| Abstract: | The primary purpose of this study was to determine the effect of acute (20-30 min) elevations of inspired CO2 partial pressure (PICO2) on whole-body O2 consumption (VO2). In human subjects, VO2 increased approximately 15 ml.min-1.m-2 with each 7-Torr increment in PICO2 from 0.4 to 28 Torr (P less than 0.05), but VO2 did not change significantly when PICO2 was increased from 28 to 35 and 42 Torr (P greater than 0.05). In ponies, VO2 did not change when PICO2 was increased from 0.7 to 7 Torr (P greater than 0.05), but it increased about 6 ml.min-1.m-2 with each 7-Torr increment in PICO2 from 7 to 28 Torr, and it increased 18 ml.min-1.m-2 when PICO2 was increased from 28 to 42 Torr (P less than 0.05). At low PICO2 the delta VO2/ delta VE was 25 and 7 ml/l for humans and ponies, respectively, where VE is pulmonary ventilation. These values exceeded the expected O2 cost of breathing; hence, some factor, such as shivering or nonshivering thermogenesis, contributed to the elevated VO2. At high PICO2, VE increased without a proportional increase in VO2; thus the delta VO2/ delta VE decreased to about 2.5 ml/l in ponies and to near 0.0 in humans. Accordingly, at high PICO2 some VO2-suppressing factor partially counteracted those factors stimulating VO2. The maximum decrease from control pHa was 0.061 and 0.038 in humans and ponies, respectively. It is questionable whether this mild acidosis was sufficient to suppress VO2. In both species, pulmonary excretion of metabolic CO2 and the respiratory exchange ratio were below control during CO2 inhalation (P less than 0.01), which suggested an increased tissue storage of CO2. |
