Counterpoint: Hypobaric hypoxia does not induce different responses from normobaric hypoxia

2012 ◽  
Vol 112 (10) ◽  
pp. 1784-1786 ◽  
Author(s):  
Remi Mounier ◽  
Julien V. Brugniaux
Keyword(s):  
Hypobaric Hypoxia ◽  
Normobaric Hypoxia

Effect of repeated normobaric hypoxia exposures during sleep on acute mountain sickness, exercise performance, and sleep during exposure to terrestrial altitude

2011 ◽  
Vol 300 (2) ◽  
pp. R428-R436 ◽  
Author(s):  
Charles S. Fulco ◽  
Stephen R. Muza ◽  
Beth A. Beidleman ◽  
Robby Demes ◽  
Janet E. Staab ◽  
...  
Keyword(s):  
Heart Rate ◽  
Exercise Performance ◽  
Hypobaric Hypoxia ◽  
Sham Group ◽  
Acute Mountain Sickness ◽  
Time Trial ◽  
Normobaric Hypoxia ◽  
Performance Decrement ◽  
Mountain Sickness ◽  
End Tidal

There is an expectation that repeated daily exposures to normobaric hypoxia (NH) will induce ventilatory acclimatization and lessen acute mountain sickness (AMS) and the exercise performance decrement during subsequent hypobaric hypoxia (HH) exposure. However, this notion has not been tested objectively. Healthy, unacclimatized sea-level (SL) residents slept for 7.5 h each night for 7 consecutive nights in hypoxia rooms under NH [ n = 14, 24 ± 5 (SD) yr] or “sham” ( n = 9, 25 ± 6 yr) conditions. The ambient percent O2 for the NH group was progressively reduced by 0.3% [150 m equivalent (equiv)] each night from 16.2% (2,200 m equiv) on night 1 to 14.4% (3,100 m equiv) on night 7, while that for the ventilatory- and exercise-matched sham group remained at 20.9%. Beginning at 25 h after sham or NH treatment, all subjects ascended and lived for 5 days at HH (4,300 m). End-tidal Pco2, O2 saturation (SaO2), AMS, and heart rate were measured repeatedly during daytime rest, sleep, or exercise (11.3-km treadmill time trial). From pre- to posttreatment at SL, resting end-tidal Pco2 decreased ( P < 0.01) for the NH (from 39 ± 3 to 35 ± 3 mmHg), but not for the sham (from 39 ± 2 to 38 ± 3 mmHg), group. Throughout HH, only sleep SaO2 was higher (80 ± 1 vs. 76 ± 1%, P < 0.05) and only AMS upon awakening was lower (0.34 ± 0.12 vs. 0.83 ± 0.14, P < 0.02) in the NH than the sham group; no other between-group rest, sleep, or exercise differences were observed at HH. These results indicate that the ventilatory acclimatization induced by NH sleep was primarily expressed during HH sleep. Under HH conditions, the higher sleep SaO2 may have contributed to a lessening of AMS upon awakening but had no impact on AMS or exercise performance for the remainder of each day.

Exposure to hypobaric hypoxia results in higher oxidative stress compared to normobaric hypoxia

2016 ◽  
Vol 223 ◽  
pp. 23-27 ◽  
Author(s):  
A. Ribon ◽  
V. Pialoux ◽  
J.J. Saugy ◽  
T. Rupp ◽  
R. Faiss ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hypobaric Hypoxia ◽  
Normobaric Hypoxia

scholarly journals Effect of Acute Exposure to Moderate Altitude on Muscle Power: Hypobaric Hypoxia vs. Normobaric Hypoxia

PLoS ONE ◽  
2014 ◽  
Vol 9 (12) ◽  
pp. e114072 ◽  
Author(s):  
Belén Feriche ◽  
Amador García-Ramos ◽  
Carmen Calderón-Soto ◽  
Franchek Drobnic ◽  
Juan G. Bonitch- Góngora ◽  
...  
Keyword(s):  
Hypobaric Hypoxia ◽  
Muscle Power ◽  
Normobaric Hypoxia ◽  
Acute Exposure ◽  
Moderate Altitude

scholarly journals The experimental study of the antihypoxic properties of harmine hydrochloride

Biomeditsina ◽  
2021 ◽  
Vol 17 (2) ◽  
pp. 71-78
Author(s):  
S. M. Adekenov ◽  
V. N. Karkischenko ◽  
M. S. Nesterov ◽  
D. A. Abaimov ◽  
A. K. Sariev
Keyword(s):  
Experimental Study ◽  
Life Expectancy ◽  
Hypobaric Hypoxia ◽  
Normobaric Hypoxia ◽  
Antihypoxic Activity ◽  
Reference Drug ◽  
Small Doses ◽  
Hypoxia With Hypercapnia ◽  
Antihypoxic Effect ◽  
Compensatory Effect

A derivative of the beta-carboline alkaloid harmine — the drug harmine hydrochloride was studied for the presence of antihypoxic properties in models of hypobaric hypoxia and normobaric hypoxia with hypercapnia. It was found that harmine hydrochloride does not have a signifi cant compensatory effect in the normobaric hypoxia test with hypercapnia. At the same time, harmine hydrochloride in small doses (2.5 and 5 mg/kg) has antihypoxic activity in the hypobaric hypoxia test, which is expressed in a statistically signifi cant increase in the life expectancy of animals treated with the drug, compared with the control, in conditions of hypoxia. According to the antihypoxic effect, harmine hydrochloride at doses of 2.5 and 5 mg/kg was found to be comparable with the reference drug (mexidol, 100 mg/kg).

