scholarly journals Respiratory and circulatory control at high altitudes.

1982 ◽  
Vol 100 (1) ◽  
pp. 147-157
Author(s):  
J B West
Keyword(s):  
Oxygen Consumption ◽  
High Altitude ◽  
Acute Hypoxia ◽  
Maximal Oxygen Consumption ◽  
Barometric Pressure ◽  
Mount Everest ◽  
Exercise Ventilation ◽  
Circulatory Control ◽  
Work Level ◽  
Oxygen Requirements

Hyperventilation is one of the most important features of acclimatization to high altitude. Resting ventilation at extreme altitudes increases up to fourfold and exercise ventilation for a given work level increases to the same extent. Hypoxic stimulation of the peripheral chemoreceptors is the chief mechanism for the hyperventilation but there is also evidence that central sensitization of the respiratory centres occurs. Permanent residents of high altitude have a blunted hypoxic ventilatory response compared to acclimatized lowlanders. Cardiac output increases in responses to acute hypoxia but returns to normal in acclimatized lowlanders. Oxygen uptake at extreme altitudes is markedly limited by the diffusion properties of the blood gas barrier. As a consequence the maximal oxygen consumption of a climber near the summit of Mount Everest is near his basal oxygen requirements. Maximal oxygen consumption is so sensitive to barometric pressure that it may be that day-to-day variations will affect the chances of a climber reaching the summit without supplementary oxygen.

Physiology in Medicine: A physiologic approach to prevention and treatment of acute high-altitude illnesses

2015 ◽  
Vol 118 (5) ◽  
pp. 509-519 ◽  
Author(s):  
Andrew M. Luks
Keyword(s):  
High Altitude ◽  
Acute Hypoxia ◽  
Acute Mountain Sickness ◽  
Travel Medicine ◽  
Barometric Pressure ◽  
Time Frame ◽  
Low Oxygen ◽  
Organ Systems ◽  
Prevention And Treatment ◽  
Physiologic Responses

With the growing interest in adventure travel and the increasing ease and affordability of air, rail, and road-based transportation, increasing numbers of individuals are traveling to high altitude. The decline in barometric pressure and ambient oxygen tensions in this environment trigger a series of physiologic responses across organ systems and over a varying time frame that help the individual acclimatize to the low oxygen conditions but occasionally lead to maladaptive responses and one or several forms of acute altitude illness. The goal of this Physiology in Medicine article is to provide information that providers can use when counseling patients who present to primary care or travel medicine clinics seeking advice about how to prevent these problems. After discussing the primary physiologic responses to acute hypoxia from the organ to the molecular level in normal individuals, the review describes the main forms of acute altitude illness—acute mountain sickness, high-altitude cerebral edema, and high-altitude pulmonary edema—and the basic approaches to their prevention and treatment of these problems, with an emphasis throughout on the physiologic basis for the development of these illnesses and their management.

Alexander M. Kellas and the physiological challenge of Mt. Everest

1987 ◽  
Vol 63 (1) ◽  
pp. 3-11 ◽  
Author(s):  
J. B. West
Keyword(s):  
Arterial Oxygen Saturation ◽  
Maximal Oxygen Consumption ◽  
Barometric Pressure ◽  
Arterial Oxygen ◽  
Full Time ◽  
Mount Everest ◽  
Unpublished Manuscript ◽  
Faculty Position ◽  
Middlesex Hospital ◽  
Extreme Altitude

Alexander M. Kellas (1868–1921) was a British physiologist who made pioneering contributions to the exploration of Everest and to the early physiology of extreme altitudes, but his physiological contributions have been almost completely overlooked. Although he had a full-time faculty position at the Middlesex Hospital Medical School in London, he was able to make eight expeditions to the Himalayas in the first two decades of the century, and by 1919 when the first official expedition to Everest was being planned, he probably knew more about the approaches than anybody else. But his most interesting contributions were made in an unpublished manuscript written in 1920 and entitled “A consideration of the possibility of ascending Mount Everest.” In this he discussed the physiology of acclimatization and most of the important variables including the summit altitude and barometric pressure, and the alveolar PO2, arterial oxygen saturation, maximal oxygen consumption, and maximal ascent rate near the summit. On the basis of this extensive analysis, he concluded that “Mount Everest could be ascended by a man of excellent physical and mental constitution in first-rate training, without adventitious aids [supplementary oxygen] if the physical difficulties of the mountain are not too great.” Kellas was one of the first physiologists to study extreme altitude, and he deserves to be better known.

