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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.

During ramp incremental cycling exercise increases in pulmonary O2 uptake (V̇o2p) are matched by a linear increase in systemic cardiac output ( Q). However, it has been suggested that blood flow in the active muscle microvasculature does not display similar linearity in blood flow relative to metabolic demand. This study simultaneously examined both systemic and regional (microvascular) blood flow and O2 extraction during incremental cycling exercise. Ten young men (V̇o2 peak = 4.2 ± 0.5 l/min) and 10 young women (V̇o2 peak = 3.2 ± 0.5 l/min) were recruited to perform two maximal incremental cycling tests on separate days. The acetylene open-circuit technique and mass spectrometry and volume turbine were used to measure Q (every minute) and breath-by-breath V̇o2p, respectively; systemic arterio-venous O2 difference (a-vO2diff) was calculated as V̇o2p/ Q on a minute-by-minute basis. Changes in near-infrared spectroscopy-derived muscle deoxygenation (Δ[HHb]) were used (in combination with V̇o2p data) to estimate the profiles of peripheral O2 extraction and blood flow of the active muscle microvasculature. The systemic Q-to-V̇o2p relationship was linear (∼5.8 l/min increase in Q for a 1 l/min increase in V̇o2p) with a-vO2diff displaying a hyperbolic response as exercise intensity increased toward V̇o2 peak. The peripheral blood flow response profile was described by an inverted sigmoid curve, indicating nonlinear responses relative to metabolic demand. The Δ[HHb] profile increased linearly with absolute V̇o2p until high-intensity exercise, thereafter displaying a “near-plateau”. Results indicate that systemic blood flow and thus O2 delivery does not reflect the profile of blood flow changes at the level of the microvasculature.

Two methods for estimating changes in microvascular O2 delivery during the on-transient of exercise were evaluated. They were tested to assess the role of the adjustment of the estimated microvascular O2 delivery in the speeding of V̇o2 kinetics during a Mod1-Hvy-Mod2 protocol (Mod, moderate-intensity exercise; Hvy, heavy-intensity “priming” exercise), in which Mod2 is preceded by a bout of Hvy. Mod pulmonary V̇o2 (V̇o2p) and deoxy-hemoglobin [HHb] data were collected in 12 males (23 ± 3 yr); response profiles were fit with a monoexponential. Signals were also 1) scaled to a relative % of the response (0–100%) to calculate the [HHb]/V̇o2 ratio for each individual and 2) rearranged in the Fick equation for estimation of capillary blood flow (Qcap). A transient [HHb]/V̇o2 “overshoot” observed in Mod1 (1.06 ± 0.05; P < 0.05) was absent during Mod2 (1.01 ± 0.06; P > 0.05); reductions in the [HHb]/V̇o2 ratio (Mod1 − Mod2) were related to reductions in phase II τV̇o2p ( r = 0.82; P < 0.05). For Qcap, a near-exponential response was observed in 8/12 subjects in Mod1 and only in 4/12 subjects in Mod2. The Qcap profile was shown to be highly dependent on the [HHb] baseline-to-amplitude ratio. Thus, accurate and physiologically consistent estimations of Qcap were not possible in most cases. This study confirmed that priming exercise results in an improved O2 delivery as shown by the decreased [HHb]/V̇o2 ratio that was related to the smaller τV̇o2 in Mod2. Additionally, this study suggested that Qcap analysis may not be valid and should be interpreted with caution when assessing microvascular delivery of O2.

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.