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  • 1
    ISSN: 1439-6327
    Keywords: Moderate exercise ; Hypoxia ; CO2 ; Leg oxygen consumption ; Leg blood flow ; Leg vascular resistance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: 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.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    European journal of applied physiology 58 (1989), S. 466-470 
    ISSN: 1439-6327
    Keywords: Blood flow ; Blood pressure ; Heart rate ; Lactate ; Oxygen uptake
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary This study was undertaken in an attempt to determine the maximal oxygen uptake in a small muscle group by measuring directly the oxygen expenditure of the forearm. Five healthy medical students volunteered. The subjects' maximal forearm work capacity was determined on a spring-loaded hand ergometer. Exercise was continued until exhaustion by pain or fatigue. Two weeks later intra-arterial and intravenous catheters were placed in the dominant arm. Blood samples for measurement of oxygen concentration were collected via the catheters. Forearm blood flow was measured by means of the indicator dilution technique. Oxygen uptake was determined according to the Fick principle. The forearm oxygen uptake attained at maximal work loads was a mean of 201 (SD±56) μmol · min−1 · 100 ml−1. It was impossible at maximal exercise to discern a plateau of the oxygen uptake curve in relation to work output. It is suggested that a plateau in the oxygen uptake curve is not a useful criterion for maximal oxygen uptake in a small muscle group. Skeletal muscle may have an unused capacity for oxygen consumption even at maximal exercise intensity where muscle work cannot be continued due to muscle pain and fatigue.
    Type of Medium: Electronic Resource
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