Persistence of the lactate paradox over 8 weeks at 3,800 m

The arterial blood lactate [La] response to exercise increases in acute hypoxia, but returns to near the normoxic (sea level, SL) response after 2 to 5 weeks of altitude acclimatization. Recently, it has been suggested that this gradual return to the SL response in [La], known as the lactate paradox (LP), unexpectedly disappears after 8 to 9 weeks at altitude. We tested this idea by recording the [La] response to exercise every 2 weeks over 8 weeks at altitude. Five normal, fit SL-residents were studied at SL and 3,800 m (Pbar = 485 torr) in both normoxia (PIO2 = 150 torr) and hypoxia (PIO2 = 91 torr approximately air at 3,800 m). Arterial [La] and blood gas values were determined at rest and during cycle exercise at the same absolute workloads (0, 25, 50, 75, 90, and 100% of initial SL-VO2Max) and exercise duration (4, 4, 4, 2, 1.5, and 0.75 min, respectively) at each time point. [La] curves were elevated in acute hypoxia at SL (p < 0.01) and at 3,800 m fell progressively toward the SL-normoxic curve (p < 0.01). On the same days, [La] responses in acute normoxia showed essentially no changes over time and were similar to initial SL normoxic responses. We also measured arterial catecholamine levels at each load and found a close relationship to [La] over time, supporting a role for adrenergic influence on [La]. In summary, extending the time at this altitude to 8 weeks produced no evidence for reversal of the LP, consistent with prior data obtained over shorter periods of altitude residence.     

Investigation of the combined effects of bedrest and mild hypoxia

Subjects were exposed to an 8-h mild hypoxia exposure (8000 ft. equivalent, 2438 m) with and without a 28-h period of 6 degrees headdown bedrest. Anticipated responses to the bedrest and the hypoxia were observed. There was no indication that bedrest affected the arterial oxygenation or the oxygen gradient across the lungs of the subjects undergoing mild hypoxia. It is concluded that there is no evidence that would preclude an alveolar O2 pressure as low as 69 torr during contingency spacecraft operation.     

Effects of sildenafil on the human response to acute hypoxia and exercise

We examined the effects of the 5-phosphodiesterase (5-PDE) inhibitor sildenafil on pulmonary arterial pressure and some oxygen transport and cardiopulmonary parameters in humans during exposure to hypobaric hypoxia at rest and after exercise. In a double-blind study, 100 mg sildenafil or placebo was administered orally to 14 healthy volunteers 45 min before exposure to 5,000 m of simulated altitude. Arterial oxygen saturation (SaO2), heart rate (HR), tidal volume (VT), respiratory rate (RR), left ventricular ejection fraction (EF), and pulmonary arterial pressure (PAP) were measured first at rest in normoxia, at rest and immediately after exercise during hypoxia, and after exercise in normoxia. The increase in systolic PAP produced by hypoxia was significantly decreased by sildenafil at rest from 40.9 +/- 2.6 to 34.9 +/- 3.0 mmHg (-14.8%; p = 0.0046); after exercise, from 49.0 +/- 3.9 to 42.9 +/- 2.6 mmHg (-12.6%; p = 0.003). No significant changes were found in normoxia either at rest or after exercise. Measurements of the effect of sildenafil on exercise capacity during hypoxia did not provide conclusive data: a slight increase in SaO2 was observed with exercise during hypoxia, and sildenafil did not cause significant changes in ventilatory parameters under any condition. Sildenafil diminishes the pulmonary hypertension induced by acute exposure to hypobaric hypoxia at rest and after exercise. Further studies are needed to determine the benefit from this treatment and to further understand the effects of sildenafil on exercise capacity at altitude.     

Degree of arterial desaturation in normoxia influences VO2max decline in mild hypoxia.

