scholarly journals DL-3-n-butylphthalide improved physical and learning and memory performance of rodents exposed to acute and chronic hypobaric hypoxia

2021 ◽  
Vol 8 (1) ◽  
Author(s):  
Gang Xu ◽  
Yi-Kun Shi ◽  
Bin-Da Sun ◽  
Lu Liu ◽  
Guo-Ji E. ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Hypobaric Hypoxia ◽  
Gastrocnemius Muscle ◽  
Chronic Hypoxia ◽  
Acute Hypoxia ◽  
Treadmill Running ◽  
Hypoxia Tolerance ◽  
Control Group ◽  
Time To Exhaustion ◽  
Atp Levels

Abstract Background Studies have revealed the protective effect of DL-3-n-butylphthalide (NBP) against diseases associated with ischemic hypoxia. However, the role of NBP in animals with hypobaric hypoxia has not been elucidated. This study investigated the effects of NBP on rodents with acute and chronic hypobaric hypoxia. Methods Sprague-Dwaley rats and Kunming mice administered with NBP (0, 60, 120, and 240 mg/kg for rats and 0, 90, 180, and 360 mg/kg for mice) were placed in a hypobaric hypoxia chamber at 10,000 m and the survival percentages at 30 min were determined. Then, the time and distance to exhaustion of drug-treated rodents were evaluated during treadmill running and motor-driven wheel-track treadmill experiments, conducted at 5800 m for 3 days or 20 days, to evaluate changes in physical functions. The frequency of active escapes and duration of active escapes were also determined for rats in a shuttle-box experiment, conducted at 5800 m for 6 days or 27 days, to evaluate changes in learning and memory function. ATP levels were measured in the gastrocnemius muscle and malonaldehyde (MDA), superoxide dismutase (SOD), hydrogen peroxide (H2O2), glutathione peroxidase (GSH-Px), and lactate were detected in sera of rats, and routine blood tests were also performed. Results Survival analysis at 10,000 m indicated NBP could improve hypoxia tolerance ability. The time and distance to exhaustion for mice (NBP, 90 mg/kg) and time to exhaustion for rats (NBP, 120 and 240 mg/kg) significantly increased under conditions of acute hypoxia compared with control group. NBP treatment also significantly increased the time to exhaustion for rats when exposed to chronic hypoxia. Moreover, 240 mg/kg NBP significantly increased the frequency of active escapes under conditions of acute hypoxia. Furthermore, the levels of MDA and H2O2 decreased but those of SOD and GSH-Px in the sera of rats increased under conditions of acute and chronic hypoxia. Additionally, ATP levels in the gastrocnemius muscle significantly increased, while lactate levels in sera significantly decreased. Conclusion NBP improved physical and learning and memory functions in rodents exposed to acute or chronic hypobaric hypoxia by increasing their anti-oxidative capacity and energy supply.

scholarly journals DL-3-n-butylphthalide improved physical and learning and memory performance of rodents exposed to acute and chronic hypobaric hypoxia

2020 ◽  
Author(s):  
Gang Xu ◽  
Yikun Shi ◽  
Binda Sun ◽  
Lu Liu ◽  
Guoji E ◽  
...  
Keyword(s):  
Survival Analysis ◽  
Learning And Memory ◽  
Hypobaric Hypoxia ◽  
Gastrocnemius Muscle ◽  
Chronic Hypoxia ◽  
Cognitive Learning ◽  
Treadmill Running ◽  
Memory Functions ◽  
Wheel Track ◽  
Active Escape

