Delayed metabolic activation of oxidative phosphorylation in skeletal muscle at exercise onset.

In "normal" conditions (e.g., normoxia, absence of pathological conditions) convective and diffusive O(2) delivery to skeletal muscle fibers do not seem to represent important determinants for the kinetics of adjustment of oxidative phosphorylation following increases in metabolic demand. Whereas a limiting role by PDH has not been experimentally confirmed, inhibition of mitochondrial respiration by NO could be partially responsible for the delayed activation of oxidative phosphorylation at exercise onset. The main determinants of muscle VO(2) kinetics, however, likely reside in the intricate 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 "PCr-Cr shuttle" concept of a regulatory role of PCr or of the products of PCr hydrolysis on oxidative phosphorylation provides a mechanism that couples VO(2), which occurs in mitochondria, to PCr hydrolysis occurring in the cytoplasm.