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The Impact of 32 Days' Exposure to Hypobaric Hypoxia on Physiological Cost of Sub-Maximal Work Performed at the Sea Level

100%

Kujach S. , Grzywacz T. , Ziemann E. , Szymczak R. , Łuszczyk M. , Laskowski R.

Baltic Journal of Health and Physical Activity

2011

tom 3

nr 1

19-25

Background: Many papers showed that long-lasting exposure to hypobaric hypoxia changed the metabolic cost of work and substrate contribution, elevating exercise energy expenditure and carbohydrates utilization. Only few of them have shown how long this adaptive changes are maintained. The aim of the study was to assess the impact of prolonged sojourn at high altitude on the physiological cost of sub-maximal work performed at the sea level.Material/Methods: Eight members of two high altitude expeditions (Lenin Peak 7,134 m a.s.l. and Somoni Peak 7,495m a.s.l.), 7 males and 1 female, mean age 26 (±4.1) years, volunteered for this study. Aerobic performance was measured by a direct method (breath-by-breath) using an expiratory gas analyser (Oxycon Pro, Jaeger) with an incremental exercise test till exhaustion. The sea level examinations were performed 7 days before the expedition (BEx) and 7 days after (AEx) the last day at over 2,500m a.s.l. Participants spent 32 (±3) days over 2,500m a.s.l. at the mean altitude of 4,712m a.s.l. (±499m).Results: Prolonged sojourn at high altitude has changed the ventilatory parameters of sub-maximal work measured at the sea level. The sojourn resulted in an increase in the ventilatory volume (tidal volume, minute ventilation and breath frequency) during the sub-maximal work performed with the same workload. However, the respiratory exchange ratio remained at a high level compared to the baseline.Conclusions: We suggest that the adaptive changes introduced during the sojourn remain at the sea level and cause increased carbohydrate metabolism.

Plasmatic hemostasis at very high altitude - a thrombelastometric approach

75%

Tobler M. , Nakas C. , Hilty M. , Huber A. , Merz T. , Hefti J.

Health Promotion & Physical Activity

2021

tom 17

nr 4

6-17

Introduction: Changes in blood coagulation during exposure to high altitude are not well understood and studies of activation and consumption of specific coagulation factors in hypoxic humans have yielded conflicting results. In this study we used thrombelastometry (TEM) which allows a global evaluation of clot formation and lysis process to study blood coagulation profiles in volunteers exposed to prolonged hypobaric hypoxia at extreme altitudes.Material and methods: We conducted a prospective observational study in 39 healthy volunteers during a research expedition up to an altitude of 7050 m. Plasma based thrombelastometric measurements and standard coagulation parameters were performed at different altitudes. Results: TEM measurements showed an increase in clotting time (CT) and maximum clot firmness (MCF) at high altitudes, paralleled by an increase in international normalized ratio (INR) and activated partial thromboplastin time (aPTT). Fibrinogen concentration increased until 6022 m. D-Dimer and Thrombin-Antithrombin complex (TAT) increased with time exposed to severe hypoxia. For both measurements high-est levels were found at 4844 m after acclimatization; in contrast, lower values were observed again at 7050m in the group of summiteers. Activated protein C resistance (APC-R) was slightly lowered at all altitudes. Conclusion: Our results suggest that activation of the coagulation and fibrinolytic system occurs with increasing hypobaric hypoxia with concurrent use of coagulation factors indicating the occurrence of a consumption-coagulopathy phenotype.

Hypobaric hypoxia and hyperbaric treatment prevents neuronal damage and affect antioxidative activity in neonatal hypoxia-ischemia rat model

63%

Gamdzyk M. , Ziembowicz A. , Salinska E.

Acta Neurobiologiae Experimentalis

2013

tom 73

nr 1

Hypoxic–ischemic encephalopathy (HIE) remains a serious condition that causes significant mortality and long-term morbidity. The aim of the study was to evaluate the effect of hyperbaric oxygen (HBO), hyperbaric air (HBA) and hypobaric hypoxia (HH) on neonatal hypoxic–ischemic (HI) brain injury within a therapeutic window of 1–6 h. We used an experimental model of perinatal hypoxia–ischemia on 7-days old rats, where left (ipsilateral) common carotid artery ligation is followed by 75 min hypoxia. HBO, HBA (2.5 ATA) and HH (0.5 atm air) were applied at 1, 3 or 6 h after HI for 60 min. Treatment was repeated for 3 following days. Brain injury was assessed by comparing ipsilateral hemisphere and contralateral hemisphere weight. Based on the evaluation of weight ratio, HH, HBO and HBA treatment, regardless of time of treatment initiation, resulted in significant reduction of brain weight loss. We observed that HBO reduced brain damage by 58.1%, 57.6% and 54.9%, respectively to the time of treatment initiation (1, 3, 6 h after HI), HBA decreased the damage by 29.9%, 38.1% and 22.0% (respectively). HH also significantly lessened brain weight loss, from 38% after untreated hypoxia–ischemia to 12.9%, 23.1% and 23.8% after HH application respectively 1, 3 and 6 h after hypoxia–ischemia. Superoxide dismutase (SOD) activity and glutathione (GSH) concentration were also measured. HI caused decrease in GSH concentration and 6-fold increase in SOD activity in ipsilateral, but not contralateral hemisphere. HBO treatment applied 1 and 3 h after HI significantly increased GSH concentration and decreased SOD activity, the effect of HBA was less pronounced. HH treatment resulted in additional increase in SOD activity in both hemispheres. However, GSH concentration after HH returned to control values. HBO and HBA altered the expression of cytoplasmic SOD1, and these changes corresponded to changes in SOD activity, suggesting significant role of this protein in neuroprotecting properties of HBO. Our results suggest that HBO, HBA and HH may serve in attenuation of the effects of HI. Early treatment gives better results in brain protection. Our results suggest that HBO and HBA probably reduce synthesis of free oxygen radicals, which manifests in decreased SOD activity. HH however, seems to act on different mechanism, because it enhances SOD activity. It may be beneficial, as it helps to neutralize superoxide anion production, provided that this SOD activity increase is accompanied by activation of glutathione peroxidase (GPx) and catalase (CAT). This assumption needs further investigation.