Respiratory sensitivity to acute hypoxia in man born at sea level living at high altitude.

It is unclear whether dogs develop pulmonary hypertension (PH) at high altitude. Beagles from sea level were exposed to an altitude of 3,100 m (PB 525 Torr) for 12-19 mo and compared with age-matched controls remaining at low altitude of 130 m (PB 750 Torr). In beagles taken to high altitude as adults, pulmonary arterial pressures (PAP) at 3,100 m were 21.6 +/- 2.6 vs. 13.2 +/- 1.2 Torr in controls. Likewise, in beagles taken to 3,100 m as puppies 2.5 mo old, PAP was 23.2 +/- 2.1 vs. 13.8 +/- 0.4 Torr in controls. This PH reflected a doubling of pulmonary vascular resistance and showed no progression with time at altitude. Pulmonary vascular reactivity to acute hypoxia was also enhanced at 3,100 m. Inhibition of prostaglandin synthesis did not attenuate the PH or the enhanced reactivity. Once established, the PH was only partially reversed by acute relief of chronic hypoxia, but reversal was virtually complete after return to low altitude. Hence, beagles do develop PH at 3,100 m of a severity comparable to that observed in humans at the same or even higher altitudes.

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Tolerance to acute anoxia in high altitude natives

Journal of Applied Physiology ◽

10.1152/jappl.1959.14.3.357 ◽

1959 ◽

Vol 14 (3) ◽

pp. 357-362 ◽

Cited By ~ 9

Author(s):

Tulio Velásquez

Keyword(s):

High Altitude ◽

Sea Level ◽

Technical Assistance ◽

Acute Hypoxia ◽

Low Pressure ◽

Pressure Chamber ◽

Relative Influence ◽

Acute Anoxia ◽

High Altitude Natives

Native residents living at an altitude of 14,900 feet were suddenly exposed to simulated higher altitudes, ranging from 30 to 40,000 feet, in a low pressure chamber. The ‘time of consciousness’ and the ceiling breathing air were determined. In addition, observations were made on the respiratory characteristics at these altitudes. Comparing the results with those given by previous investigators using sea level residents, they indicate that a man born and living at an altitude of 14,900 feet has a definitely greater tolerance to acute hypoxia than a man born and residing at sea level. The relative influence of hypoxia and hypocapnia on the symptoms which developed during this test is discussed. Note: (With the Technical Assistance of Edgard Florentini and Melquiades Huayna-Vera) Submitted on June 2, 1958

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Pulmonary gas exchange at maximal exercise in Danish lowlanders during 8 wk of acclimatization to 4,100 m and in high-altitude Aymara natives

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00725.2003 ◽

2004 ◽

Vol 287 (5) ◽

pp. R1202-R1208 ◽

Cited By ~ 71

Author(s):

Carsten Lundby ◽

Jose A. L. Calbet ◽

Gerrit van Hall ◽

Bengt Saltin ◽

Mikael Sander

Keyword(s):

Gas Exchange ◽

High Altitude ◽

Sea Level ◽

Maximal Exercise ◽

Acute Hypoxia ◽

Pulmonary Gas Exchange ◽

Maximum Exercise ◽

Altitude Acclimatization ◽

Ventilatory Equivalent ◽

High Altitude Natives

We aimed to test effects of altitude acclimatization on pulmonary gas exchange at maximal exercise. Six lowlanders were studied at sea level, in acute hypoxia (AH), and after 2 and 8 wk of acclimatization to 4,100 m (2W and 8W) and compared with Aymara high-altitude natives residing at this altitude. As expected, alveolar Po2 was reduced during AH but increased gradually during acclimatization (61 ± 0.7, 69 ± 0.9, and 72 ± 1.4 mmHg in AH, 2W, and 8W, respectively), reaching values significantly higher than in Aymaras (67 ± 0.6 mmHg). Arterial Po2 (PaO2) also decreased during exercise in AH but increased significantly with acclimatization (51 ± 1.1, 58 ± 1.7, and 62 ± 1.6 mmHg in AH, 2W, and 8W, respectively). PaO2 in lowlanders reached levels that were not different from those in high-altitude natives (66 ± 1.2 mmHg). Arterial O2 saturation (SaO2) decreased during maximum exercise compared with rest in AH and after 2W and 8W: 73.3 ± 1.4, 76.9 ± 1.7, and 79.3 ± 1.6%, respectively. After 8W, SaO2 in lowlanders was not significantly different from that in Aymaras (82.7 ± 1%). An improved pulmonary gas exchange with acclimatization was evidenced by a decreased ventilatory equivalent of O2 after 8W: 59 ± 4, 58 ± 4, and 52 ± 4 l·min·l O2−1, respectively. The ventilatory equivalent of O2 reached levels not different from that of Aymaras (51 ± 3 l·min·l O2−1). However, increases in exercise alveolar Po2 and PaO2 with acclimatization had no net effect on alveolar-arterial Po2 difference in lowlanders (10 ± 1.3, 11 ± 1.5, and 10 ± 2.1 mmHg in AH, 2W, and 8W, respectively), which remained significantly higher than in Aymaras (1 ± 1.4 mmHg). In conclusion, lowlanders substantially improve pulmonary gas exchange with acclimatization, but even acclimatization for 8 wk is insufficient to achieve levels reached by high-altitude natives.

