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The present study compared peak muscle deoxygenation ([HHb]peak) responses at three quadriceps sites during occlusion (OCC), ramp incremental (RI), severe- (SVR) and moderate-intensity (MOD) exercise. Seven healthy men (25 ± 4 yr) each completed a stationary cycling RI (20 W/min) test to determine [HHb]peak [at distal and proximal vastus lateralis (VLD and VLP) and rectus femoris (RF)], peak V̇o2 (V̇o2peak), gas exchange threshold (GET), and peak work rate (WRpeak). Subjects also completed MOD (WR = 80% GET) and SVR exercise (WR corresponding to 120% V̇o2peak) with absolute [HHb] (quantified by multichannel, time-resolved near-infrared spectroscopy) and pulmonary VO2 (V̇o2p) monitored continuously. Additionally, [HHb] and total hemoglobin ([Hb]tot) were monitored at rest and during subsequent OCC (250 mmHg). Site-specific adipose tissue thickness was assessed (B-mode ultrasound), and its relationship with resting [Hb]tot was used to correct absolute [HHb]. For VLD and RF, [HHb]peak was higher ( P < 0.05) during OCC (VLD = 111 ± 38, RF = 114 ± 26 μM) than RI (VLD 64 ± 14, RF = 85 ± 20) and SVR (VLD = 63 ± 13, RF = 81 ± 18). [HHb]peak was similar ( P > 0.05) across these conditions at the VLP (OCC = 67 ± 17, RI = 69 ± 17, SVR = 63 ± 17 μM). [HHb] peaked and then decreased prior to exercise cessation during SVR at all three muscle sites. [HHb]peak during MOD was consistently lower than other conditions at all sites. A “[HHb] reserve” exists during intense cycling at the VLD and RF, likely implying either sufficient blood flow to meet oxidative demands or insufficient diffusion time for complete equilibration. In VLP this [HHb] reserve was absent, suggesting that a critical Po2 may be challenged during intense cycling.

This study examined the separate and combined effects of acute hypoxia (Hypo) and heavy-intensity “priming” exercise (Hvy) on pulmonary O2 uptake (V̇o2p) kinetics during moderate-intensity exercise (Mod). Breath-by-breath V̇o2p 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 O2 (FiO2) = 15%, Mod 2 + Hypo] or “sham” (FiO2 = 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 V̇o2p 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-V̇o2 ratio was calculated. Compared with control (Mod 1), τV̇o2p and the O2 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, τV̇o2p was increased (30 ± 8 s, P < 0.05), yet O2 deficit was unaffected (643 ± 193 ml, P > 0.05). The modest “overshoot” in the [HHb]-to-V̇o2 ratio (reflecting an O2 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 “O2 delivery-independent” speeding of τV̇o2p following Hvy (or Hvy + Hypo); rather, this study suggests that local muscle O2 delivery likely governs the rate of adjustment of V̇o2 at τV̇o2p greater than ∼20 s.