OXYGEN UPTAKE KINETICS: WHY ARE THEY SO SLOW? AND WHAT DO THEY TELL US?

(V) over dot(O2) kinetics and O-2 deficit represent important determinants of exercise tolerance and sport performance. In "normal" conditions convective and diffusive O-2 delivery to skeletal muscle fibers do not represent important determinants of (V) over dot(O2) kinetics. Thus, in "normal" conditions (e.g. normoxia, no impediments to O-2 delivery, absence of pathological conditions) the limiting factors for (V) over dot(O2) kinetics seem mainly located within muscle fibers. Whereas a limiting role by PDH has not been experimentally confirmed, the role of inhibition of mitochondrial respiration by NO needs further investigations. Important determinants of skeletal muscle (V) over dot(O2) kinetics likely reside in the interplay between the various mechanisms of energy provision at exercise onset. By acting as high-capacitance energy buffers, PCr hydrolysis and anaerobic glycolysis would delay or attenuate the increase in [ADP] within the cell following rapid increases in ATP demand, thereby buffering a more rapid activation of oxidative phosphorylation. The different "localization" of the main limiting factors for (V) over dot(O2) kinetics and (V) over dot(O2)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 (V) over dot(O2)max is mainly limited by the capacity of the cardiovascular system to deliver O-2 to exercising muscles, by analysis of (V) over dot(O2) kinetics the functional evaluation is mainly related to skeletal muscle. In pathological conditions the situation may be less clear, and warrants further investigations.