Why the study?
Does exercise at Vo2 max under normoxic and hypoxic conditions alter mean myoglobin oxygen tension in normal nonathlete subjects?
Does exercise at Vo2 max under normoxic and hypoxic conditions alter mean myoglobin oxygen tension in normal nonathlete subjects?
Mean myoglobin Po2 falls during exercise at Vo2 max, supporting the postulate that intracellular O2 availability is one of several limiting factors for aerobic capacity.
Mean Mb PO2 falls at VO2max in nonathletes; hypothesis-generating for intracellular O2 as a limiter of aerobic capacity.
Changes in intracellular Po2 in myoglobin containing skeletal muscle during exercise were estimated in normal nonathlete subjects from measurements of shifts of CO between blood and muscle under conditions where the total body CO stores remained constant. Exercise was performed on a bicycle ergometer. In 1.5-2 and 6-7 min runs at Vo2 max with the subject breathing 21% O2, mean MbCO/HbCO increased 146 +/- 7 and 163 +/- 11% of resting values, respectively (P less than 0.05). With the subjects breathing 13-14% O2, in 1.5-2 and 6-7 min runs, Vo2 max fell an average of 4.3 +/- 5.1% and 12.0 +/- 5.2%, respectively, and mean MbCO/HbCO increased to 233 +/- 18% and 210 +/- 52% of resting value, respectively (P less than 0.05). These findings suggest that mean myoglobin Po2 fell during exercise at Vo2 max, with the subjects breathing 21% O2 and the decrease in mean myoglobin Po2 was greater with the subject breathing 13-14% O2. There was considerable variability in different subjects and in some, the data were not consistent with intracellular O2 availability limiting aerobic metabolism. The data support a postulate that there are several limiting factors for the aerobic capacity, including intracellular O2 availability.
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Clark et al. (1975) studied this question.
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