ABSTRACT
Chapter 8 presents evidence that changing the conditions of O2 delivery can adjust the phosphorylation and redox potentials necessary to achieve a given V̇O2. Thus, decreasing muscle microvascular and intracellular partial pressures (PO2) slows V̇O2 kinetics and results in a greater perturbation of the intracellular milieu (Δ[PCr], Δ[Η+], for example) across the rest-exercise transition. However, to establish that O2 supply limits the speed of V̇O2 kinetics in healthy muscle under normal circumstances it must be demonstrated that increasing muscle microvascular and intracellular PO2 and contents speed V̇O2 kinetics. This chapter focuses on carefully controlled experiments that evaluate specifically whether conditions that substantially increase mitochondrial O2 availability can speed V̇O2 kinetics. One central theme developed in this book is that the rate at which skeletal muscle oxidative metabolism (V̇O2) adjusts to a new metabolic requirement is one of the factors that determines exercise tolerance.
