高住低训过程中血氧饱和度变化及其与血红蛋白变化的关联

目的:观察低氧运动过程中脉搏血氧饱和度(SpO2)和血红蛋白(Hb)的变化规律,探讨科学进行高住低训的评价指标.方法:8名男性受试者每晚于15.4%O2低氧环境中暴露10小时,白天在常氧环境下训练.测定高住低训过程中,常氧运动、急性低氧暴露10小时、高住低训第1、2、3、4周时低氧运动(15.4%O2,76.5%VO2max强度)中SpO2及安静时Hb.结果:(1)常氧状态下运动时SpO2下降幅度最小,急性低氧暴露时最大.随着受试者对低氧运动的适应,SpO2下降幅度逐渐减小.(2)常氧运动中,SpO2在运动开始时下降.随着运动时间的延长SpO2逐渐回升到运动前水平;急性低氧运动时,SpO2一直处于低水平,至恢复期10分钟仍未恢复到运动前水平.随着受试者对低氧运动的适应,虽然运动中SpO2下降,但运动后10分钟已恢复到安静时水平.(3)高住低训过程中,Hb呈上升趋势,第4周时有所下降,且SpO2与Hb的变化存在较大个体差异.结论:进行4周HiLo,机体逐渐适应了低氧环境;个体SpO2和Hb的变化可能存有一定的关联性.提示可以将SpO2作为评价低氧适应的生理指标.     

间歇性低氧暴露对足球运动员自由基代谢的影响

16名北京体育大学体育系男子足球运动员随机分为对照组和实验组,对照组为常氧环境,实验组实施高住低训,观察间歇性低氧暴露及运动对机体自由基代谢的影响。结果:(1)对照组4周实验前后自由基代谢各指标无明显变化。(2)实验组运动前、10小时急性低氧暴露后与常氧运动前比较,血清CK明显升高,血清MDA及红细胞SOD活性有升高趋势,红细胞GSH明显下降,GSH-PX有下降趋势。(3)实验组4周低氧暴露运动前与常氧相比,血清CK进一步升高,红细胞SOD、GSH-PX有升高趋势,血清MDA无明显变化。(4)运动对自由基代谢的影响在常氧与低氧环境下无明显差异。     

间歇低氧暴露预防SD大鼠大运动负荷训练期血红蛋白下降及其机制探讨

目的:探讨大运动负荷训练期间采用间歇低氧暴露预防运动性血红蛋白低下的效果及其机制。方法:将53只SD大鼠随机分为常氧安静组和常氧运动组、运动低氧暴露1h组、运动低氧暴露2h组、运动低氧暴露(1+1)h组。各运动组进行6周递增负荷跑台运动,各低氧暴露组从第4周起在运动后分别进行人工常压低氧(14.5%O2)暴露1h、2h和(1+1)h。6周实验结束后安静时测试血液Hb、RBC、Hct及血清IL-1、IL-3、IL-6、G-CSF、T、EPO、GM-CSF含量。结果:(1)6周递增负荷运动后,常氧运动组大鼠Hb、RBC、Hct显著低于常氧安静组,而各运动低氧暴露组与常氧安静组比较未见显著下降且显著高于常氧运动组。(2)与常氧运动组相比,仅运动低氧暴露(1+1)h组IL-6显著升高,而各运动低氧暴露组G-CSF、IL-3、EPO未见显著变化,但均出现上升趋势,且运动低氧暴露(1+1)h组上升幅度最大;而GM-CSF、T和IL-1未见规律性变化。结论:间歇低氧暴露能有效预防大运动负荷训练期间血红蛋白降低的发生与发展,其作用机理可能与间歇低氧暴露提高机体红系造血生长因子水平有关。     