PURPOSE: Elite endurance athletes display varying degrees of pulmonary gas exchange limitations during maximal normoxic exercise and many demonstrate reduced arterial O2 saturations (SaO2) at VO2max--a condition referred to as exercise induced arterial hypoxemia (EIH). We asked whether mild hypoxia would cause significant declines in SaO2 and VO2max in EIH athletes while non-EIH athletes would be unaffected. METHODS: Nineteen highly trained males were divided into EIH (N = 8) or Non-EIH (N = 6) groups based on SaO2 at VO2max (EIH <90%, Non-EIH >92%). Athletes with intermediate SaO2 values (N = 5) were only included in correlational analyses. Two randomized incremental treadmill tests to exhaustion were completed--one in normoxia, one in mild hypoxia (FIO2 = 0.187; approximately 1,000 m). RESULTS: EIH subjects demonstrated a significant decline in VO2max from normoxia to mild hypoxia (71.1+/-5.3 vs. 68.1+/-5.0 mL x kg(-1) min(-1), P<0.01), whereas the non-EIH group did not show a significant deltaVO2max (67.2+/-7.6 vs. 66.2+/-8.4 mL x kg(-1) x min(-1)). For all 19 athletes, SaO2 during maximal exercise in normoxia correlated with the change in VO2max from normoxia to mild hypoxia (r = -0.54, P<0.05). However, the change in SaO2 and arterial O2 content from normoxia to mild hypoxia was equal for both EIH and Non-EIH (deltaSaO2 = 5.2% for both groups), bringing into question the mechanism by which changes in SaO2 affect VO2max in mild hypoxia. CONCLUSIONS: We conclude that athletes who display reduced measures of SaO2 during maximal exercise in normoxia are more susceptible to declines in VO2max in mild hypoxia compared with normoxemic athletes.     

Time course of cardiovascular and hematological responses in rats exposed to chronic intermittent hypobaric hypoxia (4600 m)

The aim of this study was to evaluate the effects of two periods of intermittent exposure to hypoxia (428 torr) in rats over 12 months. The conditions of CIH4x4 (4 days in hypoxia, 4 days in normoxia, n = 50) and CIH2x2 (2 days in hypoxia, 2 days in normoxia, n = 50) were selected for simulating in this animal model the chronic-intermittent exposure to high altitudes experienced by Andean miners. We assessed mortality, weight, hematological parameters, and time course of resting heart rate and systolic blood pressure. In general, mortality increased during the first month, with a tendency to stabilize during exposure; it was associated with lower weights and with higher hematocrit levels, making these possible predictor factors. Intermittence produced an increase in hematocrit and hemoglobin concentrations as previously seen in most hypoxic models, compared with normoxia (NX, n = 30), but attained lower levels compared with chronic hypoxia (CH, n = 28). CIH4x4 and CIH2x2 had similar sustained elevations of systolic blood pressure (171 +/- 3 and 174 +/- 2 mmHg, respectively) versus the basal level (163 +/- 3; 163 +/- 3 mmHg), whereas CH did not. Heart rate suffered an equally sustained decrease in all exposed groups (343 +/- 14 beats/min). Exposure to chronic-intermittent hypoxia led to a mild polycythemia and to a decrease in heart rate. The effects of hypoxia were already evident during the first month of exposure and attained a more pronounced expression and stabilization during the third month.     

Acute moderate hypoxia affects the oxygen desaturation and the performance but not the oxygen uptake response

The purpose of this study was to examine the influence of hypoxia on the O2 uptake response, on the arterial and muscular desaturation and on the test duration and test duration at VO2max during exhaustive exercise performed in normoxia and hypoxia at the same relative workload. Nine well-trained males cyclists performed an incremental test and an exhaustive constant power test at 90 % of maximal aerobic power on a cycling ergometer, both in normoxia and hypoxia (inspired O2 fraction = 16 %). Hypoxic normobar conditions were obtained using an Alti Trainer200 and muscular desaturation was monitored by near-infrared spectroscopy instrument (Niro-300). The mean response time (66 +/- 4 s vs. 44 +/- 7 s) was significantly lower in hypoxia caused by the shorter time constant of the VO2 slow component. This result was due to the lower absolute work rate in hypoxia which decreased the amplitude of the VO2 slow component. The arterial (94.6 +/- 0.3 % vs. 84.2 +/- 0.7 %) and muscular desaturation (in the vastus lateralis and the lateral gastrocnemius) were reduced by hypoxia. The test duration (440 +/- 31 s vs. 362 +/- 36 s) and the test duration at VO2max (286 +/- 53 s vs. 89 +/- 33 s) were significantly shorter in hypoxia. Only in normoxia, the test duration was correlated with arterial and muscular saturation (r = 0.823 and r = 0.828; p < 0.05). At the same relative workload, hypoxia modified performance, arterial and muscular oxygen desaturation but not the oxygen uptake response. In normoxia, correlation showed that desaturation seems to be a limiting factor of performance.     

