EFFECTS OF INSPIRED O-2 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 o nset of exercise have been proposed to initiate reflexive feedback whi ch increases ventilation (VE), via mechanoreceptors in the heart and/ or intrapulmonary CO2 flow receptors. Both lower body negative pressur e (-40 mm Hg) release (LBNP-release) and acute head-down (-30 degrees) tilt (TILT) provide physiological models to focus upon the effects of increased venous return and CO2 flow on VE, without the confounding i nfluence of limb afferents or the descending efferents associated with central command. We examined the ventilatory responses to LBNP-releas e and TILT while inhaling one of four gas mixtures: a) room air (R); b ) 95% O-2 (O); c) 95% O-2, 1.25% CO2 (LC); and d) 95% O-2, 2.25% CO2 I HC). Breath-by-breath measurements for VE end-tidal CO2 (PETCO(2)), ti dal volume (VT), and breathing frequency (fs) were taken. VE and VT fo r HC were significantly higher (p < 0.05) than those for R, O, and LC throughout the test session, while fs and PETCO(2) were not significan tly different among the gas treatments. VE increased (p < 0.05) above resting baseline with LBNP-release and TILT for R, O, LC, and HC prima rily through an elevation of fB. Further, the maximal change in VE fol lowing LBNP-release or TILT were not different among inhaled gas mixtu res. However, area under the VE 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 ar e essential in driving VE with these models. We postulate that mechano receptors in the right heart and/or pulmonary artery contribute to the elevation in VE which immediately follows LBNP-release and TILT.