模拟不同海拔高住低练对大鼠心肌VEGF和HSP70的影响

目的:探讨模拟不同海拔高住低练对大鼠心肌保护性蛋白热休克蛋白70(HSP70)和血管内皮生长因子(VEGF)表达的影响。方法:适应性喂养1周后,将48只SD大鼠按体重随机分为6组:常氧对照组(C)、14.5%O2低氧暴露组(14.5%O2LH)、12.7%O2低氧暴露组(12.7O2LH)、常氧训练组(TL)、14.5%O2高住低练组(14.5%O2LiLo)、12.7%O2高住低练组(12.7%O2HiLo),每组8只。采用20.9%、14.5%和12.7%三种氧浓度暴露和运动强度逐渐递增的高住低练模型,两LH组每天在低压氧舱中放置22 h后2 h舱外常氧生活,两HiLo组每天在低压氧舱中放置22 h后常氧生活1 h,再常氧训练1 h,所有进行低氧暴露的动物每周实验6天;TL组和两HiLo组进行一次5～10 min跑台适应性训练(速度为16 m/min,坡度为0)后,每天训练速度为35m/min,运动时间从30 min至60 min递增,每3天增加5 min,每天训练1次,每周6天,共4周。实验方案结束后24 h,麻醉大鼠取大鼠心尖肌组织,采用免疫组织化学技术检测VEGF和HSP70表达。结果:(1)与C组比较,14.5%O2LH组、TL组和12.7%O2的HiLo组VEGF阳性物质表达量显著增加(Ρ<0.05),12.7%O2LH组增加不显著(Ρ>0.05),而14.5%O2HiLo组表达量增加非常显著(Ρ<0.01);14.5%O2LH组VEGF阳性物质表达量较12.7%O2LH组显著增加(Ρ<0.05),12.7%O2HiLo组比14.5%O2HiLo组显著降低(Ρ<0.05),14.5%O2HiLo组VEGF阳性物质表达量较14.5%O2LH组显著增加(Ρ<0.05)。(2)与C组相比较,14.5%O2LH组、14.5%O2和12.7%O2两HiLo组HSP70阳性物质表达量增加(Ρ<0.05),12.7%O2LH组表达最明显,而TL组增加不显著(Ρ>0.05);14.5%O2LH和HiLo两组HSP70阳性物质表达量分别比12.7%O2LH和HiLo两组显著降低(Ρ<0.05),而两LH组HSP70阳性物质表达量分别与两HiLo组相比无显著性差异(Ρ>0.05)。结论:单纯低氧暴露、常氧运动及高住低练三种应激因素均诱导细胞保护性蛋白VEGF和HSP70表达;14.5%O2HiLo组的VEGF表达最显著,而12.7%O2LH组的HSP70表达最显著。     

间歇性低氧暴露对小鼠自由基代谢的影响

本实验选用40只雄性ICR封闭群小鼠,随机分为4组:对照组、低氧暴露组、运动组、运动 低氧组,每组10只.4周训练结束后,取心、脑、完整的腓肠肌,测试各组织MDA含量及SOD活性.实验结果提示:(1)间歇性低氧暴露提高了心肌组织的SOD水平,同时MDA水平下降,表明心肌抗氧化能力提高,有利于在长时间运动中保持正常供血功能.(2)间歇性低氧暴露提高骨骼肌组织SOD活性和降低MDA含量,表明间歇性低氧暴露可有效提高骨骼肌抗氧化能力.(3)间歇性低氧暴露可提高脑组织对过氧化脂质的清除能力和SOD活性,对于延缓中枢疲劳有意义.     

低氧暴露和运动对正常大鼠胰岛β细胞形态的影响

目的:动态观察低氧暴露和运动对正常大鼠胰岛β细胞形态的影响。方法:将SD大鼠分为安静对照组(C)、低氧暴露组(H)、常氧运动组(E)和高住低训组(HL)。运动方式为跑台运动,坡度5°,速度20 m/min,60 min/次,低氧组晚上在氧浓度为13.6%的低氧帐篷内暴露12h。分别于实验开始后1d、7d和28d时取材,用HE和醛复红对比染色观察胰岛β细胞形态,并用图像分析法计算β细胞面积百分比。结果:实验1d的低氧暴露和高住低训初期(1d和7d),胰腺腺泡细胞出现明显的中度脂肪变性,28d时腺泡细胞呈现轻度的脂肪变性。图像分析显示,实验7d和28d时常氧运动组胰岛β细胞占胰岛面积百分比都有增加的趋势,但均无显著性差异(P>0.05);实验7d时低氧暴露组以及高住低训组胰岛β细胞占胰岛面积百分比都有增加的趋势,但均无显著性差异(P>0.05)。实验28d时高住低训组胰岛β细胞占胰岛面积百分比显著性降低(P<0.05),低氧暴露组也有降低的趋势,但无显著性差异(P>0.05)。结论:①高住低训可使正常大鼠胰腺腺泡细胞发生脂肪变性,随时间延长其脂肪变性减轻。②有氧运动训练对正常大鼠胰岛β细胞的形态无显著影响,低氧暴露和高住低训可降低胰岛β细胞占胰岛面积的百分比,且高住低训组更明显,表明低氧暴露和高住低训可能对正常机体胰岛β细胞的形态产生不良影响,从而影响其内分泌功能。     