Effect of acute hypoxia on central fatigue during repeated isometric leg contractions

To determine whether hypoxia has a direct influence on the central command independently of the working muscles, 16 subjects performed intermittent isometric unilateral knee extensions until exhaustion either in normobaric hypoxia (inspired O₂ fraction=0.11, arterial oxygen saturation ∼84%) or in normoxia while the knee extensor muscles were exposed to circulatory occlusion with a 250 mmHg cuff. Among the subjects, 11 also performed the tests in hypoxia and normoxia without occlusion. Single electrical stimulations were regularly delivered to the femoral nerve to measure the changes in the knee extensor peak twitch force. With the cuff, the average slope of decrease in peak twitch did not depend on the inspired oxygen fraction. Performance was slightly but significantly lower during hypoxia than in normoxia (8.2±2.6 vs 9.4±3.1 repetitions, P <0.05) with the cuff on. The number of repetitions was much higher during hypoxia with maintaining leg blood flow (15.6±4.5 repetitions) than with circulatory occlusion in normoxia. In conclusion, this study showed that a direct effect of hypoxia in reducing the motor drive to the working muscles exists but this effect is moderate.     

In vivo 31P-MR spectroscopy of the liver in the infant rabbit to study the effect of hypoxia on the phosphorus metabolites and intracellular pH

In vivo 31P-magnetic resonance spectroscopy (MRS) with a chronically implanted detection coil was used to study the effect of hypoxia on the phosphorus metabolites and intracellular pH in the liver of infant rabbits. A two-turn 10-mm radiofrequency coil was placed between the hepatic lobes in each of four infant New Zealand white rabbits (10-16 days old). Two days later, the rabbits were anesthetized and mechanically ventilated with 1.5% isoflurane in 98.5% O2. Blood gases, heart rate, and mean arterial pressure were monitored. 31P-MR spectra were continuously obtained every 5 minutes during 15 minutes of hyperoxia (PaO2 greater than 250 torr), 15 minutes normoxia (PaO2 approximately equal to 100 torr), 60 minutes hypoxia (PaO2 = 24 torr +/- 4 S.D.), and 15 minutes recovery (hyperoxia). In addition, 31P-MR spectra of perchloric-acid extracts of the liver of an adult and of an infant rabbit, removed under normoxic conditions, were examined. The 31P-MR spectra of liver of the normoxic adult (in vitro) and infant rabbits (in vitro and in vivo) revealed a high level of phosphodiesters, namely glycerol-3-phosphorylethanolamine, glycerol-3-phosphorylcholine, and phosphoenolpyruvate, compared with that reported for adult rat and adult mouse liver. The inorganic phosphate (Pi)-to-adenosine triphosphate (ATP) ratio was about 0.90 during hyperoxia and during normoxia. Within 15 minutes after induction of hypoxia, the level of phosphorus metabolites changed markedly: The ATP decreased 41% +/- 18 S.D. (P less than .01) and the Pi increased 206% +/- 29 S.D. (P less than .01); the Pi/ATP ratio was 5.0.(ABSTRACT TRUNCATED AT 250 WORDS)     

Exercise during short‐term exposure to hypoxia or hyperoxia ‐ novel treatment strategies for type 2 diabetic patients?!

Both hypoxia (decreased oxygen availability) and hyperoxia (increased oxygen availability) have been shown to alter exercise adaptations in healthy subjects. This review aims to clarify the possible benefits of exercise during short‐term exposure to hypoxia or hyperoxia for patients with type 2 diabetes mellitus (T2DM ). There is evidence that exercise during short‐term exposure to hypoxia can acutely increase skeletal muscle glucose uptake more than exercise in normoxia, and that post‐exercise insulin sensitivity in T2DM patients is more increased when exercise is performed under hypoxic conditions. Furthermore, interventional studies show that glycemic control can be improved through regular physical exercise in short‐term hypoxia at a lower workload than in normoxia, and that exercise training in short‐term hypoxia can contribute to increased weight loss in overweight/obese (insulin‐resistant) subjects. While numerous studies involving healthy subjects report that regular exercise in hypoxia can increase vascular health (skeletal muscle capillarization and vascular dilator function) to a higher extent than exercise training in normoxia, there is no convincing evidence yet that hypoxia has such additive effects in T2DM patients in the long term. Some studies indicate that the use of hyperoxia during exercise can decrease lactate concentrations and subjective ratings of perceived exertion. Thus, there are interesting starting points for future studies to further evaluate possible beneficial effects of exercise in short‐term hypoxia or hyperoxia at different oxygen concentrations and exposure durations. In general, exposure to hypoxia/hyperoxia should be considered with caution. Possible health risks—especially for T2DM patients—are also analyzed in this review.     

