Maximal exercise and muscle oxygen extraction in acclimatizing lowlanders and high altitude natives

[EN] The tight relation between arterial oxygen content and maximum oxygen uptake (Vv(o2max)within a given person at sea level is diminished with altitude acclimatization. An explanation often suggested for this mismatch is impairment of the muscle O(2) extraction capacity with chronic hypoxia, and is the focus of the present study. We have studied six lowlanders during maximal exercise at sea level (SL) and with acute (AH) exposure to 4,100 m altitude, and again after 2 (W2) and 8 weeks (W8) of altitude sojourn, where also eight high altitude native (Nat) Aymaras were studied. Fractional arterial muscle O(2) extraction at maximal exercise was 90.0+/-1.0% in the Danish lowlanders at sea level, and remained close to this value in all situations. In contrast to this, fractional arterial O(2) extraction was 83.2+/-2.8% in the high altitude natives, and did not change with the induction of normoxia. The capillary oxygen conductance of the lower extremity, a measure of oxygen diffusing capacity, was decreased in the Danish lowlanders after 8 weeks of acclimatization, but was still higher than the value obtained from the high altitude natives. The values were (in ml min(-1) mmHg(-1)) 55.2+/-3.7 (SL), 48.0+/-1.7 (W2), 37.8+/-0.4 (W8) and 27.7+/-1.5 (Nat). However, when correcting oxygen conductance for the observed reduction in maximal leg blood flow with acclimatization the effect diminished. When calculating a hypothetical leg V(o2max)at altitude using either the leg blood flow or the O(2) conductance values obtained at sea level, the former values were almost completely restored to sea level values. This would suggest that the major determinant V(o2max)for not to increase with acclimatization is the observed reduction in maximal leg blood flow and O(2) conductance.

On the mechanisms that limit oxygen uptake during exercise in acute and chronic hypoxia: role of muscle mass

[EN] Peak aerobic power in humans (VO2,peak) is markedly affected by inspired O2 tension (FIO2). The question to be answered in this study is what factor plays a major role in the limitation of muscle peak VO2 in hypoxia: arterial O2 partial pressure (Pa,O2) or O2 content (Ca,O2)? Thus, cardiac output (dye dilution with Cardio-green), leg blood flow (thermodilution), intra-arterial blood pressure and femoral arterial-to-venous differences in blood gases were determined in nine lowlanders studied during incremental exercise using a large (two-legged cycle ergometer exercise: Bike) and a small (one-legged knee extension exercise: Knee)muscle mass in normoxia, acute hypoxia (AH) (FIO2 = 0.105) and after 9 weeks of residence at 5260 m (CH). Reducing the size of the active muscle mass blunted by 62% the effect of hypoxia on VO2,peak in AH and abolished completely the effect of hypoxia on VO2,peak after altitude acclimatization. Acclimatization improved Bike peak exercise Pa,O2 from 34 +/- 1 in AH to 45 +/- 1 mmHg in CH(P <0.05) and Knee Pa,O2 from 38 +/- 1 to 55 +/- 2 mmHg(P <0.05). Peak cardiac output and leg blood flow were reduced in hypoxia only during Bike. Acute hypoxia resulted in reduction of systemic O2 delivery (46 and 21%) and leg O2 delivery (47 and 26%) during Bike and Knee, respectively, almost matching the corresponding reduction in VO2,peak. Altitude acclimatization restored fully peak systemic and leg O(2) delivery in CH (2.69 +/- 0.27 and 1.28 +/- 0.11 l min(-1), respectively) to sea level values (2.65 +/- 0.15 and 1.16 +/- 0.11 l min(-1), respectively) during Knee, but not during Bike. During Knee in CH, leg oxygen delivery was similar to normoxia and, therefore, also VO2,peak in spite of a Pa,O2 of 55 mmHg. Reducing the size of the active mass improves pulmonary gas exchange during hypoxic exercise, attenuates the Bohr effect on oxygen uploading at the lungs and preserves sea level convective O2 transport to the active muscles. Thus, the altitude-acclimatized human has potentially a similar exercising capacity as at sea level when the exercise model allows for an adequate oxygen delivery (blood flow x Ca,O2), with only a minor role of Pa,O2 per se, when Pa,O2 is more than 55 mmHg.

Leg and arm lactate and substrate kinetics during exercise

[EN] To study the role of muscle mass and muscle activity on lactate and energy kinetics during exercise, whole body and limb lactate, glucose, and fatty acid fluxes were determined in six elite cross-country skiers during roller-skiing for 40 min with the diagonal stride (Continuous Arm + Leg) followed by 10 min of double poling and diagonal stride at 72-76% maximal O(2) uptake. A high lactate appearance rate (R(a), 184 +/- 17 micromol x kg(-1) x min(-1)) but a low arterial lactate concentration ( approximately 2.5 mmol/l) were observed during Continuous Arm + Leg despite a substantial net lactate release by the arm of approximately 2.1 mmol/min, which was balanced by a similar net lactate uptake by the leg. Whole body and limb lactate oxidation during Continuous Arm + Leg was approximately 45% at rest and approximately 95% of disappearance rate and limb lactate uptake, respectively. Limb lactate kinetics changed multiple times when exercise mode was changed. Whole body glucose and glycerol turnover was unchanged during the different skiing modes; however, limb net glucose uptake changed severalfold. In conclusion, the arterial lactate concentration can be maintained at a relatively low level despite high lactate R(a) during exercise with a large muscle mass because of the large capacity of active skeletal muscle to take up lactate, which is tightly correlated with lactate delivery. The limb lactate uptake during exercise is oxidized at rates far above resting oxygen consumption, implying that lactate uptake and subsequent oxidation are also dependent on an elevated metabolic rate. The relative contribution of whole body and limb lactate oxidation is between 20 and 30% of total carbohydrate oxidation at rest and during exercise under the various conditions. Skeletal muscle can change its limb net glucose uptake severalfold within minutes, causing a redistribution of the available glucose because whole body glucose turnover was unchanged.