Oxygen Uptake Kinetics

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 (VO2) kinetics response are highly conserved across the animal kingdom. For a given metabolic demand, fast VO2 kinetics mandates a smaller O2 deficit, less substrate-level phosphorylation and high exercise tolerance. By the same token, slow VO2 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, VO2 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 VO2 kinetics control more proximally within the O2-transport system. Greater understanding of VO2 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 VO2 kinetics as well as the burgeoning elderly population.

Inorganic nitrate supplementation improves muscle oxygenation, O2uptake kinetics, and exercise tolerance at high but not low pedal rates

“…Providing the higher cadence condition in the current study increased the contribution of type II muscle fibers to force production (6, 7; but see 1), the increased muscle [O 2 Hb] with BR supplementation at the higher cadence might have attenuated the mismatch between muscle O 2 supply and muscle O 2 demand, facilitating a higher driving pressure for blood-tomyocyte O 2 flux and a more rapid adjustment of V O 2 during the step exercise test. This interpretation is in keeping with the O 2 'tipping point' theory proposed by Poole and Jones (51), which stipulates that phase II V O 2 kinetics is only speeded by interventions which enhance muscle O 2 delivery when muscle O 2 delivery is initially limited, at least in healthy adults. Alternatively, or in conjunction with enhanced fast-twitch muscle perfusion, inorganic NO 3 Ϫ supplementation has been shown to enhance calcium-handling proteins in fast-twitch muscle and to increase cytoplasmic [calcium] (34).…”

Increased peripheral vascular disease risk progressively constrains perfusion adaptability in the skeletal muscle microcirculation

“…It has become commonly accepted that NO bioavailability represents a critical contributor to the regulation of vascular tone under normal physiological conditions, and that the loss of this pathway represents a major element in vasculopathies and altered mass transport and exchange during challenged conditions (27,35,47,48,54). In this regard, the results from the present study may provide new insight into these relationships.…”

Modeling V?O2 and V?CO2 with Hammerstein-Wiener Models

“…A detailed review and historical account of the mathematical modeling of theV O 2 kinetics for constant work rate has recently been given by Poole and Jones (2012), containing over 800 references. See also Jones and Poole (2005) and, for a clarification, Ma et al (2010).…”