EN
O2 kinetics and O2 deficit are important determinants of exercise tolerance. In "normal" conditions convective and diffusive O2 delivery to skeletal muscle fibers do not represent important determinants of O2 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 O2 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 O2 kinetics and O2max offers the opportunity to perform a functional evaluation of oxidative metabolism at two different levels of the pathway for O2, from ambient air to mitochondria. WhereasO2max is mainly limited by the capacity of the cardiovascular system to deliver O2 to exercising muscles, by analysis of O2 kinetics the functional evaluation is mainly related to skeletal muscle. In pathological conditions the situation may be less clear, and warrants further investigations.