Exercise Hyperemia is Preserved During Augmented Basal Oxygen Delivery in Humans

Abstract

The coupling between skeletal muscle blood flow and metabolic demand is largely attributed to feedback regulation of oxygen delivery. However, the relative importance of feedforward mechanisms in increasing blood flow in proportion to contractile work is unknown. We hypothesized that the change in blood flow following initiation of exercise is preserved independent of the level of baseline oxygen delivery, and that reciprocal reductions in oxygen extraction occur during elevations in resting blood flow. In 6 young healthy adults (4M/2F, 22±1 y) we quantified forearm blood flow (FBF; Doppler ultrasound), oxygen extraction (O2 extraction; based on venous O2 content), and forearm oxygen consumption (mVO2; Fick equation). Measurements were taken at rest and during 5 minutes of rhythmic handgrip exercise under control conditions and during intra‐arterial infusion of the vasodilator sodium nitroprusside (SNP) to pharmacologically manipulate oxygen delivery (O2D) prior to initiation of contractions. We elevated resting blood flow to levels that matched (MAT) and exceeded (EXC) steady‐state hyperemia during control (CON) exercise trials. Steady‐state FBF and O2D during dynamic forearm contractions at an intensity equivalent to 10% of participants maximal voluntary contraction under CON conditions were 159 ± 24 ml · min−1 and 32 ± 4.9 ml O2 · min−1, respectively. As intended, SNP infusion increased resting FBF (152 ± 26 ml · min−1) and O2D (31 ± 5.3 ml O2 · min−1) to levels similar to those observed during CON exercise in MAT (both P = NS), and further elevated FBF (196 ± 19 ml · min−1) and O2D (40 ± 4.0 ml O2 · min−1) to levels exceeding CON exercise in EXC (both P < 0.05). However, resting O2 extraction decreased in MAT (9 ± 5 %) and EXC (7 ± 4 %) compared to CON (49 ± 7 %; P < 0.05), and thus resting mVO2 was not different between conditions (range: ~2–3 ml O2 · min−1; P = NS). Despite elevating resting FBF and O2D to levels adequate to sustain muscle contractile work, the change in FBF in response to exercise remained intact during MAT (Δ FBF; 112 ± 20 ml · min−1) and EXC (Δ FBF; 133 ± 18 ml · min−1) compared to CON (Δ FBF; 123 ± 24 ml · min−1; all P = NS). As predicted, O2 extraction remained lower during steady‐state exercise in the MAT (45 ± 7 %) and EXC (39 ± 7 %) conditions compared to CON (66 ± 3 %; P < 0.05). However, the change in O2 extraction from rest to steady‐state exercise was not reduced (Δ O2 extraction: CON; 17 ± 5, MAT; 36 ± 5, EXC; 32 ± 5 %; P = NS), and thus mVO2 was not different between conditions (CON; 21 ± 2.9, MAT; 24 ± 4.5, EXC; 27 ± 5.6 ml O2 · min−1; P = NS). We conclude that changes in blood flow and oxygen extraction remain intact when oxygen delivery is artificially elevated prior to exercise, which highlights the importance of feedforward mechanisms capable of initiating changes in skeletal muscle blood flow independent of oxygen delivery. Support or Funding Information NIH HL119337