Evidence of decrease in peak heart rate in acute hypoxia: effect of exercise-induced arterial hypoxemia

This study focuses on the influence of the arterial oxygen saturation level at exhaustion on peak heart rate under acute moderate hypoxia, in endurance-trained subjects. Nineteen competing male cyclists performed exhaustive ramp exercise (cycle ergometer) under normoxia and normobaric hypoxia (15 % O (2)). After the normoxic trial, the subjects were divided into those demonstrating exercise-induced arterial hypoxemia during exercise (> 5 % decrease in SaO (2) between rest and the end of exercise, n = 10) and those who did not (n = 9). O (2) uptake, heart rate and arterial O (2) saturation (ear-oximeter) levels were measured. Under hypoxia, peak heart rate decreased for both groups (p < 0.001) and to a greater extent for hypoxemic subjects (p < 0.01). Arterial O (2) saturation under hypoxia was lower for the hypoxemic than for the non-hypoxemic subjects (p < 0.001) and it was correlated to the fall in peak heart rate between normoxia and hypoxia for all subjects (p < 0.01; r = 0.65). Hypoxemic subjects presented greater decrease in maximal O (2) uptake than non-hypoxemic ones (19.6 vs. 15.6 %; p < 0.05). The results confirm the greater decrement in arterial O (2) saturation under hypoxia in hypoxemic subjects and demonstrates a more pronounced reduction in peak heart rate in those subjects compared with non-hypoxemic ones. These data confirm the possible influence of arterial oxygenation on the decrease in peak heart rate in acute hypoxia.     

Arterial haemoglobin oxygen saturation is affected by F1O2 at submaximal running velocities in elite athletes

This study was conducted to determine whether arterial desaturation would occur at submaximal workloads in highly trained endurance athletes and whether saturation is affected by the fraction of oxygen in inspired air (F(I)O2). Six highly trained endurance athletes (5 women and 1 man, aged 25+/-4 yr, VO2max 71.3+/-5.0 ml x kg(-1) x min(-1)) ran 4x4 min on a treadmill in normoxia (F(I)O2 0.209), hypoxia (F(I)O2 0.155) and hyperoxia (F(I)O2 0.293) in a randomized order. The running velocities corresponded to 50, 60, 70 and 80% of their normoxic maximal oxygen uptake (VO2max). In hypoxia, the arterial haemoglobin oxygen saturation percentage (SpO2%) was significantly lower than in hyperoxia and normoxia throughout the test, and the difference became more evident with increasing running intensity. In hyperoxia, the SpO2% was significantly higher than in normoxia at 70% running intensity as well as during recovery. The lowest values of SpO2% were 94.0+/-3.8% (P<0.05, compared with rest) in hyperoxia, 91.0+/-3.6% (P<0.001) in normoxia and 72.8+/-10.2% (P<0.001) in hypoxia. Although the SpO2% varied with the F(I)O2, the VO2 was very similar between the trials, but the blood lactate concentration was elevated in hypoxia and decreased in hyperoxia at the 70% and 80% workloads. In conclusion, elite endurance athletes may show an F(I)O2-dependent limitation for arterial O2 saturation even at submaximal running intensities. In hyperoxia and normoxia, the desaturation is partly transient, but in hypoxia the desaturation worsens parallel with the increase in exercise intensity.     

Heart rate variability in rats acclimatized to high altitude

The aims of this study were to relate heart morphology and functions changes to heart rate variability (HRV) components after acclimatization to high altitude and to define whether preadaptation to hypoxia could modulate HRV responses to acute hypoxic stress. Doppler-echocardiographic studies of the left ventricle were performed in female Wistar rats before, during, and after a 10-week exposure to moderate hypobaric hypoxia (CH rats, approximately 4000 m simulated) or normoxia (N rats, approximately 55 m). Right ventricular morphology and function and pulmonary artery pressure were evaluated using heart catheterization. Spectral analysis of HRV was studied after exposure in conscious unrestrained rats in normoxia and during acute hypoxic stress. Necropsy right ventricular hypertrophy and intraventricular and pulmonary artery hypertension were found in CH rats compared with N rats. Echocardiographic left ventricular morphology and functions were similar between the groups after exposures. Compared to the control group, CH rats had similar heart rates and HRV components when measured in normoxia. During acute hypoxic stress, HRV decreased in all rats, but less in CH rats. These results support the hypothesis that long-term mild hypoxia may moderate sympathetic activation induced by acute hypoxia and that right ventricular hypertrophy cannot be the direct cause of such a shift in sympathovagal nerve interaction during acute hypoxic stress.     

