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.     

Regional pulmonary perfusion in patients with acute pulmonary edema.

Redistribution of pulmonary blood flow (PBF) away from edematous regions of the lung is characteristic of experimental acute lung injury (ALI), helping to preserve ventilation-perfusion matching and gas exchange. The purpose of this study was to determine if such perfusion redistribution occurs in acute pulmonary edema in humans. METHODS: We measured the regional distribution of lung water concentration (LWC) and PBF with PET in 9 patients with ALI, 7 patients with non-ALI pulmonary edema, and 7 healthy subjects. RESULTS: The average patient chest radiographic score was 7.5 +/- 2.2 (scale: 0-12, where > or =4 met our criterion for pulmonary edema). The mean partial pressure of oxygen, arterial/fraction of inspired oxygen ratio (PaO(2)/FIO(2)) was 192 +/- 78. LWC was 35 +/- 4 mL H(2)O/100 mL lung versus 20 +/- 5 mL H(2)O/100 mL lung in the healthy subjects (P < 0.05). On average, the ventral-to-dorsal regional distribution of PBF was similar in patients with pulmonary edema and healthy subjects, regardless of the etiology of the pulmonary edema. However, LWC and an index of perfusion redistribution away from edematous lung regions, when combined, were a significant determinant of the PaO(2)/FIO(2) (coefficient of determination [R2] = 0.53; P = 0.03). CONCLUSION: These results suggest that hypoxic vasoconstriction is severely blunted in ALI. The perfusion redistribution that does exist contributes slightly to improved oxygenation during early pulmonary edema in humans.     

Oxygen consumption, lactate accumulation, and sympathetic response during prolonged exercise under hypoxia

Six men (33 +/- 3 years old) performed 1 h ergocycle exercise (60% VO2 max) at sea level and at a simulated altitude of 3000 m. A similar relative exercise intensity corresponded to a lower absolute work load (139 +/- 4 W) in hypoxic than normoxic (163 +/- 4 W) conditions. Lower oxygen uptake (VO2) with no change in ventilation (VE), respiratory exchange ratio (R), and heart rate (Hr) were observed during exercise under hypoxia compared to normoxia. A slow rise in VO2, after the initial 5 min exercise, was observed in normoxic (+ 230 ml/min) as well as in hypoxic (250 ml/min) conditions that might be, in part, related to oxidative removal of blood lactate. Peak blood lactate concentration reached at 30 min of exercise was similar in normoxia (4.5 +/- 0.4) and in hypoxia (4.7 +/- 0.5). However, while the lactate level decreased during exercise at sea level, it remained elevated throughout exercise in altitude. Blood lactate concentration measured at the end of exercise was significantly (P less than 0.05) higher in hypoxic (4.4 +/- 0.3) than in normoxic (3.2 +/- 0.4) conditions. Catecholamine response to exercise was similar in both conditions. We conclude that during prolonged exercise at a given relative work load, hypoxia does not affect cardiorespiratory and sympathetic responses but tends to increase blood lactate accumulation. Higher blood lactate concentrations during hypoxic exercise seems to reflect alterations in the removal of blood lactate rather than changes in glycolytic flux.     

Training in hypoxia: modulation of metabolic and cardiovascular risk factors in men

PURPOSE: This study was designed to determine changes in metabolic and cardiovascular risk factors following normobaric hypoxic exercise training in healthy men. METHODS: Following a randomized baseline maximal exercise test in hypoxia and/or normoxia, 34 physically active subjects were randomly assigned to either a normoxic (N = 14) or a hypoxic (N = 18) training group. Training involved 4 wk of cycling exercise inspiring either a normobaric normoxic (F(IO2) = approximately 20.9%) or a normobaric hypoxic (F(IO2) = approximately 16.0%) gas, respectively, in a double-blind manner. Cycling exercise was performed three times per week for 20-30 min at 70-85% of maximum heart rate determined either in normoxia or hypoxia. Resting plasma concentrations of blood lipids, lipoproteins, total homocysteine, and auscultatory arterial blood pressure responses at rest and in response to submaximal and maximal exercise were measured before and 4 d after physical training. RESULTS: Total power output during the training period was identical in both normoxic and hypoxic groups. Lean body mass increased by 1.4 +/- 1.5 kg following hypoxic training only (P < 0.001). While dietary composition and nutrient intake did not change during the study, both normoxic and hypoxic training decreased resting plasma concentrations of nonesterified fatty acids, total cholesterol, high density lipoprotein (HDL), and low density lipoprotein (LDL) (P < 0.05 - < 0.001). Apolipoproteins AI and B decreased following normoxic training only (P < or = 0.001). Plasma concentrations of resting total homocysteine decreased by 11% following hypoxic training (P < or = 0.05) and increased by 10% (P < 0.05) following normoxic training. These changes were independent of changes in serum vitamin B12 and red cell folate which remained stable throughout. A decreased lactate concentration during submaximal exercise was observed in response to both normoxic and hypoxic training. Hypoxic training decreased maximal systolic blood pressure by 10 +/- 9 mm Hg (P < 0.001) and the rate pressure product by 14 +/- 23 mm Hg x beats x min(-1)/100 (P < or = 0.001) and increased maximal oxygen uptake by 0.47 +/- 0.77 L x min(-1) (P < 0.05). CONCLUSION: Normoxic and hypoxic training was associated with significant improvements in selected risk factors and exercise capacity. The stimulus of intermittent normobaric hypoxia invoked an additive cardioprotective effect which may have important clinical implications.     