低氧暴露对运动诱导的血红蛋白低下大鼠红细胞参数和某些造血因子的影响

目的:探讨低氧暴露对运动性血红蛋白低下机体红细胞参数和某些造血因子的影响及其机制。方法:采用6周递增负荷跑台运动建立大鼠运动性血红蛋白低下模型,人工常压低氧环境下(14.5%O2)分别采用每天1h、2h和(1+1)h三种暴露方式进行恢复,3周后测定运动性血红蛋白低下大鼠血红蛋白含量(Hb)、红细胞数目(RBC)、红细胞压积(Hct)、肾脏促红细胞生成素(EPO)与血清白细胞介素-3(IL-3)含量,并与常氧恢复组比较。结果:1h、2h和(1+1)h低氧暴露恢复组大鼠的Hb、RBC、Hct水平均显著高于常氧恢复组(P<0.05,P<0.01),肾脏EPO水平显著高于常氧恢复组(P<0.05),而血清IL-3水平虽有增高趋势,但无显著意义(P>0.05)。三种低氧暴露方式大鼠各指标之间未见显著性差异(P>0.05)。结论:低氧暴露能加速红细胞的生成,有助于运动性血红蛋白低下的恢复,其作用机理可能与低氧暴露提高机体某些红细胞造血生长因子水平有关。     

低氧训练对AMPKα2三种基因状态鼠骨骼肌HIF-1α mRNA表达的影响

目的:探讨低氧耐力训练对AMPKα2基因敲除(KO)、高表达转基因(OE)及野生型(WT)小鼠骨骼肌HIF-1α mRNA表达的影响。方法:WT、KO及OE鼠各30只,分别随机分为常氧对照组、低氧暴露组和低氧训练组。常氧对照组在常氧状态下饲养14天;低氧暴露组在低氧环境(模拟海拔4000米高度,氧浓度约12.3%)下饲养14天;低氧训练组在与低氧暴露组相同的低氧环境下饲养并连续14天进行跑台训练(12 m/min,1 h/day)。14天后断食12 h取材,测定小鼠骨骼肌AMPKα2蛋白和HIF-1α mRNA表达。结果:(1)OE和WT鼠低氧暴露组、低氧训练组骨骼肌AMPKα2蛋白表达与常氧对照组相比均无显著性差异,KO鼠骨骼肌无AMPKα2蛋白表达。(2)OE鼠、KO鼠和WT鼠低氧训练组骨骼肌HIF-1α mRNA表达量与低氧暴露组相比显著增加。(3)低氧训练下,OE鼠骨骼肌HIF-1α mRNA表达量与WT鼠相比有显著性差异。结论:低氧训练中AMPKα2对骨骼肌HIF-1α mRNA表达起重要作用,但并非HIF-1α表达的必要条件。     

人红细胞抗氧化蛋白和抗氧化酶在间歇性低氧暴露后的变化

目的 :观察人体血液中红细胞抗氧化蛋白 (HRPRP)、SOD酶、GSH -PX酶在间歇性低氧暴露后的变化 ,观察抗氧化系统在间歇性低氧暴露后的反应是否有利于运动能力的提高。方法 :男性大学生 1 5名随机分成对照组和实验组 ,两组从事相同身体活动 ,实验组每天安静状态下间歇吸低氧 (浓度 1 4 %～ 1 0 %) 5 0～ 6 0分钟 ,连续 4周。两组均在实验开始前、结束后按Bruce方案进行力竭运动 ,并在安静和运动后取血测试HRPRP、SOD、GSH -PX、MDA。结果 :间歇性低氧暴露后 ,HRPRP含量和红细胞抗氧化酶SOD、GSH -PX活性在安静时和力竭运动后明显提高 ,运动时间延长 ,最大吸氧量增加。结论 :间歇性低氧暴露有助于增强红细胞抗氧化能力 ,改善和提高运动能力。     

