No abstract

Moreover, the anemia ϩ hypoxia condition caused a very extreme arterial hypoxemia. We have previously reported some of these data, and they solely focused on comparing normoxia with hypoxia (9), or normal with low [Hb] (10). METHODSSubjects. Seven young men (age 24 Ϯ 1 yr) participated in the study. Their mean height and weight were 183 Ϯ 3 cm and 85.1 Ϯ 4.6 kg, respectively. Their maximal pulmonary O 2 consumption (V O 2 ), determined by cycle ergometry, was 55 Ϯ 5 ml·kg Ϫ1 · min Ϫ1 (range 41-70), and maximal cardiac output (Q TOT ) was 26 Ϯ 0.8 l/min (range 23-28). Additional description of anthropometric and muscle characteristics of these seven subjects as well as more details on methods and study design are available in a previous publication (10). All subjects were informed about the procedures and risks of the study before giving written informed consent to participate as approved by the Copenhagen Fredriksberg Ethical Committee.Experimental protocol. Subjects were studied on two occasions: once with their normal [Hb] and at least 1 wk later after blood withdrawal with low [Hb]. The afternoon before the low [Hb] experiment, 1-1.5 l of whole blood (average 1.3 Ϯ 0.05 l, ϳ20% of subject's blood volume) were withdrawn from each subject and replaced by an equal volume of human serum albumin (5% albumin). After normovolemic hemodilution, the blood volume was maintained (7.06 Ϯ 0.46 to 6.93 Ϯ 0.48 l, pre-post blood removal, P Ͼ 0.8), and [Hb] and hematocrit dropped ϳ20%, to 114.7 Ϯ 1.9 g/l and 34.4 Ϯ 0.4%, respectively (10). At the end of the low [Hb] experiment, the previously removed whole blood was reinfused to the subject. During the normal and low [Hb] experiments, the subjects inspired 0.21 and 0.11 FI O 2 in N 2 administered in random order. These tests were separated by at least 1 h of rest in the semirecumbent position while subjects breathed room air. In those subjects who breathed hypoxic gas first, in some cases the subsequent resting measurements for lactate were above baseline, although no effects of order of hypoxia were observed during exercise.

We hypothesized that exercise would cause greater severity and incidence of acute mountain sickness (AMS) in the early hours of exposure to altitude. After passive ascent to simulated high altitude in a decompression chamber [barometric pressure = 429 Torr, approximately 4,800 m (J. B. West, J. Appl. Physiol. 81: 1850-1854, 1996)], seven men exercised (Ex) at 50% of their altitude-specific maximal workload four times for 30 min in the first 6 h of a 10-h exposure. On another day they completed the same protocol but were sedentary (Sed). Measurements included an AMS symptom score, resting minute ventilation (VE), pulmonary function, arterial oxygen saturation (Sa(O(2))), fluid input, and urine volume. Symptoms of AMS were worse in Ex than Sed, with peak AMS scores of 4.4 +/- 1.0 and 1.3 +/- 0.4 in Ex and Sed, respectively (P < 0.01); but resting VE and Sa(O(2)) were not different between trials. However, Sa(O(2)) during the exercise bouts in Ex was at 76.3 +/- 1.7%, lower than during either Sed or at rest in Ex (81.4 +/- 1.8 and 82.2 +/- 2.6%, respectively, P < 0.01). Fluid intake-urine volume shifted to slightly positive values in Ex at 3-6 h (P = 0.06). The mechanism(s) responsible for the rise in severity and incidence of AMS in Ex may be sought in the observed exercise-induced exaggeration of arterial hypoxemia, in the minor fluid shift, or in a combination of these factors.

the cardiovascular response to dynamic knee-extensor exercise. Am. J. Physiol. 272 (Heart Circ. Physiol. 41): H2655-H2663,1997.-Hypoxia affects 02 transport and aerobic exercise capacity. In two previous studies, conflicting results have been reported regarding whether 02 delivery to the muscle is increased with hypoxia or whether there is a more efficient 02 extraction to allow for compensation of the decreased 02 availability at submaximal and maximal exercise. To reconcile this discrepancy, we measured limb blood flow (LBF), cardiac output, and O2 uptake during two-legged knee-extensor exercise in eight healthy young men. They completed studies at rest, at two submaximal workloads, and at peak effort under normoxia (inspired O2 fraction 0.21) and two levels of hypoxia (inspired O2 fractions 0.16 and 0.11). During submaximal exercise, LBF increased in hypoxia and compensated for the decrement in arterial 02 content. At peak effort, however, our subjects did not achieve a higher cardiac output or LBF. Thus O2 delivery was not maintained and peak power output and leg 02 uptake were reduced proportionately.These data are consistent then with the findings of an increased LBF to compensate for hypoxemia at submaximal exercise, but no such increase occurs at peak effort despite substantial cardiac capacity for an elevation in LBF. (18) concluded that, as long as the mass of active muscle is too small to tax the pumping capacity of the heart, vasodilatation and LBF can rise to higher values than those attained under normoxemia. The elevation can be of such a magnitude as to compensate, even in severe hypoxemia, for the lowered arterial O2 content (Ca,z>, not only at light to moderate exercise but also at intense exhaustive work. Thus Rowe11 et al. found that O2 delivery to the exercising muscle was maintained and similar peak muscle O2 uptake (90~) and power output values were achieved with hypoxemia. Richardson et al. (17), using the same exercise model, i.e., one-legged dynamic knee-extension exercise, found contradictory results: their endurancetrained subjects had similar LBFs under submaximal and lower LBFs under maximal exercise with hypoxia, resulting in decreased O2 delivery and peak power output. During submaximal work, O2 extraction was increased to compensate for the low O2 delivery in hypoxia but not at the exhaustive level. The subjects in this latter study were able to produce power outputs almost twice as high as those in the investigation by Rowe11 et al. (18). The training status may then be an explanatory factor for being able not only to produce a large arterially transported amount of O2 but also to better utilize this supply.Neither study included measurement 'of cardiac output (CO), but it has been repeatedly shown (2, 11, 19, 22) in ordinary bicycle exercise that CO is elevated by acute hypoxemia at a given submaximal vo2, whereas peak CO remains the same or is lower. If the submaximally elevated CO is not reflectedin a higher blood flow to the exercising skeletal muscles, a larger fractio...