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Respiratory Sensitivity to Acute Hypoxia in Goat Kids Born at High Altitude

Acta Physiologica Scandinavica ◽

10.1111/j.1748-1716.1969.tb04587.x ◽

1969 ◽

Vol 77 (4) ◽

pp. 439-441

Author(s):

Allan H. Mines ◽

Søren C. Sørensen

Keyword(s):

High Altitude ◽

Acute Hypoxia ◽

Respiratory Sensitivity

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Cardiorespiratory response to exercise in men repeatedly exposed to extreme altitude

Journal of Applied Physiology ◽

10.1152/jappl.1983.55.5.1379 ◽

1983 ◽

Vol 55 (5) ◽

pp. 1379-1385 ◽

Cited By ~ 12

Author(s):

J. S. Milledge ◽

M. P. Ward ◽

E. S. Williams ◽

C. R. Clarke

Keyword(s):

Heart Rate ◽

High Altitude ◽

Sea Level ◽

Heart Rate Response ◽

Ventilatory Response ◽

Acute Hypoxia ◽

Cardiorespiratory Response ◽

Extreme Altitude ◽

High Altitude Natives ◽

Response To Exercise

The ventilatory and heart rate responses to exercise were studied in four experienced high-altitude climbers at sea level and during a 6-wk period above 4,500 m to discover whether their responses to hypoxia were similar to those of high-altitude natives. Comparison was made with results from four scientists who lacked their frequent exposure to extreme altitude. The climbers had greater Vo2max at sea level and altitude but similar ventilatory responses to increasing exercise. On acute hypoxia at sea level their ventilatory response was less than that of scientists. Their heart rate response did not differ from that of scientists at sea level, but with acclimatization the reduction in response was significantly greater. Alveolar gas concentrations were similar after acclimatization, but climbers achieved these changes more rapidly. The increase in hematocrit was similar in the two groups. It is concluded that these climbers, unlike high-altitude residents, have cardiorespiratory responses to exercise similar to those of other lowlanders except that their ventilatory response was lower and the reduction in their heart rate response was greater.

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Ventilatory interaction between hypoxia and [H+] at chemoreceptors of man

Journal of Applied Physiology ◽

10.1152/jappl.1975.39.2.292 ◽

1975 ◽

Vol 39 (2) ◽

pp. 292-296 ◽

Cited By ~ 22

Author(s):

R. A. Gabel ◽

R. B. Weiskopf

Keyword(s):

Experimental Design ◽

High Altitude ◽

Sea Level ◽

Acute Hypoxia ◽

Simulated Altitude ◽

Peripheral Chemoreceptor ◽

Peripheral Chemoreceptors ◽

Central Chemoreceptors ◽

Progressive Hypoxia ◽

The Mean

By measuring ventilation during isocapnic progressive hypoxia, peripheral chemoreceptor sensitivity to acute hypoxia (deltaV40) was measured in five normal young men under four sets of conditions: 1) at sea level at the subject's resting PCO2, 2) at sea level with PCO2 5 Torr above resting PCO2, 3) after 24 h at a simulated altitude of 4,267 m (PB = 447 Torr) at the subject's resting PCO2 measured during acute hyperoxia, and 4) after 24 h at high altitude, with PCO2 elevated to the subject's sea-level resting PCO2. With this experimental design, we were able to systematically vary the PCO2 and [H+] at the peripheral and central chemoreceptors of man. When mean pHa was decreased from 7.424 to 7.377 without significant change in PACO2, the mean deltaV40 increased from 18.0 to 55.9 1/min. Conversely, when mean PACO2 was altered between 33.8 and 41.6 Torr with pHa held relatively constant, the mean deltaV40 did not change. This suggests that it is the H+ and not CO2 which interacts with hypoxia in stimulating the ventilation of man. An additional finding was that the intrinsic sensitivity of the peripheral chemoreceptors to acute hypoxia did not change during 24 h of acclimatization to high altitude.