间断减压缺氧适应对脑血流的影响

16名身体健康男性青年为受试对象.用脑血流图(REG)评价间断缺氧适应后再暴露5000m急性缺氧时的脑血流(CBF)改变.结果表明,适应组急性高山反应的发生率低,发病程度较轻.分析REG的主峰波幅,流入容积速度、重搏波深度、上升角和顶峰角等参数显示,急性缺氧时适应组CBF减少,对照组CBF增加.高山反应轻度者CBF减少;中度者CBF改变不明显;重度者CBF增多.这提示:(1)急性高山病的发生可能与CBF的改变有关.(2)间断减压缺氧适应可以改善脑循环和减轻高山反应症状.     

Regulation of cerebral blood flow during exercise

Constant cerebral blood flow (CBF) is vital to human survival. Originally thought to receive steady blood flow, the brain has shown to experience increases in blood flow during exercise. Although increases have not consistently been documented, the overwhelming evidence supporting an increase may be a result of an increase in brain metabolism. While an increase in metabolism may be the underlying causative factor for the increase in CBF during exercise, there are many modulating variables. Arterial blood gas tensions, most specifically the partial pressure of carbon dioxide, strongly regulate CBF by affecting cerebral vessel diameter through changes in pH, while carbon dioxide reactivity increases from rest to exercise. Muscle mechanoreceptors may contribute to the initial increase in CBF at the onset of exercise, after which exercise-induced hyperventilation tends to decrease flow by pial vessel vasoconstriction. Although elite athletes may benefit from hyperoxia during intense exercise, cerebral tissue is well protected during exercise, and cerebral oxygenation does not appear to pose a limiting factor to exercise performance. The role of arterial blood pressure is important to the increase in CBF during exercise; however, during times of acute hypotension such as during diastole at high-intensity exercise or post-exercise hypotension, cerebral autoregulation may be impaired. The impairment of an increase in cardiac output during exercise with a large muscle mass similarly impairs the increase in CBF velocity, suggesting that cardiac output may play a key role in the CBF response to exercise. Glucose uptake and CBF do not appear to be related; however, there is growing evidence to suggest that lactate is used as a substrate when glucose levels are low. Traditionally thought to have no influence, neural innervation appears to be a protective mechanism to large increases in cardiac output. Changes in middle cerebral arterial velocity are independent of changes in muscle sympathetic nerve activity, suggesting that sympathetic activity does not alter medium-sized arteries (middle cerebral artery).CBF does not remain steady, as seen by apparent increases during exercise, which is accomplished by a multi-factorial system, operating in a way that does not pose any clear danger to cerebral tissue during exercise under normal circumstances.     

高原头痛头昏与脑血流改变的关系

在西藏山南（3600m)观察了高原头痛、头昏的发生情况和与脑血流的关系。结果表明，快速进驻高原和久居高原人头痛、头昏的人数均达一半以上，快速进驻高原头痛、头昏者的脑血流图（REG）主峰波幅、流入容积速度和上升角明显高于无症状者，久居高原头痛、头昏者的REG主峰波幅明显高于无症状者，流入容积速度和上升角明显小于无症状者，提示高原急、慢性缺氧头痛、头昏的原因不同，急性缺氧头痛，头昏同脑血流过度增加有关；慢性缺氧头痛、头昏主要同脑血管的顺应性降低、脑血流减少有关。     

Effects of intermittent hypoxia on heart rate variability during rest and exercise

