Post-exercise accumulation of interstitial lung water is greater in hypobaric than normobaric hypoxia in adults born prematurely

2022 ◽  
Vol 297 ◽  
pp. 103828
Author(s):  
Tadej Debevec ◽  
Mathias Poussel ◽  
Damjan Osredkar ◽  
Sarah J. Willis ◽  
Claudio Sartori ◽  
...  
Keyword(s):  
Normobaric Hypoxia ◽  
Lung Water ◽  
Post Exercise

Acute Normobaric Hypoxia Exposure and Excess Post-Exercise Oxygen Consumption

2018 ◽  
Vol 89 (12) ◽  
pp. 1031-1035
Author(s):  
James W. Navalta ◽  
Elizabeth A. Tanner ◽  
Nathaniel G. Bodell
Keyword(s):  
Oxygen Consumption ◽  
Normobaric Hypoxia ◽  
Post Exercise ◽  
Hypoxia Exposure

scholarly journals A pilot investigation into the effects of acute normobaric hypoxia, high altitude exposure and exercise on serum angiotensin-converting enzyme, aldosterone and cortisol

2018 ◽  
Vol 19 (2) ◽  
pp. 147032031878278 ◽  
Author(s):  
Mark Cooke ◽  
Richard Cruttenden ◽  
Adrian Mellor ◽  
Andrew Lumb ◽  
Stewart Pattman ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
High Altitude ◽  
Prolonged Exposure ◽  
Normobaric Hypoxia ◽  
Converting Enzyme ◽  
Serum Angiotensin Converting Enzyme ◽  
Post Exercise ◽  
Altitude Exposure ◽  
Pilot Investigation ◽  
Ace Activity

Introduction: Aldosterone decreases at high altitude (HA) but the effect of hypoxia on angiotensin-converting enzyme (ACE), a key step in the renin-angiotensin-aldosterone system, is unclear. Methods: We investigated the effects of exercise and acute normobaric hypoxia (NH, ~11.0% FiO2) on nine participants and six controls undertaking the same exercise at sea level (SL). NH exposure lasted 5 hours with 90 minutes of submaximal treadmill walking. Blood samples for aldosterone, ACE and cortisol were taken throughout exposure and at rest during a trek to HA (5140 m) in eight separate participants. Results: There was no difference in cortisol or aldosterone between groups pre-exercise. Aldosterone rose with exercise to a greater extent at SL than in NH (post-exercise: 700 ± 325 versus 335 ± 238 pmol/L, mean ± SD, p = 0.044). Conversely, cortisol rose to a greater extent in NH (post-exercise: 734 ± 165 versus 344 ± 159 nmol/L, mean ± SD, p = 0.001). There were no differences in ACE activity. During the trek to HA, resting aldosterone and cortisol reduced with no change in ACE. Conclusions: Acute NH subdues the exercise-associated rise in aldosteroe but stimulates cortisol, whereas prolonged exposure at HA reduces both resting aldosterone and cortisol. As ACE activity was unchanged in both environments, this is not the mechanism underlying the fall in aldosterone.

Cognitive Function During Post-Exercise in Normobaric Hypoxia

2016 ◽  
Vol 48 ◽  
pp. 572
Author(s):  
Yongsuk Seo ◽  
Hayden Gerhart ◽  
Jon Stavres ◽  
Shane Draper ◽  
Ellen L. Glickman
Keyword(s):  
Cognitive Function ◽  
Normobaric Hypoxia ◽  
Post Exercise

The Effect of Acute Normobaric Hypoxia On Heart Rate And Mean Arterial Pressure at Rest, During annd Post Exercise

2011 ◽  
Vol 43 (Suppl 1) ◽  
pp. 286
Author(s):  
Yongsuk Seo ◽  
Chul-Ho Kim ◽  
Corey A. Peacock ◽  
Edward J. Ryan ◽  
Zack Sax ◽  
...  
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Normobaric Hypoxia ◽  
Post Exercise

Oxygen radicals participate in alloxan-induced pulmonary EDEMA

1990 ◽  
Vol 48 (3) ◽  
pp. 298-299
Author(s):  
Tomoo Kawada ◽  
Michio Arakawa ◽  
Kenjiro Kambara ◽  
Takashi Segawa ◽  
Fumio Ando ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
Oxygen Radicals ◽  
Bolus Injection ◽  
Physiological Saline ◽  
Baseline Period ◽  
Alveolar Epithelial Cells ◽  
Control Group ◽  
Intervention Period ◽  
Lung Water ◽  
Electron Microscopic

We know that alloxan causes increased-permeability pulmonary edema and that alloxan generates oxygen radicals (H2O2, O2−, ·OH) in blood. Therefore, we hypothesize that alloxan-generated oxygen radicals damage pulmonary capillary endothelial cells, and, possibly, alveolar epithelial cells as well. We examined whether oxygen radical scavengers, such as catalase or dimethylsulfoxide (DMSO), protected against alloxaninduced pulmonary edema.Five dogs in each following group were anesthetized: control group: physiological saline (20ml/kg/h); alloxan group: physiological saline + alloxan (75mg/kg) bolus injection at the beginning of the experiment; catalase group: physiological saline + catalase (150,000u/kg) bolus injection before injection of alloxan; DMSO group: physiological saline + DMSO (0.4mg/kg) bolus injection before alloxan. All dogs had 30-min baseline period and 3-h intervention period. Hemodynamics and circulating substances were measured at the specific points of time. At the end of intervention period, the dogs were killed and had the lungs removed for electron microscopic study and lung water measurement with direct destructive method.

The Basis for the Increase in Factor VIII Procoagulant Activity During Exercise

1983 ◽  
Vol 49 (01) ◽  
pp. 053-057 ◽  
Author(s):  
Robert G Kopitsky ◽  
Mary Ellen P Switzer ◽  
R Sanders Williams ◽  
Patrick A McKee
Keyword(s):  
Factor Viii ◽  
Acute Exercise ◽  
Post Exercise ◽  
Fviii Activity ◽  
Plasma Factor ◽  
The Subject ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Healthy Males ◽  
Related Increase

SummaryWe studied the effect of acute exercise on the ability of thrombin to activate plasma factor VIII (FVIII) activity in 20 healthy males. The subject showed an average exercise-related increase in FVIII activity of 54.5±8.2% over pre-exercise FVIII activity (p<0.001). When exposed to the same concentration of thrombin, post-exercise FVIII activity showed greater enhancement than pre-exercise FVIII activity: 157.1±12.8% increase in activity versus 117.3±9.9%, respectively (p<0.01). The degree of the potentiated thrombin effect in post-exercise samples relative to pre-exercise samples was linearly correlated with the degree of the exercise-related increase in FVIII activity. Taken together with our previous observations that the extent of thrombin enhancement of FVIII activity varies inversely with the mole ratio of FVIII/von Willebrand factor subunits to thrombin, these findings imply that release of FVIII does not occur during exercise, and that the exercise-related increase in FVIII activity results primarily, if not completely, from activation of already circulating but inactive FVIII.

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