Abstract Background: Studies revealed the protective effect of DL-3-n-butylphthalide (NBP) against ischemic hypoxia diseases. However, the role of NBP in animals with hypobaric hypoxia is elusive. This study investigated the effect of NBP on animals with acute and chronic hypobaric hypoxia. Methods: SD rats and Kunming mice administrated with NBP ( 90, 180 and 360 mg/kg for mice, 60, 120, and 240 mg/kg for rats and 90, 180 and 360 mg/kg for mice 60, 120, and 240 mg/kg for rats ) were placed located in 10,000 m hypobaric hypoxia chamber. And survival analysis of animals implied that NBP could significantly improve and survival percent at 30 min were analyzed . Then, drug treated animals rats (mice) were evaluated for exhaustive exhausted time and exhaustive exhausted distance in forced exercise wheel-track treadmill and treadmill running and motor-driven wheel-track treadmill experiments at 5,800 m (5,000 m) for 3 or 21 days or 21 days , to evaluate changes of physical functions. Rats were also evaluated for times of active escape , and average time of active escape , time of passive escape, and average time of passive escape in a shuttle-box experiment at 5,800 m for 7 days or 28 days 7 or 28 days , to evaluate changes of cognitive learning and memory function s . ATP level was evaluated measured in the gastrocnemius muscle and maloaldehyde (MDA), superoxide dismutase (SOD), hydrogen peroxide (H 2 O 2 ), lactate, and glutathione peroxiase (GSH-Px) measurements and routine blood tests were detected in serum of rats . Results: Survival analysis in 10,000 m indicated NBP could improve hypoxia tolerance ability. Exhaustive Exhausted time for rats (NBP, 120 and 240 mg/kg) and exhaustive exhausted time and distance for mice (NBP, 90 mg/kg) significantly increased under acute hypoxia. And NBP treatment also significantly increased the exhaustive exhausted time for rats under chronic hypoxia. Moreover, NBP of 120 and 240 mg/kg significantly increased the average time s of passive active escape under acute and chronic hypoxia. These results suggested that NBP could improve physical and cognitive learning and memory functions under acute and chronic hypobaric hypoxia. Furthermore, the levels of MDA and H 2 O 2 decreased but those of SOD and GSH-Px in serum of rats increased under acute and chronic hypoxia. Furthermore, Additionally, the content of ATP in gastrocnemius muscle significantly increased, while lactate in serum level significantly decreased. The results presented suggested that NBP could regulate redox homeostasis and improve energy metabolism of hypobaric hypoxic rats. Conclusion: NBP could improve physical and cognitive learning and memory functions under acute and chronic hypobaric hypoxia by increasing anti-oxidative capacity and energy supply.

scholarly journals DL-3-n-Butylphthalide Improves Physical and Cognitive Performance of Animals with Acute and Chronic Hypobaric Hypoxia

2020 ◽  
Author(s):  
Gang Xu ◽  
Yikun Shi ◽  
Binda Sun ◽  
Lu Liu ◽  
Guoji E ◽  
...  
Keyword(s):  
Cognitive Functions ◽  
Hypobaric Hypoxia ◽  
Chronic Hypoxia ◽  
Acute Hypoxia ◽  
Redox Homeostasis ◽  
Oxidative Capacity ◽  
Treadmill Running ◽  
Escape Time ◽  
Physical Functions ◽  
Active Escape

Abstract Background: Studies revealed the protective effect of DL-3-n-butylphthalide (NBP) against ischemic hypoxia diseases. However, the role of NBP in animals with hypobaric hypoxia is elusive. This study investigated the effect of NBP on animals with acute and chronic hypobaric hypoxia.Methods: SD rats and Kunming mice administrated with NBP (90, 180 and 360 mg/kg for mice, and 60, 120, and 240 mg/kg for rats) were located in 10,000 m hypobaric hypoxia chamber. And survival analysis of animals implied that NBP could significantly improve survival percent at 30 min. Then, treated animals were evaluated for exhaustive time and exhaustive distance in forced exercise wheel-track treadmill and treadmill running experiments at 5,800 m for 3 or 21 days, to evaluate physical functions. Rats were also evaluated for times of active escape, average time of active escape, time of passive escape, and average time of passive escape in a shuttle-box experiment at 5,800 m for 7 or 28 days, to evaluate cognitive functions. ATP level was evaluated in the gastrocnemius muscle and maloaldehyde (MDA), superoxide dismutase (SOD), hydrogen peroxide (H2O2), lactate, and glutathione peroxiase (GSH-Px) measurements and routine blood tests were detected.Results: Exhaustive time for rats (NBP, 120 and 240 mg/kg) and exhaustive time and distance for mice (NBP, 90 mg/kg) significantly increased under acute hypoxia. And NBP treatment significantly increased the exhaustive time for rats under chronic hypoxia. Moreover, NBP of 120 and 240 mg/kg significantly increased the average time of passive escape under acute and chronic hypoxia. These results suggested that NBP could improve physical and cognitive functions under acute and chronic hypobaric hypoxia. Furthermore, the levels of MDA and H2O2 decreased but those of SOD and GSH-Px increased under acute and chronic hypoxia. Furthermore, the content of ATP significantly increased, while lactate level significantly decreased. The results presented that NBP could regulate redox homeostasis and improve energy metabolism.Conclusion: NBP could improve physical and cognitive functions under acute and chronic hypobaric hypoxia by increasing anti-oxidative capacity and energy supply.

