Regulation of V̇O ₂ kinetics by O ₂ delivery: Insights from acute hypoxia and heavy-intensity priming exercise in young men

This study examined the separate and combined effects of acute hypoxia (Hypo) and heavy-intensity "priming" exercise (Hvy) on pulmonary O ₂ uptake (V̇O _2p) kinetics during moderate-intensity exercise (Mod). Breath-by-breath V̇ O _2p and near-infrared spectroscopy-derived muscle deoxygenation {deoxyhemoglobin concentration [HHb]} were monitored continuously in 10 men (23 ± 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 (FI _O2) = 15%, Mod 2 + Hypo] or "sham" (FI _O2 = 20.9%, Mod 2-N) 2 min following Hvy in half of these repetitions; Mod was also performed in Hypo without Hvy (Mod 1 + Hypo). On-transient V̇O _2p 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-V̇O ₂ ratio was calculated. Compared with control (Mod 1), τV̇O _2p and the O ₂ deficit (26 ± 7 s and 638 ± 144 ml, respectively) were reduced (P < 0.05) in Mod 2-N (20 ± 5 s and 529 ± 196 ml) and increased (P < 0.05) in Mod 1 + Hypo (34 ± 14 s and 783 ± 184 ml); in Mod 2 + Hypo, τV̇O _2p was increased (30 ± 8 s, P < 0.05), yet O ₂ deficit was unaffected (643 ± 193 ml, P > 0.05). The modest "overshoot" in the [HHb]-to-V̇O ₂ ratio (reflecting an O ₂ delivery-to-utilization mismatch) in Mod 1 (1.06 ± 0.04) was abolished in Mod 2-N (1.00 ± 0.05), persisted in Mod 2 + Hypo (1.09 ± 0.07), and tended to increase in Mod 1 + Hypo (1.10 ± 0.09, P ± 0.13). The present data do not support an "O ₂ delivery-independent" speeding of τV̇O _2p following Hvy (or Hvy + Hypo); rather, this study suggests that local muscle O ₂ delivery likely governs the rate of adjustment of V̇O ₂ at τV̇O _2p greater than ∼20 s.