Oxygen Uptake Kinetics

Publisher Website
Google Scholar
Abstract
Muscular exercise requires transitions to and from metabolic rates often exceeding an order of magnitude above resting and places prodigious demands on the oxidative machinery and O2‐transport pathway. The science of kinetics seeks to characterize the dynamic profiles of the respiratory, cardiovascular, and muscular systems and their integration to resolve the essential control mechanisms of muscle energetics and oxidative function: a goal not feasible using the steady‐state response. Essential features of the O2 uptake ( o2) kinetics response are highly conserved across the animal kingdom. For a given metabolic demand, fast o2 kinetics mandates a smaller O2 deficit, less substrate‐level phosphorylation and high exercise tolerance. By the same token, slow o2 kinetics incurs a high O2 deficit, presents a greater challenge to homeostasis and presages poor exercise tolerance. Compelling evidence supports that, in healthy individuals walking, running, or cycling upright, o2 kinetics control resides within the exercising muscle(s) and is therefore not dependent upon, or limited by, upstream O2‐transport systems. However, disease, aging, and other imposed constraints may redistribute o2 kinetics control more proximally within the O2‐transport system. Greater understanding of o2 kinetics control and, in particular, its relation to the plasticity of the O2‐transport/utilization system is considered important for improving the human condition, not just in athletic populations, but crucially for patients suffering from pathologically slowed o2 kinetics as well as the burgeoning elderly population. © 2012 American Physiological Society. Compr Physiol 2:933‐996, 2012.