Skeletal muscle lipid peroxidation in exercised and food-restricted rats during aging

1989 ◽  
Vol 67 (1) ◽  
pp. 69-75 ◽  
Author(s):  
J. W. Starnes ◽  
G. Cantu ◽  
R. P. Farrar ◽  
J. P. Kehrer
Keyword(s):  
Lipid Peroxidation ◽  
Gastrocnemius Muscle ◽  
Thiobarbituric Acid ◽  
Exercise Group ◽  
Alpha Tocopherol ◽  
Treadmill Running ◽  
Control Group ◽  
Muscle Lipid ◽  
Fischer 344 ◽  
Skeletal Muscle Lipid

The effects of chronic endurance exercise and food restriction on nonenzymatic lipid peroxidation (LP) of gastrocnemius muscle during aging were studied in male, Fischer 344 rats. One set of rats aged 6 and 18 mo were assigned to an exercise group (treadmill running) or an age-matched sedentary control group. After 6 mo (at the ages of 12 and 24 mo), LP and levels of alpha-tocopherol and its oxidized form, alpha-tocopheryl quinone, were measured. The extent of LP was determined in homogenates by measuring the content of thiobarbituric acid-reactive substances. After homogenization, the muscles were immediately evaluated for basal LP and also incubated in the presence of oxidant stressors for 2 h to assess antioxidant capacity (AOC) and for 24 h to estimate total peroxidizable lipid (TPL). Basal LP was not affected by age or exercise. AOC was not affected by exercise at either age. However aging significantly decreased AOC and increased alpha-tocopheryl quinone in both sedentary and exercised groups. TPL was not affected by age, but was increased by exercise training (P less than 0.05). Another set of rats was divided into the following three groups at 3 mo of age: sedentary, fed ad libitum (S); sedentary, caloric restricted by alternate day feeding (R); and exercised by forced treadmill running (E). Two years later, when the rats were 27 mo of age, the extent of LP was assessed.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac and respiratory effects of digitalis during chronic hypoxia in intact conscious dogs

1975 ◽  
Vol 229 (2) ◽  
pp. 270-274 ◽  
Author(s):  
GA Beller ◽  
SR Giamber ◽  
SB Saltz ◽  
TW Smith
Keyword(s):  
Sea Level ◽  
Chronic Hypoxia ◽  
Acute Hypoxia ◽  
Left Ventricular ◽  
Control Group ◽  
Continuous Exposure ◽  
Ventricular Performance ◽  
Toxic Dose ◽  
Respiratory Effects ◽  
Significant Difference

The arrhythmogenic and respiratory effects of ouabain during chronic hypoxia were studied in 10 unanesthetized dogs in a hypobaric chamber (446 mmHg) following 7-19 (mean 14.7) days of continuous exposure at this altitude. Another 15 dogs studied at sea level comprised the normoxic control group. In both groups, a 7.5-mug/kg loading dose of ouabain was followed by infusion of ouabain at 3.0 mug/kg per min to ECG evidence of toxicity. Mean arterial Po2 was 46 +/- 5 mmHg in chronically hypoxic dogs as compared to 86 +/- 7 mmHg in normoxic animals (P less than 0.001). Mean hematocrit was 54 +/- 1% in hypoxic and 43 +/- 2% in normoxic groups (P less than 0.001). In five dogs studied first at sea level and subsequently under conditions of chronic hypoxia, mean maximum left ventricular dP/dt and peak (dP/dt)P-1 were unchanged. Marked hyperventilation during ouabain infusion was observed. In normoxic dogs mean arterial pH rose from 7.43 +/- 0.05 to 7.70 +/- 0.02 U, and Pco2 fell from 41 +/- 4 to 15 +/- 1 mmHg during ouabain administration (P less than 0.001). Similar changes were observed in hypoxic dogs. There was no significant difference in the mean toxic dose of ouabain in chronically hypoxic (71 +/- 11 mug/kg) versus normoxic (78 +/- 12 mug/kg) animals. Thus, in contrast to acute hypoxia, chronic hypoxia in unanesthetized dogs was not associated with a significant reduction in the dose of ouabain required to produce toxic arrhythmias. Chronic hypoxia was also not associated with alterations in left ventricular performance.

