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21.
With hypoxic exposure ventilation is elevated through the hypoxic ventilatory response. We tested the hypothesis that the resulting hypocapnia reduces maximal exercise capacity by decreasing (i) cerebral blood flow and oxygenation and (ii) the ventilatory drive.  相似文献   
22.
Human exposure to altitude is a model to study the role of oxygen in different areas of physiology and pathophysiology. The aim of this study was to evaluate whether a short exposure to hypoxia (5 days) combined with exercise, at altitude ranging from 900 m above sea level to 5895 m above sea level (Kilimanjaro Expedition) can modify seminal and reproductive hormonal parameter levels in human beings. During the ascent, blood oxygen saturation at 3.848 m above sea level was found to be decreased when compared to sea level (P < 0.02). The sperm forward motility at sea level after the expedition showed a significant reduction ??(P < 0.02). There were no changes in other seminal parameters among those compared. Determination of the hormonal plasma concentrations showed that baseline values of follicle‐stimulating hormone, total testosterone, prolactin and oestradiol were unchanged at sea level after the hypoxic experience, with respect to baseline values at sea level. On the other hand, luteinising hormone levels after altitudes trekking significantly increased compared to levels before the expedition (P < 0.05). Because of the short‐term exposure, we can assume that the reduced forward motility described here may result from the effects of the acute altitude hypoxia on spermatozoa during the epididymal transit where they mature acquiring their motility.  相似文献   
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24.

Background

Modulation of the mitochondrial permeability transition pore (MPTP) and inhibition of the apoptotic signaling are critically associated with the cardioprotective phenotypes afforded by both intermittent hypobaric-hypoxia (IHH) and endurance-training (ET). We recently proposed that IHH and ET improve cardiac function and basic mitochondrial capacity, although without showing addictive effects. Here we investigate whether a combination of IHH and ET alters cardiac mitochondrial vulnerability to MPTP and related apoptotic signaling.

Methods

Male Wistar rats were divided into normoxic-sedentary (NS), normoxic-exercised (NE, 1 h/day/5 week treadmill-running), hypoxic-sedentary (HS, 6000 m, 5 h/day/5 weeks) and hypoxic-exercised (HE) to study susceptibility to calcium-induced cardiac MPTP opening. Mitochondrial cyclophilin D (CypD), adenine nucleotide translocator (ANT), Bax and Bcl-2 protein contents were semi-quantified by Western blotting. Cardiac caspase 3-, 8- and 9-like activities were measured. Mitochondrial aconitase and superoxide dismutase (MnSOD) activity and malondialdehyde (MDA) and sulphydryl group (–SH) content were determined.

Results

Susceptibility to MPTP decreased in NE and HS vs. NS and even further in HE. The ANT content increased in HE vs. NS. Bcl-2/Bax ratio increased in NE and HS compared to NS. Decreased activities in tissue caspase 3-like (HE vs. NS) and caspase 9-like (HS and HE vs. NS) were observed. Mitochondrial aconitase increased in NE and HS vs. NS. No alterations between groups were observed for caspase 8-like activity, MnSOD, CypD, MDA and –SH.

Conclusions

Data confirm that IHH and ET modulate cardiac mitochondria to a protective phenotype characterized by decreased MPTP induction and apoptotic signaling, although without visible addictive effects as initially hypothesized.  相似文献   
25.
We have previously formulated and validated a mathematical model specifically designed to describe human respiratory behavior at altitude. In that model, we assumed equality of alveolar and end-pulmonary-capillary oxygen tensions. However, this equality may not hold true during rapid and prolonged changes to high altitudes producing severe hypoxia as can occur in aircraft cabin decompressions and in some respiratory diseases. We currently investigate this possibility by modifying our previous model to include the dynamics of oxygen exchange across the pulmonary capillary. The updated model was validated against limited experimental data on ventilation and gas tensions in various altitude-decompression scenarios. The updated model predicts that during rapid and sustained decompressions to high altitudes the disequilibrium of gas tensions between alveolar gas and capillary blood could be 10 Torr, or larger. Neglecting this effect underestimates the severity of a decompression and its potential to produce unconsciousness and subsequent brain damage. In light of these results, we also examined the effect of this disequilibrium on the diminished oxygen diffusion capacity that can occur in some respiratory diseases. We found that decreases in diffusion capacity which would have minimal effects at sea level produced significant disequilibrium of gas tensions and a large fall in hemoglobin oxygen saturation at a cabin altitude of 4000–8000 ft. As demonstrated, this new model could serve as an important tool to examine the important physiological consequences of decompression scenarios in aircraft and the pathophysiological situations in which the equilibrium of gas tensions along the pulmonary capillary are particularly critical.  相似文献   
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27.
本文对低压舱内模拟快速进入高原和移居高原健康青年战士的体能及心功能之间的关系进行了对比探讨,结果表明:①测试的VO2max、AT值和PWC(150)均随海拔高度的升高而呈线性降低,且三项指标在同海拔高度的降低率近乎一致;②高原现场选用PWC(150)和AT替代VO2max,可避免VO2max高原应用欠安全性;③移居高原者测试的各项体能指标均明显优于模拟快速进入同高度者;④测试移居高原1.7年者的心功能,提示已基本获得高原适应。  相似文献   
28.
葛淼 《河北医药》1998,20(6):322-324
目的:为制定中国健康老年男性全血比粘度参考值的统一标准提供科学依据,方法:收集了中国各地用毛细管法测定的健康老年男性全血比粘度参考值,并对其与海拔高度的关系进行了研究。结果:发现随着海拔高度的逐渐增大,健康老年男性全血比粘度参考值也在逐渐地增大,相关性很显著。用一元回归分析的方法推导出了一个回归方程。结论:如果知道了中国某地的海拔高度,就可以用回归方程估算这个地区的健康老年男性全血比粘度考值。  相似文献   
29.
为了解高原地区特殊情况下发生的坏血病,对海拔4300m地区世居藏族未发病的15例健康人和6例临床表现膝关节肿痛、皮肤出血等为特征的维生素C缺乏症,测定Hb、血清总蛋白,白蛋白等25项。结果显示:病人组和对照组均有轻度贫血,尤以病人组明显,病人组血清总蛋白和白蛋白低于对照组,而肾功能,血脂,免疫等测定结果均在正常范围,同期测定的血清维生素C含量两组均显著低于正常人含量。提示在高原地区特殊情况下,饮食  相似文献   
30.
In 1976, Paolo Cerretelli published an article entitled Limiting factors to oxygen transport on Mount Everest in the Journal of Applied Physiology . The paper demonstrated the role of cardiovascular oxygen transport in limiting maximal oxygen consumption (O2max). In agreement with the predominant view of O2max limitation at that time, however, its results were taken to mean that cardiovascular oxygen transport does not limit O2max at altitude. So it was argued that the limiting factor could be in the periphery, and muscle blood flow was proposed as a possible candidate. Despite this suggestion, the conclusion generated a series of papers on muscle structural characteristics. These experiments demonstrated a loss of muscle oxidative capacity in chronic hypoxia, and thus provided an unambiguous refutation of the then widespread hypothesis that an increased muscle oxidative capacity is needed at altitude to compensate for the lack of oxygen. This analysis is followed by a short account of Cerretellis more recent work, with a special attention to the subject of the so-called lactate paradox.  相似文献   
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