Increased steady-state VO2 and larger O2 deficit with CO2 inhalation during exercise

To examine whether inhalation of CO(2) -enriched gas would increase steady-state VO(2) during exercise and enlarge O(2) deficit.

Ten physically active men (VO(2) 53.7 ± 3.6 mL min(-1) kg(-1) ; x ± SD) performed transitions from low-load cycling (baseline; 40 W) to work rates representing light (≈ 45% VO(2); 122 ± 15 W) and heavy (≈ 80% VO(2); 253 ± 29 W) exercise while inhaling normal air (air) or a CO(2) mixture (4.2% CO(2) , 21% O(2) , balance N(2) ). Gas exchange was measured with Douglas bag technique at baseline and at min 0-2, 2-3 and 5-6.

Inhalation of CO(2) -enriched air consistently induced respiratory acidosis with increases in PCO(2) and decreases in capillary blood pH (P < 0.01). Hypercapnic steady-state VO(2) was on average about 6% greater (P < 0.01) than with air in both light and heavy exercise, presumably because of increased cost of breathing (ΔVE 40-50 L min(-1) ; P < 0.01), and a substrate shift towards increased lipid oxidation (decline in R 0.12; P < 0.01). VO(2) during the first 2 min of exercise were not significantly different whereas the increase in VO(2) from min 2-3 to min 5-6 in heavy exercise was larger with CO(2) than with air suggesting a greater VO(2) slow component. As a result, O(2) deficit was greater with hypercapnia in heavy exercise (2.24 ± 0.51 L vs. 1.91 ± 0.45 L; P < 0.05) but not in light (0.64 ± 0.21 L vs. 0.54 ± 0.20 L; ns).

Inhalation of CO(2)-enriched air and the ensuing respiratory acidosis increase steady-state VO(2) in both light and heavy exercise and enlarges O(2) deficit in heavy exercise.