Changes in heart rate variability induced by an intermittent exposure to hypoxia were evaluated in athletes unacclimatized to altitude. Twenty national elite athletes trained for 13 days at 1200 m and either lived and slept at 1200 m (live low, train low, LLTL) or between 2500 and 3000 m (live high, train low, LHTL). Subjects were investigated at 1200 m prior to and at the end of the 13-day training camp. Exposure to acute hypoxia (11.5% O(2)) during exercise resulted in a significant decrease in spectral components of heart rate variability in comparison with exercise in normoxia: total power (p < 0.001), low-frequency component. LF (p < 0.001), high-frequency component, HF (p < 0.05). Following acclimatization, the LHTL group increased its LF component (p < 0.01) and LF/HF ratio during exercise in hypoxia after the training period. In parallel, exposure to intermittent hypoxia caused an increased ventilatory response to hypoxia. Acclimatization modified the correlation between the ventilatory response to hypoxia at rest and the difference in total power between normoxia and hypoxia (r (2) = 0.65, p < 0.001). The increase in total power, LF component, and LF/HF ratio suggests that intermittent hypoxic training increased the response of the autonomic nervous system mainly through increased sympathetic activity.     

Physiological effects of intermittent hypoxia

Intermittent hypoxia (IH), or periodic exposure to hypoxia interrupted by return to normoxia or less hypoxic conditions, occurs in many circumstances. In high altitude mountaineering, IH is used to optimize acclimatization although laboratory studies have not generally revealed physiologically significant benefits. IH enhances athletic performance at sea level if blood oxygen capacity increases and the usual level of training is not decreased significantly. IH for high altitude workers who commute from low altitude homes is of considerable practical interest and the ideal commuting schedule for physical and mental performance is being studied. The effect of oxygen enrichment at altitude (i.e., intermittent normoxia on a background of chronic hypoxia) on human performance is under study also. Physiological mechanisms of IH, and specifically the differences between effects of IH and acute or chronic continuous hypoxia remains to be determined. Biomedical researchers are defining the molecular and cellular mechanisms for effects of hypoxia on the body in health and disease. A comparative approach may provide additional insight about the biological significance of these effects.     

Autonomic control of cerebral circulation: exercise

On the basis of measurement techniques that require steady-state hemodynamic conditions when the measurement of cerebral blood flow (CBF) is being obtained, cerebral autoregulation (CA) maintains CBF stable over a wide range of cerebral perfusion pressures. When an acute (or dynamic) change in cerebral perfusion pressure (seconds) is imposed, CBF is not maintained. For example, after thigh cuff occlusion, its release induces an acute drop in arterial blood pressure (ABP). The sharp decrease in CBF indicates that CA was unable to respond to the dynamic (or rapid) changes in cerebral perfusion pressure. Therefore, control mechanisms of arterial pressure with short time constants must contribute importantly to CBF regulation. In order for CA to be effective, the cerebral perfusion pressure must lie within an autoregulatory range of perfusion pressures. The traditional thinking is that changes in sympathetic tone have a limited effect on CBF at rest. However, moderate- to heavy-intensity exercise causes only moderate increases in CBF despite large increases in sympathetic activity and ABP. Animal studies demonstrate that increases in sympathetic nerve activity cause cerebral vasoconstriction and protection against disruption of the blood-brain barrier. These findings suggest that the regulation of CBF during exercise is modulated not only by CA but also by autonomic nervous system and the arterial baroreflex-mediated control of the systemic circulation.     

体位改变和昼夜节律对大脑血流速度的影响

为研究头低位倾斜（ＨＤＴ）、直立位和昼夜节律对大脑血流速度的影响，采用经颅多普勒（ＴＣＤ）新技术在上述三种情况下对１２名青年健康男性的脑血流速度进行了观察。结果显示：－６°头低位倾斜１ｈ后大脑中动脉血流速度增加；直立位１５ｍｉｎ后大脑中动脉血流速度降低；在昼夜２４ｈ中，夜间睡眠时大脑中动脉血流速度较白天低；ＴＣＤ技术重复性好，可适用于航天医学研究     

Redistribution of pulmonary blood flow during hypoxic exercise.