Pulmonary function alterations after 3 wk of exposure to hypobaria and/or hypoxia in growing rats

1995 ◽  
Vol 78 (5) ◽  
pp. 1787-1792 ◽  
Author(s):  
H. S. Sekhon ◽  
J. L. Wright ◽  
W. M. Thurlbeck
Keyword(s):  
Lung Function ◽  
Forced Vital Capacity ◽  
Hypobaric Hypoxia ◽  
Vital Capacity ◽  
Total Lung Capacity ◽  
Ambient Pressure ◽  
Normobaric Hypoxia ◽  
Lung Growth ◽  
Lung Capacity ◽  
Expiratory Flow

We studied lung growth in rats between 4 and 7 wk of age under different conditions. There were five groups, seven animals in each: 1) general controls (ambient pressure and room air, food ad libitum); 2) hypobaric normoxic [barometric pressure (PB) 410 mmHg, PO2 153 Torr]; 3) normobaric hypoxic (ambient pressure, PO2 80 Torr); 4) hypobaric hypoxic (PB 410 mmHg, PO2 80 Torr); and 5) weight-matched controls to hypobaric hypoxic. Residual volume, functional residual capacity, vital capacity, and total lung capacity grew 10–20% more in both hypoxic groups than in weight-matched and general controls. Expiratory flow rates corrected for forced vital capacity decreased, and specific airway resistance increased significantly. In addition, the ratio of forced expiratory volume in 0.1 s to %forced vital capacity, peak expiratory flow rate, and forced maximal midexpiratory flow were also lower in normobaric hypoxic animals compared with weight-matched controls. Above a transpulmonary pressure of 6 cmH2O, flows were reduced in both hypoxic groups. No differences were observed between hypobaric normoxic and general control groups for lung volume and lung function. In weight-matched animals, total lung capacity decreased but lung function remained unchanged. We conclude that accelerated lung growth in hypobaric hypoxia and normobaric hypoxia is dysanaptic. Lung growth in hypobaric hypoxia is primarily induced by low oxygen, but differences between hypobaric hypoxia and normobaric hypoxia suggest a beneficial effect of low pressure.

scholarly journals Markers of physiological stress during exercise under conditions of normoxia, normobaric hypoxia, hypobaric hypoxia, and genuine high altitude

2017 ◽  
Vol 117 (5) ◽  
pp. 893-900 ◽  
Author(s):  
David Richard Woods ◽  
John Paul O’Hara ◽  
Christopher John Boos ◽  
Peter David Hodkinson ◽  
Costas Tsakirides ◽  
...  
Keyword(s):  
High Altitude ◽  
Hypobaric Hypoxia ◽  
Physiological Stress ◽  
Normobaric Hypoxia

scholarly journals Increase in slow-wave vasomotion by hypoxia and ischemia in lowlanders and highlanders

2018 ◽  
Vol 125 (3) ◽  
pp. 780-789 ◽  
Author(s):  
Paolo Salvi ◽  
Andrea Faini ◽  
Paolo Castiglioni ◽  
Fausto Brunacci ◽  
Luca Montaguti ◽  
...  
Keyword(s):  
Spectral Density ◽  
Power Spectral Density ◽  
Slow Wave ◽  
Hypobaric Hypoxia ◽  
Oxygen Supply ◽  
Tissue Oxygenation ◽  
Low Frequency ◽  
Normobaric Hypoxia ◽  
Geometric Standard Deviation ◽  
Power Spectral

The physiological relevance of slow-wave vasomotion is still unclear, even though it has been hypothesized that it could be a compensatory mechanism for enhancing tissue oxygenation in conditions of reduced oxygen supply. The aim of our study was to explore the effects of hypoxia and ischemia on slow-wave vasomotion in microcirculation. Peripheral oxygen saturation and forearm microcirculation flow (laser-Doppler flowmetry) were recorded at baseline and during postocclusive reactive hyperemia in the Himalaya region from 8 European lowlanders (6 men; aged 29–39 yr) at 1,350, 3,400, and 5,050 m and from 10 Nepalese male highlanders (aged 21–39 yr) at 3,400 and 5,050 m of altitude. The same measurements were also performed at sea level in 16 healthy volunteers (aged 23–61 yr) during a short-term exposure to normobaric hypoxia. In lowlanders, exposure to progressively higher altitude under baseline flow conditions progressively increased 0.06–0.15 Hz vasomotion amplitude [power spectral density % was expressed as geometric means (geometric standard deviation) = 14.0 (3.6) at 1,350 m; 87.0(2.3) at 3,400 m and 249.8 (3.6) at 5,050 m; P = 0.006 and P < 0.001 vs. 1,350 m, respectively]. In highlanders, low frequency vasomotion amplitude was similarly enhanced at different altitudes [power spectral density % = 183.4 (4.1) at 3,400 m vs. 236.0 (3.0) at 5,050 m; P = 0.139]. In both groups at altitude, it was further increased after ischemic stimulus ( P < 0.001). At baseline, acute short lasting normobaric hypoxia did not induce low frequency vasomotion, which was conversely induced by ischemia, even under normal oxygenation and barometric pressure. This study offers the demonstration of a significant increase in slow-wave vasomotion under prolonged hypobaric-hypoxia exposure at high altitude, with a further enhancement after ischemia induction. NEW & NOTEWORTHY This study offers the demonstration in humans of the occurrence of enhanced slow-wave vasomotion in microcirculation induced by exposure to hypobaric hypoxia, ischemia, and their combination. This phenomenon, where vasomotion can be hypothesized to behave as a “peripheral heart,” may represent a compensating adaptive change aimed at improving peripheral flow and tissue oxygenation in conditions of reduced oxygen supply, such as altitude-induced hypobaric hypoxia and postocclusion ischemia.

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