Contributions of the peripheral respiratory chemoreceptors to hyperpnea at intensities below the respiratory compensation point

We evaluated the contribution of the peripheral chemoreflex to the breathing response during steady-state exercise at intensities below the respiratory compensation point (RCP). Eighteen healthy, young participants (nine females) completed a maximal exercise protocol (<i>visit 1</i>) and three step-incremental protocols (<i>visits 2-4</i>) over 4 days. The step-incremental protocol involved two 8-min stages in the lower and upper regions of the moderate-intensity domain (MOD₁ and MOD₂; below lactate threshold, LT) and two 12-min stages within the heavy-intensity domain (HVY₁ and HVY₂; between LT and RCP). Six-to-10 breaths of 100% oxygen were administered twice at rest and at three time points during steady-state exercise at each intensity (<i>visits 2</i> and <i>3</i>), and arterialized-venous blood samples were obtained for blood gases and metabolites (<i>visit 4</i>). Gas exchange and ventilatory variables were measured breath-by-breath by metabolic cart and pneumotach. Peripheral chemoreflex contribution was determined as the absolute change in minute ventilation (ΔV̇e) between the average of breaths between 10 and ∼20 s after O₂ breathing and those in the 30 s before O₂ breathing. The average ΔV̇e at rest was -0.3 ± 1.0 L·min^-1 and this value decreased to -2.7 ± 1.6 L·min^-1 at MOD₁, -4.2 ± 1.8 L·min^-1 at MOD₂, -5.8 ± 2.5 L·min^-1 at HVY₁, and -7.0 ± 2.7 L·min^-1 at HVY₂ (one-way ANOVA; <i>P</i> < 0.001). However, the intensity-dependent reduction in ΔV̇e was no longer significant when accounting for [H⁺] [one-way analysis of covariance (ANCOVA); <i>P</i> = 0.515]. Therefore, the peripheral chemoreflex drive to breathe (in L·min^-1) increases with exercise intensity below RCP and may stem from a reflexive response to rising [H⁺].<b>NEW & NOTEWORTHY</b> We assessed peripheral chemoreflex (PChR) contributions to steady-state breathing at rest and at four exercise intensities below the respiratory compensation point by quantifying the fall in ventilation in response to surreptitious oxygen breathing. The magnitude by which ventilation fell increased progressively from rest to the highest intensity, indicating a rising PChR drive. Proton concentration from arterialized-venous blood also increased with intensity. Intensity-dependent increases in PChR drive may reflect a reflexive response to rising proton concentration.