Pulmonary blood flow (PBF) distribution was studied at rest and during exercise in rats acclimatized to chronic hypoxia (barometric pressure [PB] 370 Torr for 3 weeks, A rats) and non-acclimatized (NA) littermates. Both A and NA rats exercised in hypoxia (inspired O2 pressure [PIO2] approximately 70 Torr) or in normoxia (PlO2 approximately 145 Torr). PBF distribution was determined using fluorescent-labeled microspheres injected into the right atrium. The lungs were cut into 28 samples to determine relative scatter of specific PBF ([sample fluorescence intensity/sample dry weight)/(total lung fluorescence intensity/total lung dry weight]). Exercise produced redistribution of PBF both in NA and A rats, and this effect was larger in hypoxia than in normoxia, with minimal redistribution occurring during normoxic exercise in NA rats. The pattern of distribution varies considerably among individual animals. As a result of distribution, the previous high flow areas would be overperfused during hypoxic exercise in some rats. The results support the concept that hypoxic pulmonary vasoconstriction is not uniform and suggest that the combination of hypoxia and exercise may lead to overperfusion and capillary leak in some individuals.     

Cerebral artery blood velocity in normal subjects during acute decreases in barometric pressure.

To investigate the effect of acute changes in barometric pressure on regional cerebral perfusion we studied the middle cerebral artery (MCA) blood velocity in five healthy male volunteers by means of a low-pressure chamber. The MCA blood velocity, arterial blood and respiratory gases were measured at the barometric pressures of 1, 0.8, 0.65, and 0.5 atmospheres. The observed blood velocity (Vo) showed no systematic changes. Decreases in barometric pressure induced hypoxia and hypocapnia. When normalizing the MCA blood velocity (Vn) to a standard P(CO2) (5.3 kPa), thereby correcting for the hypoxic induced hypocapnia, we obtained an inverse relationship between cerebral artery blood velocity and arterial blood oxygen content (CaO2). The oxygen supply to the brain, estimated as the product of Vo and CaO2, decreased with lowering of the barometric pressure. However, the product of Vn and CaO2 remained constant. This suggests the existence of a regulatory mechanism attempting to maintain a constant oxygen supply to the brain during acute changes in CaO2, if the hyperventilation induced decrease in PCO2 can be omitted. In the artificial situation of a low pressure chamber, our findings are quite similar to those obtained at sea level. This indicates that the underlying mechanisms of control of cerebral blood flow do not change during acute exposure to altitude.     

Oxygen administration, cerebral blood flow velocity, and dynamic cerebral autoregulation

INTRODUCTION: Hyperoxia is reported to decrease steady-state cerebral blood flow (CBF). In addition, dynamic cerebral autoregulation would be altered. Hyperoxia may improve dynamic cerebral autoregulation, contrary to hypoxia. However, no previous studies have examined changes in steady-state CBF velocity (CBFV) and alterations of dynamic cerebral autoregulation during acute exposure to hyperoxia. We, therefore, evaluated dynamic cerebral autoregulation simultaneously with steady-state CBFV during stepwise hyperoxia under oxygen administration. METHODS: There were eight healthy volunteers who were examined under normoxic (21% O2) and hyperoxic conditions in stepwise fashion to 40%, 70%, and 100% O2. Mean blood pressure (MBP) in the radial artery was measured via tonometry, and CBFV in the middle cerebral artery was measured by transcranial Doppler ultrasonography. Dynamic cerebral autoregulation was assessed by spectral and transfer function analysis of beat-to-beat changes in MBP and CBFV. RESULTS: End-tidal CO2 decreased significantly at 70% and 100% O2. Steady-state CBFV decreased significantly at F1O2 > or = 40%, while MBP was unchanged. Associated with these changes, cerebral vascular resistance index increased at 70% and 100% O2. Transfer function gain and coherence remained unchanged at all levels of F1O2. DISCUSSION: These results suggest that hyperoxemia and hypocapnia reduce steady-state CBFV and increase cerebral vascular resistance during oxygen administration. This reduction in steady-state CBFV occurs even during mild hyperoxia < or = 40% O2 and becomes obvious at 70% O2 with hypocapnia. However, dynamic cerebral autoregulation may remain unchanged during hyperoxia, even with apparent changes in steady-state CBFV.