Acute in vitro hypoxia and high-altitude (4,559 m) exposure decreases leukocyte oxygen consumption

2011 ◽  
Vol 300 (1) ◽  
pp. R32-R39 ◽  
Author(s):  
Vitalie Faoro ◽  
Bruno Fink ◽  
Sarah Taudorf ◽  
Christoph Dehnert ◽  
Marc M. Berger ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
High Altitude ◽  
Respiratory Burst ◽  
Acute Hypoxia ◽  
Resonance Spectroscopy ◽  
Metabolic Functions ◽  
Spin Resonance ◽  
Ros Formation ◽  
Low Altitude

Hypoxia impairs metabolic functions by decreasing activity and expression of ATP-consuming processes. To separate hypoxia from systemic effects, we tested whether hypoxia at high altitude affects basal and PMA-stimulated leukocyte metabolism and how this compares to acute (15 min) and 24 h of in vitro hypoxia. Leukocytes were prepared at low altitude and ∼24 h after arrival at 4559 m. Mitochondrial oxygen consumption (JO2) was measured by respirometry, oxygen radicals by electron spin resonance spectroscopy, both at a Po2= 100 mmHg (JO2,100) and 20 mmHg (JO2,20). Acute hypoxia of leukocytes decreased JO2at low altitude. Exposure to high altitude decreased JO2,100, whereas JO2,20was not affected. Acute hypoxia of low-altitude samples decreased the activity of complexes I, II, and III. At high altitude, activity of complexes I and III were decreased when measured in normoxia. Stimulation of leukocytes with PMA increased JO2,100at low (twofold) and high altitude (five-fold). At both locations, PMA-stimulated JO2was decreased by acute hypoxia. Basal and PMA-stimulated reactive oxygen species (ROS) production were unchanged at high altitude. Separate in vitro experiments performed at low altitude show that ∼75% of PMA-induced increase in JO2was due to increased extra-mitochondrial JO2(JO2,res; in the presence of rotenone and antimycin A). JO2,reswas doubled by PMA. Acute hypoxia decreased basal JO2,resby ∼70% and PMA-stimulated JO2,resby about 50% in cells cultured in normoxia and hypoxia (1.5% O2; 24 h). Conversely, 24 h in vitro hypoxia decreased mitochondrial JO2,100and JO2,20, extra-mitochondrial, basal, and PMA-stimulated JO2were not affected. These results show that 24 h of high altitude but not 24 h in vitro hypoxia decreased basal leukocyte metabolism, whereas PMA-induced JO2and ROS formation were not affected, indicating that prolonged high-altitude hypoxia impairs mitochondrial metabolism but does not impair respiratory burst. In contrast, acute hypoxia impairs respiratory burst at either altitude.

scholarly journals Maximal oxygen consumption in national elite triathletes that train in high altitude

2013 ◽  
Vol 8 (2) ◽  
pp. 342-349 ◽  
Author(s):  
Gilberto González-Parra ◽  
Rigoberto Mora ◽  
Bernhard Hoeger
Keyword(s):  
Oxygen Consumption ◽  
High Altitude ◽  
Maximal Oxygen Consumption

Hypoxia, Hypocapnia and Spirometry at Altitude

1997 ◽  
Vol 92 (6) ◽  
pp. 593-598 ◽  
Author(s):  
Andrew J. Pollard ◽  
Peter W. Barry ◽  
Nick P. Mason ◽  
David J. Collier ◽  
Rachel C. Pollard ◽  
...  
Keyword(s):  
Oxygen Saturation ◽  
High Altitude ◽  
Sea Level ◽  
Barometric Pressure ◽  
Supplementary Oxygen ◽  
Mount Everest ◽  
Base Camp ◽  
Lower Oxygen ◽  
Significant Change ◽  
Β2 Agonist

