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Pulmonary gas exchange and acid-base state were compared in nine Danish lowlanders (L) acclimatized to 5,260 m for 9 wk and seven native Bolivian residents (N) of La Paz (altitude 3,600–4,100 m) brought acutely to this altitude. We evaluated normalcy of arterial pH and assessed pulmonary gas exchange and acid-base balance at rest and during peak exercise when breathing room air and 55% O2. Despite 9 wk at 5,260 m and considerable renal bicarbonate excretion (arterial plasma HCO3 − concentration = 15.1 meq/l), resting arterial pH in L was 7.48 ± 0.007 (significantly greater than 7.40). On the other hand, arterial pH in N was only 7.43 ± 0.004 (despite arterial O2 saturation of 77%) after ascent from 3,600–4,100 to 5,260 m in 2 h. Maximal power output was similar in the two groups breathing air, whereas on 55% O2only L showed a significant increase. During exercise in air, arterial Pco 2 was 8 Torr lower in L than in N ( P < 0.001), yet Po 2 was the same such that, at maximal O2 uptake,alveolar-arterial Po 2 difference was lower in N (5.3 ± 1.3 Torr) than in L (10.5 ± 0.8 Torr), P = 0.004. Calculated O2 diffusing capacity was 40% higher in N than in L and, if referenced to maximal hyperoxic work, capacity was 73% greater in N. Buffering of lactic acid was greater in N, with 20% less increase in base deficit per millimole per liter rise in lactate. These data show in L persistent alkalosis even after 9 wk at 5,260 m. In N, the data show 1) insignificant reduction in exercise capacity when breathing air at 5,260 m compared with breathing 55% O2; 2) very little ventilatory response to acute hypoxemia (judged by arterial pH and arterial Pco 2 responses to hyperoxia); 3) during exercise, greater pulmonary diffusing capacity than in L, allowing maintenance of arterial Po 2despite lower ventilation; and 4) better buffering of lactic acid. These results support and extend similar observations concerning adaptation in lung function in these and other high-altitude native groups previously performed at much lower altitudes.

In sea-level natives, exposure to hypoxia for a few weeks is characterized by an increased dependence on blood glucose and a decreased reliance on lactate for energy metabolism during exercise. These metabolic adjustments have been attributed to behavioral changes in the sympathoadrenergic and pancreatic systems. The aim of this study was to test the hypothesis of a reduced sympathoadrenergic activation and subsequent metabolic changes when high-altitude natives are acutely exposed to normoxia. Young Andean natives performed incremental exercise to exhaustion during hypoxia (arterial PO2 55.1 +/- 1.1 Torr) or during acute normoxia (arterial PO2 78.7 +/- 1.7 Torr). As a whole, oxygen uptake was increased in normoxia compared with hypoxia during graded exercise. This finding is not related to a decrease in anaerobic metabolism but rather is interpreted as a consequence of a shift in substrate utilization during exercise (increased contribution of fat as assessed by a reduction in the respiratory exchange ratio). These metabolic changes are not accompanied by modifications of glucoregulatory hormones (catecholamines, insulin, and glucagon). In particular, the exercise-induced catecholamine secretion was similar in chronic hypoxia and acute normoxia. As a consequence, blood lactate accumulation during incremental exercise was similar in both conditions. It is concluded that high-altitude natives do not display any sign of a greater sympathoadrenergic activation during chronic hypoxia and that the exercise-induced hormonal changes remained unaffected by acute inhalation of a normoxic gas mixture.

The present study was performed to evaluate the effects of chronic inspiratory hypoxia and its combination with physical exercise on plasma erythropoietin concentration ([EPO]). Eight natives from the Bolivian Plateau were investigated at 3,600 m above sea level at rest as well as during and up to 48 h after exhaustive exercise (EE) and 60 min of submaximal (60%) cycle ergometer exercise (SE). Ten sea-level subjects were used as a control group for resting values. The mean resting plasma [EPO] of the high-altitude group (19.5 +/- 0.7 mU/ml) did not differ from that of the sea-level group (18.1 +/- 0.4 mU/ml) but was higher than would be expected from the relationship between [EPO] and hematocrit at sea level. Five hours after both types of exercise, [EPO] decreased by 2.1 +/- 0.8 (EE, P < 0.01) and 1.6 +/- 0.8 mU/ml (SE, P < 0.05); 48 h after SE, [EPO] increased by 2.6 +/- 0.9 mU/ml (P < 0.05). It is concluded that 1) high-altitude natives need relatively high [EPO] to maintain their high hematocrit and 2) exercise at low basal arterial PO2 does not directly increase plasma [EPO] in high-altitude residents but seems to exert suppressive effects.

The effects of high altitude (HA, 3,700 m) on performance during a force-velocity test (maximal anaerobic power, MAnP) and a 30-s Wingate test (mean power, P) were studied in boys 7-15 yr of age. Forty-seven children acclimatized to HA were compared with 101 living at low altitude (LA, 330 m). They had the same good nutritional status and the same level of physical activities [average 5.4 +/- 1.1 (SD) and 5.2 +/- 1.9 h/wk at HA and LA, respectively]. They performed the two tests using the same calibrated cycle ergometer. For the Wingate test, O2 uptake (VO2) during the 30 s and the peak of blood lactate concentration ([L]p) during the recovery were also measured. No difference in MAnP was observed between HA and LA. P, [L]p, and VO2 were lower at HA. This suggests that the altitude of 3,700 m did not affect the performance of the force-velocity test but reduced that of the Wingate test. This decrease in P was linked to a lower participation of glycolysis and aerobic metabolism. The latter is related to a reduced aerobic performance at HA. In addition, the slopes of the relationships between age and MAnP, P, and [L]p were the same at HA and LA, indicating that chronic hypoxia did not alter the development of the anaerobic metabolism during puberty.

In a previous study we showed that there were no differences in anaerobic metabolism between groups of 11-yr-old children living at high (3,700 m) and low (330 m) altitudes. The aim of this study is to investigate changes in this metabolism during pubertal development. We compare blood lactate concentration ([L]) after maximal bicycle exercise in 20 boys acclimatized to high altitude (HA, 12 yr old) and at low altitude in 14 boys (LA1, 12 yr old) and in 13 boys (LA2, 14 yr old). The subjects had the same level of physical fitness and the same nutritional and socioeconomic status. Pubertal development was identified by salivary testosterone concentration ([T]). Results (means ± SE) showed 1) at the age of 12 years, [L] and [T] in HA were significantly higher than in LA1 ([L] was 9.2 ± 0.5 vs. 6.8 ± 0.5 mmol/l, [T] was 233 ± 66 vs. 132 ± 30 pmol/l), 2) [L] and [T] in HA were statistically the same as in LA2, and 3) a linear relationship between [L] and [T] was significant (P less than 0.05) in all HA and LA subjects. This suggests that the higher [L] in 12-yr-old boys living at HA could result in an enhanced anaerobic metabolism linked to an earlier gonadal maturation evaluated by testosterone level.