scholarly journals Effect of chronic hypoxia and hypercapnia on learning and memory function in mice and the expression of NT and CGRP in brain

2018 ◽  
Vol 16 ◽  
pp. 205873921881895 ◽  
Author(s):  
Hangyu Xu ◽  
Hao Xu
Keyword(s):  
Learning And Memory ◽  
Brain Tissue ◽  
Chronic Hypoxia ◽  
Memory Function ◽  
Normal Pressure ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Sod Activity ◽  
Stress Injury ◽  
Experimental Group

The aim of this study is to investigate the effects of chronic hypoxia and hypercapnia on learning and memory function of mice and the expression of neurotensin (NT) and calcitonin gene–related peptide (CGRP) in mice brain. A total of 30 C57BL/6J male mice were randomly divided into normoxia control group (control group, n = 15) and chronic hypoxia and hypercapnia stress group (experimental group, n = 15). The control group was kept under normal temperature and pressure conditions, while the experimental group was kept in a chamber at normal pressure, hypoxia and hypercapnia for 8 h daily and 6 days a week for 4 weeks. On the 28th day, the learning and memory ability of mice was examined by 8-arm maze. The content of 8-hydroxy-deoxyguanosine (8-OHdG) in brain was detected by enzyme-linked immunosorbent assay (ELISA) analysis. Superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were determined by spectrophotometry, and the derangement of hippocampal ultrastructures and numbers of apoptotic neurons were observed by microscope. The expression of NT and CGRP in brain tissue was observed by immunochemistry. Compared to control group, the content of 8-OHdG in hippocampal and serum MDA were significantly increased by 1.3 and 1.78 times, while the activity of SOD in serum was decreased by 27.28% in experimental group. Besides, the cellular structure of the hippocampus was disorderly arranged, the shape is irregular and the quantity is markedly reduced obviously in experimental group. In addition, the content of NT and CGRP in brain tissue was higher in experimental group than in control group ( P < 0.05). The stress of chronic hypoxia and hypercapnia not only can induce learning and memory disorders in mice which may be related to increased neuronal apoptosis and oxidative stress injury but also can increase the expression of NT and CGRP in brain tissue which may have some impact on gastrointestinal motility in mice.

The effects of nightly normobaric hypoxia and high intensity training under intermittent normobaric hypoxia on running economy and hemoglobin mass

2007 ◽  
Vol 103 (3) ◽  
pp. 828-834 ◽  
Author(s):  
Mituso Neya ◽  
Taisuke Enoki ◽  
Yasuko Kumai ◽  
Takayuki Sugoh ◽  
Takashi Kawahara
Keyword(s):  
High Intensity ◽  
Intermittent Hypoxia ◽  
Training Group ◽  
Normobaric Hypoxia ◽  
Running Economy ◽  
Treadmill Running ◽  
Control Group ◽  
Time To Exhaustion ◽  
Simulated Altitude ◽  
Hemoglobin Mass

We investigated the effects of nightly intermittent exposure to hypoxia and of training during intermittent hypoxia on both erythropoiesis and running economy (RE), which is indicated by the oxygen cost during running at submaximal speeds. Twenty-five college long- and middle- distance runners [maximal oxygen uptake (V̇o2max) 60.3 ± 4.7 ml·kg−1·min−1] were randomly assigned to one of three groups: hypoxic residential group (HypR, 11 h/night at 3,000 m simulated altitude), hypoxic training group (HypT), or control group (Con), for an intervention of 29 nights. All subjects trained in Tokyo (altitude of 60 m) but HypT had additional high-intensity treadmill running for 30 min at 3,000 m simulated altitude on 12 days during the night intervention. V̇o2 was measured at standing rest during four submaximal speeds (12, 14, 16, and 18 km/h) and during a maximal stage to volitional exhaustion on a treadmill. Total hemoglobin mass (THb) was measured by carbon monoxide rebreathing. There were no significant changes in V̇o2max, THb, and the time to exhaustion in all three groups after the intervention. Nevertheless, HypR showed ∼5% improvement of RE in normoxia ( P < 0.01) after the intervention, reflected by reduced V̇o2 at 18 km/h and the decreased regression slope fitted to V̇o2 measured during rest position and the four submaximal speeds ( P < 0.05), whereas no significant corresponding changes were found in HypT and Con. We concluded that our dose of intermittent hypoxia (3,000 m for ∼11 h/night for 29 nights) was insufficient to enhance erythropoiesis or V̇o2max, but improved the RE at race speed of college runners.

