送系统中线粒体调节功能的了解。他们的研究暗示线粒体氧亲和力，尤其是在控制基础代谢率（BMR）和运动效率，2肌肉质量相关的氧提取3和训练引起的有氧能力改善方面。1个