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Spleen contraction elevates hemoglobin concentration at high altitude during rest and exercise

European Journal of Applied Physiology ◽

10.1007/s00421-020-04471-w ◽

2020 ◽

Vol 120 (12) ◽

pp. 2693-2704

Author(s):

Erika Schagatay ◽

Alexander Lunde ◽

Simon Nilsson ◽

Oscar Palm ◽

Angelica Lodin-Sundström

Keyword(s):

High Altitude ◽

Acute Hypoxia ◽

Arterial Oxygen Saturation ◽

Hemoglobin Concentration ◽

Step Test ◽

Arterial Oxygen ◽

Spleen Volume ◽

Spleen Contraction ◽

Response To Exercise ◽

Rest And Exercise

Abstract Purpose Hypoxia and exercise are known to separately trigger spleen contraction, leading to release of stored erythrocytes. We studied spleen volume and hemoglobin concentration (Hb) during rest and exercise at three altitudes. Methods Eleven healthy lowlanders did a 5-min modified Harvard step test at 1370, 3700 and 4200 m altitude. Spleen volume was measured via ultrasonic imaging and capillary Hb with Hemocue during rest and after the step test, and arterial oxygen saturation (SaO2), heart rate (HR), expiratory CO2 (ETCO2) and respiratory rate (RR) across the test. Results Resting spleen volume was reduced with increasing altitude and further reduced with exercise at all altitudes. Mean (SE) baseline spleen volume at 1370 m was 252 (20) mL and after exercise, it was 199 (15) mL (P < 0.01). At 3700 m, baseline spleen volume was 231 (22) mL and after exercise 166 (12) mL (P < 0.05). At 4200 m baseline volume was 210 (23) mL and after exercise 172 (20) mL (P < 0.05). After 10 min, spleen volume increased to baseline at all altitudes (NS). Baseline Hb increased with altitude from 138.9 (6.1) g/L at 1370 m, to 141.2 (4.1) at 3700 m and 152.4 (4.0) at 4200 m (P < 0.01). At all altitudes Hb increased from baseline during exercise to 146.8 (5.7) g/L at 1370 m, 150.4 (3.8) g/L at 3700 m and 157.3 (3.8) g/L at 4200 m (all P < 0.05 from baseline). Hb had returned to baseline after 10 min rest at all altitudes (NS). The spleen-derived Hb elevation during exercise was smaller at 4200 m compared to 3700 m (P < 0.05). Cardiorespiratory variables were also affected by altitude during both rest and exercise. Conclusions The spleen contracts and mobilizes stored red blood cells during rest at high altitude and contracts further during exercise, to increase oxygen delivery to tissues during acute hypoxia. The attenuated Hb response to exercise at the highest altitude is likely due to the greater recruitment of the spleen reserve during rest, and that maximal spleen contraction is reached with exercise.

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Effect of high altitude on human placental amino acid transport

Journal of Applied Physiology ◽

10.1152/japplphysiol.00691.2019 ◽

2020 ◽

Vol 128 (1) ◽

pp. 127-133 ◽

Cited By ~ 2

Author(s):

Owen. R. Vaughan ◽

Fredrick Thompson ◽

Ramón. A. Lorca ◽

Colleen G. Julian ◽

Theresa L. Powell ◽

...

Keyword(s):

Birth Weight ◽

Amino Acid ◽

High Altitude ◽

Sea Level ◽

Amino Acid Transport ◽

Acid Uptake ◽

Acid Transport ◽

Transport Capacity ◽

System A ◽

Low Altitude

Women residing at high altitudes deliver infants of lower birth weight than at sea level. Birth weight correlates with placental system A-mediated amino acid transport capacity, and severe environmental hypoxia reduces system A activity in isolated trophoblast and the mouse placenta. However, the effect of high altitude on human placental amino acid transport remains unknown. We hypothesized that microvillous membrane (MVM) system A and system L amino acid transporter activity is lower in placentas of women living at high altitude compared with low-altitude controls. Placentas were collected at term from healthy pregnant women residing at high altitude (HA; >2,500 m; n = 14) or low altitude (LA; <1,700 m; n = 14) following planned, unlabored cesarean section. Birth weight, but not placenta weight, was 13% lower in HA pregnancies (2.88 ± 0.11 kg) compared with LA (3.30 ± 0.07 kg, P < 0.01). MVM erythropoietin receptor abundance, determined by immunoblot, was greater in HA than in LA placentas, consistent with lower placental oxygen levels at HA. However, there was no effect of altitude on MVM system A or L activity, determined by Na+-dependent [14C]methylaminoisobutyric acid uptake and [3H]leucine uptake, respectively. MVM abundance of glucose transporters (GLUTs) 1 and 4 and basal membrane GLUT4 were also similar in LA and HA placentas. Low birth weights in the neonates of women residing at high altitude are not a consequence of reduced placental amino acid transport capacity. These observations are in general agreement with studies of IUGR babies at low altitude, in which MVM system A activity is downregulated only in growth-restricted babies with significant compromise. NEW & NOTEWORTHY Babies born at high altitude are smaller than at sea level. Birth weight is dependent on growth in utero and, in turn, placental nutrient transport. We determined amino acid transport capacity in placentas collected from women resident at low and high altitude. Altitude did not affect system A amino acid transport across the syncytiotrophoblast microvillous membrane, suggesting that impaired placental amino acid transport does not contribute to reduced birth weight in this high-altitude population.

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