scholarly journals Regulation of catecholamine release from the adrenal medulla is altered in deer mice (Peromyscus maniculatus) native to high altitudes

2019 ◽  
Vol 317 (3) ◽  
pp. R407-R417 ◽  
Author(s):  
Angela L. Scott ◽  
Nicole A. Pranckevicius ◽  
Colin A. Nurse ◽  
Graham R. Scott
Keyword(s):  
High Altitude ◽  
Adrenal Medulla ◽  
Hypobaric Hypoxia ◽  
Chronic Hypoxia ◽  
Acute Hypoxia ◽  
Catecholamine Secretion ◽  
Deer Mice ◽  
Dopa Decarboxylase ◽  
Plasma Epinephrine ◽  
High Altitude Natives

High-altitude natives have evolved to overcome environmental hypoxia and provide a compelling system to understand physiological function during reductions in oxygen availability. The sympathoadrenal system plays a key role in responses to acute hypoxia, but prolonged activation of this system in chronic hypoxia may be maladaptive. Here, we examined how chronic hypoxia exposure alters adrenal catecholamine secretion and how adrenal function is altered further in high-altitude natives. Populations of deer mice ( Peromyscus maniculatus) native to low and high altitudes were each born and raised in captivity at sea level, and adults from each population were exposed to normoxia or hypobaric hypoxia for 5 mo. Using carbon fiber amperometry on adrenal slices, catecholamine secretion evoked by low doses of nicotine (10 µM) or acute hypoxia (Po2∼15–20 mmHg) was reduced in lowlanders exposed to hypobaric hypoxia, which was attributable mainly to a decrease in quantal charge rather than event frequency. However, secretion evoked by high doses of nicotine (50 µM) was unaffected. Hypobaric hypoxia also reduced plasma epinephrine and protein expression of 3,4-dihydroxyphenylalanine (DOPA) decarboxylase in the adrenal medulla of lowlanders. In contrast, highlanders were unresponsive to hypobaric hypoxia, exhibiting typically low adrenal catecholamine secretion, plasma epinephrine, and DOPA decarboxylase. Highlanders also had consistently lower catecholamine secretion evoked by high nicotine, smaller adrenal medullae with fewer chromaffin cells, and a larger adrenal cortex compared with lowlanders across both acclimation environments. Our results suggest that plastic responses to chronic hypoxia along with evolved changes in adrenal function attenuate catecholamine release in deer mice at high altitude.

scholarly journals OR-048 Effects and Mechanism of myokines in exercise mediated improving obesity rats skeletal muscle remodeling

2018 ◽  
Vol 1 (2) ◽  
Author(s):  
Liang Zhang ◽  
Hongtao Yang ◽  
Jin Ma ◽  
Linjie Li
Keyword(s):  
Skeletal Muscle ◽  
Muscle Fiber ◽  
High Fat Diet ◽  
Gastrocnemius Muscle ◽  
Receptor Expression ◽  
Treadmill Running ◽  
Endocrine Function ◽  
Control Group ◽  
High Fat ◽  
Muscle Remodeling