1. Both hypoxia and hypocapnia can cause broncho-constriction in humans, and this could have a bearing on performance at high altitude or contribute to altitude sickness. We studied the relationship between spirometry, arterial oxygen saturation and end-tidal carbon dioxide (ETCO2) concentration in a group of healthy lowland adults during a stay at high altitude, and then evaluated the response to supplementary oxygen and administration of a β2 agonist 2. We collected spirometric data from 51 members of the 1994 British Mount Everest Medical Expedition at sea level (barometric pressure 101.2–101.6 kPa) and at Mount Everest Base Camp in Nepal (altitude 5300 m, barometric pressure 53–54.7 kPa) using a pocket turbine spirometer. A total of 205 spirometric measurements were made on the 51 subjects during the first 6 days after arrival at Base Camp. Further measurements were made before and after inhalation of oxygen (n = 47) or a β2 agonist (n = 39). ETCO2 tensions were measured on the same day as spirometric measurements in 30 of these subjects. 3. In the first 6 days after arrival at 5300 m, lower oxygen saturations were associated with lower forced expiratory volume in 1 s (FEV1; P < 0.02) and forced vital capacity (FVC; P < 0.01), but not with peak expiratory flow (PEF). Administration of supplementary oxygen for 5 min increased oxygen saturation from a mean of 81%–94%, but there was no significant change in FEV1 or FVC, whilst PEF fell by 2.3% [P < 0.001; 95% confidence intervals (CI) −4 to −0.7%]. After salbutamol administration, there was no significant change in PEF, FEV1 or FVC in 35 non-asthmatic subjects. Mean ETCO2 at Everest Base Camp was 26 mmHg, and a low ETCO2 was weakly associated with a larger drop in FVC at altitude compared with sea level (r = 0.38, P < 0.05). There was no correlation between either ETCO2 or oxygen saturation and changes in FEV1 or PEF compared with sea-level values. 4. In this study, in normal subjects who were acclimatized to hypobaric hypoxia at an altitude of 5300 m, we found no evidence of hypoxic broncho-constriction. Individuals did not have lower PEF when they were more hypoxic, and neither PEF nor FEV1 were increased by either supplementary oxygen or salbutamol. FVC fell at altitude, and there was a greater fall in FVC for subjects with lower oxygen saturations and probably lower ETCO2.

Maximal exercise performance in chronic hypoxia and acute normoxia in high-altitude natives

1995 ◽  
Vol 78 (5) ◽  
pp. 1868-1874 ◽  
Author(s):  
R. Favier ◽  
H. Spielvogel ◽  
D. Desplanches ◽  
G. Ferretti ◽  
B. Kayser ◽  
...  
Keyword(s):  
High Altitude ◽  
Chronic Hypoxia ◽  
Acute Hypoxia ◽  
Bicycle Ergometer ◽  
La Paz ◽  
Altitude Exposure ◽  
Exercise Ventilation ◽  
High Altitude Natives ◽  
The Difference ◽  
Arterial O2 Saturation

Maximal O2 uptake (VO2max) was determined on a bicycle ergometer in chronic hypoxia (CH) and during acute exposure to normoxia (AN) in 50 healthy young men who were born and had lived at 3,600 m altitude (La Paz, Bolivia). VO2max was significantly improved (approximately 8%) by AN. However, the difference in VO2max measured in CH and AN (delta VO2max) was lower than that reported in sea-level natives (SN) who exercised in chronic normoxia and acute hypoxia. It is shown that high-altitude natives (HN) and SN have a similar VO2max in normoxia, but highlanders can attain a greater VO2max when O2 availability is reduced by altitude exposure. In addition, in HN, the higher the subject's VO2max in hypoxia, the smaller his delta VO2max. These results contrast with the data obtained in 14 lowlanders acclimatized to high altitude who showed that their delta VO2max was positively related to their VO2max in hypoxia, as previously reported in SN who exercised in acute hypoxia (A. J. Young, A. Cymerman, and R. L. Burse. Eur. J. Appl. Physiol. Occup. Physiol. 54: 12–15, 1985). Furthermore, arterial O2 saturation of HN behaved differently from acclimatized lowland natives, inasmuch as it fell less during exercise both in CH and AN. HN with high aerobic capacity display a lower exercise ventilation and a reduced arterial saturation, which could explain their inability to improve VO2max with normoxia.(ABSTRACT TRUNCATED AT 250 WORDS)

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

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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