Oxygen uptake kinetics: why are they so slow? And what do they tell us?

VO(2) kinetics and O(2) deficit are important determinants of exercise tolerance. In "normal" conditions convective and diffusive O(2) delivery to skeletal muscle fibers do not represent important determinants of VO(2) kinetics, whose limiting factors seem mainly located within muscle fibers. Whereas a limiting role by PDH has not been confirmed, the role of inhibition of mitochondrial respiration by NO needs further investigations. Important determinants of skeletal muscle VO(2) kinetics likely reside in the interplay between bioenergetic mechanisms at exercise onset. By acting as high-capacitance energy buffers, PCr hydrolysis and anaerobic glycolysis would delay or attenuate the increase in [ADP] within muscle fibers following rapid increases in ATP demand, preventing a more rapid activation of oxidative phosphorylation. The different "localization" of the main limiting factors for VO(2) kinetics and VO(2)max offers the opportunity to perform a functional evaluation of oxidative metabolism at two different levels of the pathway for O(2), from ambient air to mitochondria. Whereas VO(2)max is mainly limited by the capacity of the cardiovascular system to deliver O(2) to exercising muscles, by analysis of VO(2) kinetics the functional evaluation is mainly related to skeletal muscle. In pathological conditions the situation may be less clear, and warrants further investigations.