Short-term intermittent normobaric hypoxia-haematological, physiological and mental effects

Effects on erythropoiesis and blood pressure as well as physical performance and mental effects were studied in 15 healthy subjects during intermittent exposure to normobaric hypoxia corresponding to either 2000 m (6 persons) or 2700 m (9 persons) above sea level; another group (5 persons) also served as controls at normoxia. The concept "live hightrain low" was used for 10 d consecutively and the exposure to hypoxia was 12 h/d. Blood pO₂ and oxygen saturation were significantly decreased during the 10 d at hypoxia. [Hb] and Hct decreased significantly after 2 d in hypoxia and then returned to pre-study levels. Erythropoietin was significantly elevated in both hypoxia groups during the initial 3–5 d. Reticulocytes were significantly increased during 7 d of hypoxia. Submaximal and maximal oxygen uptake, blood pressure at rest and during exercise and the profile of mood states (POMS test) did not change during the study. In conclusion, intermittent normobaric hypoxia for 10 d resulted in a significant stimulation of erythropoiesis. Staying at normobaric hypoxia may serve as a complement to an ordinary altitude level sojourn.     

Effect of hypoxia on VO2 kinetics during pseudorandom binary sequence exercise

The dynamic response characteristics of the oxygen uptake (VO2) response were investigated during upright cycle ergometer exercise in six healthy male volunteers. The exercise test consisted of a pseudorandom binary sequence (PRBS) with 15 units per sequence, each unit 15 s long, for a total period of 225 s. Six identical sequences were completed in a single test session. Each subject exercised under both normoxic and hypoxic (FIO2 = 14%) conditions. VO2 was measured breath-by-breath. The data were analyzed in the frequency domain by Fourier analysis to yield amplitude and phase shift coefficients for the relationship between the input work rate and the output responses of VO2 and heart rate (HR). The amplitude of the VO2/work rate was significantly reduced by hypoxia compared to normoxia over a wide range of frequencies. The mean VO2 was not different between hypoxia and normoxia. The phase shift for the VO2/work rate response was significantly greater for hypoxia than normoxia. The amplitude of the HR/work rate relationship was not significantly altered by hypoxia; however, the mean HR was higher during hypoxia. The phase shift of the HR/work rate response was significantly different between hypoxia and normoxia only at certain frequencies. These data indicate that the effects of hypoxia on the cardiorespiratory response to exercise can be characterized by the use of PRBS exercise and Fourier analysis techniques. A significant reduction in the ability of the cardiorespiratory system to adapt to changes in work rate appears to be caused by a reduction in the arterial O2 content.     

Absolute and relative work capacity in women at 758, 586, and 523 torr barometric pressure

Six young women performed an incremental bicycle work test at sea level barometric pressure (PB = 758 torr) and during acute exposure (1 h) to simulated altitudes of PB 586 and 523 torr. Submaximal oxygen uptake (VO2) for a given workload was independent of altitude but maximal oxygen uptake (VO2 max) decreased 10 and 13%, respectively, at the higher altitudes. Although heart rate (fC) was consistently higher at altitude for a given VO2, the slope of fC vs, VO2 was independent of altitude and VO2 max. Exercise fC appeared to be a function of the relative workload i.e. VO2 as a percentage of VO2 max measured at each PB. Carbon dioxide (CO2) elimination increased with altitude for a given VO2 but also was a function of the relative workload. Pulmonary ventilation (BTPS), however, was consistently 10-15% higher at altitude when expressed as a percent of VO2 max, primarily due to an increase in respiratory rate. Compared to published studies on males, this increased ventilation may impart a slight advantage to women in maintaining arterial oxygenation, but ventilatory reserve may be decreased and limited at higher altitudes. At altitudes down to PB 523 torr, the control of fC responses and decrements in maximal oxygen uptake in women were similar to males, but ventilatory control mechanisms differed.     