Objective Aims From the year 2000, many experimental research data have indicated that skeletal muscle could express, synthesis and secrete multiple cytokines and polypeptides. The cytokines and polypeptides, not only regulate skeletal muscle growth, metabolism and motor function by paracrine/autocrine pathway, but also regulate functions of peripheral tissue and organs by endocrine pathway. Further researches proposed muscle as a secretory organ played a key role in mediating the health-promoting effects of physical activity and proteins expressed and released by skeletal muscle have been termed as myokines. Disorders of skeletal muscle endocrine function have related to the occurrence and development of multiple metabolic diseases, and myokines participate in obesity skeletal muscle remodeling. This study aims to investigate the expression changes of myokines and its effects in exercise mediated improving skeletal muscle remodeling on obesity mice, and explore the underlying mechanism of its functions. Methods Methods Five-week-old male Sprague-Dawley(SD) rats were randomly divided into a control group of 8 and a high-fat diet（HFD）group of 16. The control group was given normal food，while the HFD group were provided with high-fat diet for eight weeks and further divided into a sedentary HFD group and a treadmill running HFD group，each of 8. The exercise mice underwent 60 min treadmill running at 26 m/min each day，5 days/week for 8 weeks. Biochemical analyses, immune-histochemical, ELISA, RT-PCR and Western Blot methods were used to investigate multiple myokines expression changes and its mechanism. Results Results 1) Exercise significantly upregulated the expression of IL-15 in soleus and gastrocnemius muscle of obesity rats, indicating IL-15 could inhibit skeletal muscle endoplasmic reticulum stress and improve insulin sensitivity. 2) Exercise significantly inhibited the expression of myostatin (MSTN) in gastrocnemius muscle and mediated the changes of muscle fiber types. 3) Exercise markedly promoted the expression of apelin/APJ and angiogenesis function in obesity skeletal muscle. 4) Exercise upregulated skeletal muscle vascular endothelial growth factor B receptor expression and improved skeletal muscle ectopic lipid accumulation. Conclusions Conclusion Exercise regulates skeletal muscle myokines expression and secretion and have the effects on skeletal muscle fiber type changes, myofiber capillary density, glucose and lipid metabolism, thus improves the skeletal muscle remodeling and maintain body homeostasis.

Mechanism and effects of fructose diphosphate on anti-hypoxia fatigue and learning memory ability

2020 ◽  
Vol 98 (10) ◽  
pp. 733-740
Author(s):  
Chunna Liu ◽  
Chunhua Shao ◽  
Qi Du ◽  
Chaoran He ◽  
Xinyuan Sun ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Glucose Transporter ◽  
Potassium Cyanide ◽  
Hypoxia Tolerance ◽  
Control Group ◽  
High Dose ◽  
Memory Ability ◽  
Nitrogen Levels ◽  
Cerebral Ischemic ◽  
The Impact

This study aims to investigate the mechanisms through which fructose diphosphate (FDP) causes anti-hypoxia and anti-fatigue effects and improves learning and memory. Mice were divided into three groups: low-dose FDP (FDP-L), high-dose FDP (FDP-H), and a control group. Acute toxic hypoxia induced by carbon monoxide, sodium nitrite, and potassium cyanide and acute cerebral ischemic hypoxia were used to investigate the anti-hypoxia ability of FDP. The tests of rod-rotating, mouse tail suspension, and swimming endurance were used to explore the anti-fatigue effects of FDP. The Morris water maze experiment was used to determine the impact of FDP on learning and memory ability. Poisoning-induced hypoxic tests showed that mouse survival time was significantly prolonged in the FDP-L and FDP-H groups compared with the control group (p < 0.05). In the exhaustive swimming test, FDP significantly shortened struggling time and prolonged the time of mass-loaded swimming; the rod-rotating test showed that endurance time was significantly prolonged by using FDP (p < 0.05). FDP significantly decreased lactate and urea nitrogen levels and increased hepatic and muscle glycogen and glucose transporter-4 and Na+-K+-ATPase (p < 0.05). To conclude, FDP enhances hypoxia tolerance and fatigue resistance and improves learning and memory ability through regulating glucose and energy metabolism.

Continuous Adaptation of Rats to Hypobaric Hypoxia Prevents Stressor Hyperglycemia and Optimizes Mitochondrial Respiration in Acute Hypoxia

2013 ◽  
Vol 4 (2) ◽  
pp. 137-147
Author(s):  
Vladimir I. Portnichenko ◽  
Valentina I. Nosar ◽  
Alla M. Sydorenko ◽  
Alla G. Portnychenko ◽  
Irina N. Mankovska
Keyword(s):  
Mitochondrial Respiration ◽  
Hypobaric Hypoxia ◽  
Acute Hypoxia
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