Regulation of V̇o₂ kinetics by O₂ delivery: insights from acute hypoxia and heavy-intensity priming exercise in young men

Abstract

Spencer MD, Murias JM, Grey TM, Paterson DH. Regulation of VO 2 kinetics by O2 delivery: insights from acute hypoxia and heavy-intensity priming exercise in young men. J Appl Physiol 112: 1023-1032, 2012. First published December 22, 2011 doi:10.1152/japplphysiol.01215.2011.-This study examined the separate and combined effects of acute hypoxia (Hypo) and heavy-intensity "priming" exercise (Hvy) on pulmonary O 2 uptake (V O2p) kinetics during moderate-intensity exercise (Mod). Breath-by-breath V O2p and near-infrared spectroscopy-derived muscle deoxygenation {deoxyhemoglobin concentration [HHb]} were monitored continuously in 10 men (23 Ϯ 4 yr) during repetitions of a Mod 1-Hvy-Mod 2 protocol, where each of the 6-min (Mod or Hvy) leg-cycling bouts was separated by 6 min at 20 W. Subjects were exposed to Hypo [fraction of inspired O 2 (FIO 2 ) ϭ 15%, Mod 2 ϩ Hypo] or "sham" (FI O 2 ϭ 20.9%, Mod 2-N) 2 min following Hvy in half of these repetitions; Mod was also performed in Hypo without Hvy (Mod 1 ϩ Hypo). On-transient V O2p and [HHb] responses were modeled as a monoexponential. Data were scaled to a relative percentage of the response (0 -100%), the signals were time-aligned, and the individual [HHb]-to-V O2 ratio was calculated. Compared with control (Mod 1), V O2p and the O2 deficit (26 Ϯ 7 s and 638 Ϯ 144 ml, respectively) were reduced (P Ͻ 0.05) in Mod 2-N (20 Ϯ 5 s and 529 Ϯ 196 ml) and increased (P Ͻ 0.05) in Mod 1 ϩ Hypo (34 Ϯ 14 s and 783 Ϯ 184 ml); in Mod 2 ϩ Hypo, V O2p was increased (30 Ϯ 8 s, P Ͻ 0.05), yet O 2 deficit was unaffected (643 Ϯ 193 ml, P Ͼ 0.05). The modest "overshoot" in the [HHb]-to-V O2 ratio (reflecting an O 2 delivery-to-utilization mismatch) in Mod 1 (1.06 Ϯ 0.04) was abolished in Mod 2-N (1.00 Ϯ 0.05), persisted in Mod 2 ϩ Hypo (1.09 Ϯ 0.07), and tended to increase in Mod 1 ϩ Hypo (1.10 Ϯ 0.09, P ϭ 0.13). The present data do not support an "O 2 delivery-independent" speeding of V O2p following Hvy (or Hvy ϩ Hypo); rather, this study suggests that local muscle O2 delivery likely governs the rate of adjustment of V O2 at V O2p greater than ϳ20 s. oxygen extraction; oxygen distribution; muscle blood flow; nearinfrared spectroscopy THE FUNDAMENTAL ADJUSTMENT of pulmonary O 2 uptake (V O 2p ) kinetics displays an exponential profile during the on-transient to moderate-intensity exercise (Mod). Whether the rate of this adjustment, given by the V O 2p time constant (V O 2p ), is limited by factors related to local muscle O 2 availability, intracellular factors related to metabolic substrate provision and enzyme activation, or a combination of both remains a topic of debate. Poole et al. (30) proposed that there is a "point" beyond which O 2 uptake (V O 2 ) kinetics are O 2 -dependent, such that the provision of O 2 becomes limiting and, thus, V O 2 is lengthened. While this proposal has received much attention within the literature, it has yet to be demonstrated that provision of "additional" O 2 resolves any potential O 2 delivery limitation.In contrast to this possibility, Grassi et...

Noninvasive estimation of microvascular O2 provision during exercise on-transients in healthy young males

“…The data presented in this study are part of a larger project also looking at the effects of hypoxia on V O2 kinetics. As such, parts of the data regarding the effects of priming exercise on the V O2 and [HHb] kinetics response from 9 of the 12 subjects were previously presented as the control data relative to an hypoxia intervention (22), whereas the present paper adds the focus on the Q cap kinetics. All procedures were approved by The University of Western Ontario Research Ethics Board for Health Sciences Research Involving Human Subjects.…”

“…These studies collectively showed that, although intracellular mechanisms are likely the principal putative factors controlling the adjustment of V O 2 kinetics during the initial response to a step increment in power output, for pulmonary V O 2p time constant (V O 2p ) values greater than ϳ20 s, the rate of adjustment of phase II V O 2p is also constrained by the matching of local O 2 delivery to muscle V O 2 . More specifically, we have shown recently that a significant reduction in the phase II V O 2p when moderate-intensity exercise is preceded by a bout of heavy-intensity (i.e., supra-lactate threshold) "priming" exercise was related to improvements in the matching of O 2 delivery to O 2 utilization, as reflected by reductions in the [HHb]/V O 2 ratio (16,22). Using a somewhat similar approach, Buchheit et al (4) indicated that a smaller V O 2p during the second bout of moderate-intensity running in those participants in whom the first bout showed a rather slow rate of adjustment for phase II V O 2p was related to improvements in O 2 provision, as reflected by a faster adjustment of Q cap [i.e., Q cap mean response time (MRT)].…”

The Complex Reality of VO2 Kinetics to Steady State: Reassessment of the Models Used to Quantify and Interpret VO2 Kinetics, Steady State, and Time to Steady State

“…Most commonly, the literature will refer to either the anaerobic threshold, lactate threshold, metabolic threshold, gas exchange threshold, or ventilation threshold (VT) when designing steady state exercise protocols (Hughson & Morrisey, 1982;Rossiter et al, 1999;Koppo et al, 2004;Murias et al, 2010;Spencer et al, 2012;McNulty et al, 2015). Surpassing of the lactate threshold is 14…”

“…Nevertheless, some researchers quantify the time difference between the onset of exercise and the end of phase-I (i.e. the phase-I duration) as a time delay Barstow & Mole, 1991;Grassi et al, 1996;Spencer et al, 2012). See Figure 2-4 for a graphical representation of all three phases.…”

“…The kinetic parameters of the V O2 response to an increased work-rate to steady state are based on complete kinetic modelling by a mono-exponential equation (Whipp, 1971;Linnarson, 1974;Whipp et al, 1982;Rossiter et al, 1999;Koppo et al, 2004;Spencer et al, 2012). Despite past experimentation contradicting the linearity of the response kinetics (Hughson & Morrissey, 1982;Brittain et al, 2001;McNulty et al, 2015), and commentaries on the over-simplification of a monoexponential model to explain V O2 kinetics (Stirling et al, 2005), the use of this processing method has continued, mostly undeterred.…”