Effects of acute hypoxia and CO2 inhalation on systemic and peripheral oxygen uptake and circulatory responses during moderate exercise |
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Authors: | B Schibye K Klausen J Trap-Jensen J O Lund O Hartling |
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Institution: | (1) Laboratory for the Theory of Gymnastics, August Krogh Institute, University of Copenhagen, Denmark;(2) Department of Clinical Physiology, Frederiksberg Hospital, Denmark;(3) School of Physiotherapy, Lersø Parkalle 38, DK-2100 Copenhagen Ø, Denmark |
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Abstract: | 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
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, 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
) 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
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
causes change in the central regulation of vascular tonus in the muscles. |
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Keywords: | Moderate exercise Hypoxia CO2 Leg oxygen consumption Leg blood flow Leg vascular resistance |
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