Exercise & Sport Sciences Reviews:
Commentary to Accompany
School of Kinesiology and Health Studies, Queen’s University, Kingston, Ontario, Canada.
Authors for this section are recruited by Commentary Editor: Russell R. Pate, Ph.D., FACSM, Department of Exercise Science, University of South Carolina, Columbia, SC 29208 (E-mail: email@example.com).
The debate over whether oxygen (O2) delivery to exercising muscle does or does not limit oxygen uptake(V˙O2) kinetics has seen a number of swings in the pendulum of accepted understanding. The dominant current view is the “tipping point” hypothesis formulated by Poole and colleagues (2), which contends that, if reduced enough (tipping point crossed; experimentally, disease, aging), O2 delivery can limit V˙O2 kinetics. However, the normal healthy young human engaged in upright lower limb exercise is not beyond the tipping point. It is in this context that Murias and colleagues (1) present their recent work arguing that, even for young healthy individuals performing upright cycling exercise, microvascular O2 delivery can limit V˙O2 kinetics.
The evidence they present is based on a novel measurement/analysis approach they developed. Muscle microvascular Hb deoxygenation ([HHb] via near-infrared spectroscopy) and estimated muscle O2 consumption (breath by breath pulmonary V˙O2) is measured during the on-transient of cycling exercise. Normalization of the change in [HHb] and V˙O2 to 100% of their steady state levels and quantification of the normalized [HHb]/V˙O2 then allows for inferences to be made about the adequacy of microvascular O2 delivery in support of utilization demand. The principle behind utilization of [HHb]/V˙O2 and its interpretation is illustrated in the Figure. A reduction in the overshoot of [HHb]/V˙O2 indicates improved matching of microvascular O2 delivery to utilization. The case for a microvascular O2 delivery limitation in young healthy humans in cycling exercise is based on 1) differences in [HHb]/V˙O2 accounting for much of the interindividual variability in V˙O2 kinetics, 2) reductions in [HHb]/V˙O2 correlating strongly with improvement in V˙O2 kinetics with exercise training and previous heavy exercise interventions, and 3) the previous heavy exercise effect being abolished when hypoxia is used to (supposedly) offset previous exercise-evoked increased muscle perfusion.
The author’s interpretation certainly is plausible and may prove to be correct. However, there remains a fundamental limitation of the author’s measurement/analysis approach. Consideration of the Figure illustrates that speeding of V˙O2 kinetics with exercise training or previous heavy exercise also would be observed in response to faster increases in the activation of O2 utilization mechanisms. Although on its own this would either not reduce or perhaps even increase [HHb]/V˙O2 during the on-transient of exercise, the observed reduction in ratio overshoot also could reflect relatively greater improvement of microvascular O2 delivery matching demand that is coincident with, but not responsible for, faster V˙O2 kinetics.
Nevertheless, the work of Paterson’s group has important implications for advancing our understanding of the underlying composition of integrated mechanisms determining V˙O2 kinetics. First, it does urge a serious reconsideration of where a normal healthy young human sits relative to the tipping point and highlights the need to consider this in terms of individual differences. Furthermore, it proposes an O2 utilization constraint on V˙O2 kinetics (the tipping point) that is characterized by a time constant of approximately 20 s and suggests that improvements in microvascular O2 delivery are required for an individual to approach this limit.
This sets the stage for future work to determine whether and to what degree individual differences in V˙O2 kinetics are a function of different combinations of O2 delivery and utilization constraints, and what do these differences reveal about the integrated effects of O2 delivery and utilization mechanisms on these kinetics?
In summary, the work of Murias et al. (1) may swing the pendulum of accepted understanding again. However, this pendulum is unlikely to come to a stop until experimental methods allow for the definitive approach in which myocyte intracellular PO2 can be increased experimentally and monitored quantitatively in upright exercising healthy young humans to determine whether normal O2 provision is or is not limiting V˙O2 kinetics.
1. Murias JM, Spencer MD, Paterson DH. The critical role of O2
provision in the dynamic adjustment of oxidative phosphorylation. Exerc. Sport Sci. Rev. 2014; 42: 4–11.
2. Poole DC, Barstow TJ, McDonough P, Jones AM. Control of oxygen uptake during exercise. Med. Sci. Sports Exerc. 2008; 40: 462–74.