The long-acting phosphodiesterase inhibitor tadalafil does not influence athletes' VO2max, aerobic, and anaerobic thresholds in normoxia

Whereas experimental studies showed that in healthy trained subjects, the phosphodiesterase-5 inhibitor (PDE-5i) sildenafil improves exercise capacity in hypoxia and not in normoxia, no studies on the effects of the long half-life PDE-5i tadalafil exist. In order to evaluate whether tadalafil influences functional parameters and performance during a maximal exercise test in normoxia, we studied 14 healthy male athletes in a double-blind cross-over protocol. Each athlete performed two tests on a cycle ergometer, both after placebo or tadalafil (at therapeutic dose: 20 mg) administration. Oxygen consumption (VO2), blood lactate, respiratory exchange ratio, rate of perceived exertion, arterial blood pressure (BP), heart frequency (HR) and oxygen pulse (VO2/HR) were evaluated before exercise, at individual ventilatory and anaerobic thresholds (IVT and IAT), at VO2max and during recovery. Compared to placebo, a single tadalafil administration significantly reduced systolic BP before and after exercise (p < 0.05), decreased VO2/HR at IVT (13.3 +/- 1.8 vs. 14.5 +/- 2.1 mL . beat (-1); p = 0.03), but did not modify individual VO2max, IVT, or IAT. In healthy athletes, 20 mg of tadalafil does not substantially influence physical fitness-related parameters, exercise tolerance, and cardiopulmonary responses to maximal exercise in normoxia; it remains to be verified if higher doses/prolonged use influence health and/or sport performance in field conditions.     

间歇性低氧暴露期间运动对体育系大学生脑血流速度的影响

目的:探讨不同低氧暴露期间运动对人体脑血流速度的影响.方法:以6名体育系男性大学生为实验对象,采用经颅多普勒技术测试了其在4周实验期内,常氧(21% O2)、急性低氧暴露(15.4%O2)和慢性间歇性低氧暴露(15.4%O2)运动时脑中动脉血流速度.结果:常氧环境中运动可以增加脑血流速度.急性和慢性间歇性低氧暴露时,运动虽然也能提高脑血流速度,但增加幅度明显小于常氧环境.急性和慢性间歇性低氧暴露时,运动会降低舒张期血流速度.随着低氧暴露刺激时间的延长,脑血流速度的变化特点与幅度逐渐与常氧时一致.低氧暴露对运动后脑血流的恢复速度影响不大.     

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.     

缺氧复合氰化钠中毒对家兔动脉血气成分的影响

目的探讨缺氧复合氰化钠(NaCN)中毒对家兔动脉血气成分的影响。方法以人工低压氧舱模拟4 000m高原缺氧环境。20只家兔随机均分为4组:高原高剂量组(2mg/kg),高原低剂量组(1.5mg/kg),平原高剂量组(2mg/kg),平原低剂量组(1.5mg/kg)。高原组动物在低压氧舱内预处理72h后进行实验。以戊巴比妥钠(30mg/kg)麻醉动物后进行股动脉插管,腹腔注射NaCN毒剂(2mg/kg或1.5mg/kg)。分别于NaCN中毒前10min(-10min),中毒后5、10、15、20、30、60、120和180min采血测定动脉血气变化。结果高原缺氧72h后动物的动脉血氧分压(PaO2)和二氧化碳分压(PaCO2)明显降低,与平原组中毒前比较差异有统计学意义(P<0.01),而pH值和碳酸氢根(HCO-3)浓度与平原组中毒前比较,差异无统计学意义(P>0.05)。各组NaCN中毒后动脉血pH值先升高后降低,PaO2显著升高,PaCO2和HCO-3浓度显著降低。结论NaCN中毒后酸碱平衡紊乱,早期表现为呼吸性碱中毒,后期表现为代谢性酸中毒。     

Exercise performance in hypoxia after novel erythropoiesis stimulating protein treatment

Maximal aerobic power at high altitude (<4000 m) does not increase with altitude acclimatization. In order to investigate the isolated effects of increased arterial oxygen content (CaO2) on maximal oxygen uptake (VO2max) in hypoxia, we studied 10 subjects during exercise in acute exposure to 12.6% O2 before and after novel erythropoiesis stimulating protein (NESP) induced increases in CaO2. Over a period of 1 month, weekly NESP treatment increased resting hemoglobin (Hb) from 13.8+/-0.9 to 16.2+/-0.5 g/dL, hematocrit from 42.1+/-0.6% to 49.0+/-1.5%, and CaO2 from 189.7+/-3.0 to 218.6+/-5.7 mL/L. At maximal exercise CaO2 was increased from 172.3+/-3.7 to 191.5+/-3.8 mL/L with NESP treatment, and although maximal heart rate was similar in both conditions (178.4+/-2.6 and 180.9+/-2.5 b.p.m.) VO2max remained unaltered, the values being 3.12+/-2.0 and 3.12+/-2.0, before and after NESP treatment, respectively. NESP-injections in human subjects causes Hb and accordingly CaO2 to increase both in normoxia and hypoxia. Despite increases in CaO2 at maximal exercise in hypoxia VO2max is not increased.