Effects of inspired O₂ and CO₂ on ventilatory responses to LBNP-release and acute head-down tilt

Increases in blood flow and CO₂ return to the heart and lungs at the onset of exercise have been proposed to initiate reflexive feedback which increases ventilation (V̇E), via mechanoreceptors in the heart and/or intrapulmonary CO₂ flow receptors. Both lower body negative pressure (-40 mm Hg) release (LBNP-release) and acute head-down (-30°) tilt (TILT) provide physiological models to focus upon the effects of increased venous return and CO₂ flow on V̇E, without the confounding influence of limb afferents or the descending efferents associated with central command. We examined the ventilatory responses to LBNP-release and TILT while inhaling one of four gas mixtures: a) room air (R); b) 95% O₂ (O); c) 95% O₂, 1.25% CO₂ (LC); and d) 95% O₂, 2.25% CO₂ (HC). Breath-by-breath measurements for V̇E end- tidal CO₂ (PETCO₂), tidal volume (VT), and breathing frequency (fB) were taken. V̇E and VT for HC were significantly higher (p < 0.05) than those for R, O, and LC throughout the test session, while fB and PETCO₂ were not significantly different among the gas treatments. V̇E increased (p < 0.05) above resting baseline with LBNP-release and TILT for R, O, LC, and HC primarily through an elevation of fB. Further, the maximal change in V̇E following LBNP-release or TILT were not different among inhaled gas mixtures. However, area under the V̇E curve following LBNP-release and TILT was higher for HC compared to the other gas mixtures. We conclude that these results are inconsistent with the theory that carotid bodies are essential in driving V̇E with these models. We postulate that mechanoreceptors in the right heart and/or pulmonary artery contribute to the elevation in V̇E which immediately follows LBNP-release and TILT.