Effects of acute hypoxia and CO₂ inhalation on systemic and peripheral oxygen uptake and circulatory responses during moderate exercise

Summary

The effect of acute hypoxia and CO₂ inhalation on leg blood flow (LBF), on leg vascular resistance (LVR) and on oxygen supply to and oxygen consumption in the exercising leg was studied in nine healthy male subjects during moderate one-leg exercise. Each subject exercised for 20 min on a cycle ergometer in four different conditions: normoxia, normoxia +2% CO₂, hypoxia corresponding to an altitude of 4000 m above sea level, and hypoxia +1.2% CO₂. Gas exchange, heart rate (HR), arterial blood pressure, and LBF were measured, and arterial and venous blood samples were analysed for $P_{{\text{CO}}_{\text{2}} }$, $P_{{\text{O}}_{\text{2}} }$, oxygen saturation, haematocrit and haemoglobin concentration. Systemic oxygen consumption was 1.83 l · min⁻¹ (1.48–2.59) and was not affected by hypoxia or CO₂ inhalation in hypoxia. HR was unaffected by CO₂, but increased from 136 beat · min⁻¹ (111–141) in normoxia to 155 (139–169) in hypoxia. LBF was 6.5 l · min⁻¹ (5.4–7.6) in normoxia and increased significantly in hypoxia to 8.4 (5.9–10.1). LVR decreased significantly from 2.23 kPa · l⁻¹ · min (1.89–2.99) in normoxia to 1.89 (1.53–2.52) in hypoxia. The increase in LBF from normoxia to hypoxia correlated significantly with the decrease in LVR. When CO₂ was added in hypoxia a significant correlation was also found between the decrease in LBF and the increase in LVR. In normoxia, the addition of CO₂ caused a significant increase in mean blood pressure. Oxygen consumption in the exercising leg (leg $\dot V_{{\text{O}}_{\text{2}} }$) in normoxia was 0.97 l · min⁻¹ (0.72–1.10), and was unaffected by hypoxia and CO₂. It is concluded that the O₂ supply to the exercising leg and its $\dot V_{{\text{O}}_{\text{2}} }$ are unaffected by hypoxia and CO₂. The increase in LBF in hypoxia is caused by a decrease in LVR. These changes can be counteracted by CO₂ inhalation. It is proposed that the regulatory mechanism behind these changes is that change in brain $P_{{\text{CO}}_{\text{2}} }$ causes change in the central regulation of vascular tonus in the muscles.