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.     

低氧性肺动脉高压大鼠肺组织中介素的分布

目的观察低氧性肺动脉高压大鼠血浆中介素含量及肺组织中介素的分布。方法成年雄性Wistar大鼠被随机分为对照组,低氧1w组、2w组、3w组。对照组置于舱外常氧环境中饲养;其他3组动物置于低压舱内,模拟海拔5000m高度缺氧,每天连续7h。各组大鼠颈总动脉取血,应用放射免疫法检测血浆中介素含量,用免疫组织化学法检测中介素在肺内的分布。结果对照组,低氧1w组、2w组、3w组血浆中介素含量依次为（138．6±5．3）、（154．6±20．2）、（158．8±21．3）、（166．3±12．2）pg／ml,低氧各组大鼠血浆中介素含量增高。低氧3w时升高最明显,明显高于对照组（P〈0．05）。中介素在大鼠肺组织多种细胞中广泛分布。结论中介素在肺动脉高压的病理生理过程中发挥显著作用。     

缺氧复合氰化钠中毒对大鼠BALF和肺组织磷脂含量的影响

目的研究缺氧合并氰化钠(NaCN)中毒对大鼠肺支气管灌洗液(BALF)和肺组织中磷脂含量的影响。方法雄性SD大鼠72只,随机分为平原实验组和高原实验组。高原实验组动物置于低压舱(4000m,61kPa,舱内温度20±3℃)内,平原实验组置于普通试验室(海拔308m,大气压97.7kPa,室温20±3℃)内3d后进行实验。每组设0、0.5、1、2、4、6h等6个观测点,0h时点大鼠不注射NaCN,其余大鼠腹腔注射NaCN(3.6mg/kg),于注射后0、0.5、1、2、4h和6h时点放血处死动物,取全肺,分别检测肺/体比值,肺干/湿重比,制取BALF及肺组织匀浆,定磷法测总磷脂(TPL)含量。结果高原实验组部分大鼠鼻腔有少量泡沫状血性分泌物流出,注射后1h内3只动物中毒死亡。平原实验组大鼠NaCN中毒后,肺/体比值、肺干/湿重比、BALF中TPL含量显著增加(P<0.05),而肺组织中TPL含量明显降低(P<0.05)。高原实验组大鼠NaCN中毒后,肺/体比值、肺干/湿重比、BALF中TPL含量增加更显著(P<0.05),肺组织中TPL含量降低更明显(P<0.05)。结论缺氧和氰化物中毒可能对肺组织存在联合损伤效应。     

Individual variation in the reduction of heart rate and performance at lactate thresholds in acute normobaric hypoxia

Heart rate monitoring and lactate measurements are used to control exercise intensity during training at moderate altitude although there is some uncertainty about hypoxia-induced changes in these parameters at equivalent submaximal exercise intensities compared to normoxia. To study the influence of acute normobaric hypoxia (FiO2 0.15) on heart rate and performance at the individual anaerobic lactate threshold (IAT), at the 4 mmol x l(-1) threshold (AT) and at an intensity requiring 80 % of VO2max measured in the respective environment, 20 endurance-trained male athletes performed an incremental treadmill test in normoxia and normobaric hypoxia. During exercise in normobaric hypoxia, heart rate and velocity were significantly (p < 0.001) reduced with a wide individual variation at the IAT (range: - 1 to - 17 min(-1), - 0.3 to - 3.5 km x h(-1)), at the AT (- 2 to - 13 min(-1), - 0.2 to - 3.3 km x h(-1)) as well as at an intensity requiring 80 % of VO2max (0 to - 18 min(-1), - 1.1 to - 3.7 km x h(-1)). Relative VO2 at the lactate thresholds expressed as a percentage of VO2max was not significantly different compared to normoxia (86 +/- 6 % vs. 84 +/- 5 %, IAT; 90 +/- 5 % vs. 88 +/- 6 %, AT), but also showed a considerable individual variation. In conclusion, heart rate and performance have to be reduced individually to a varying extent during exercise in a hypoxic environment in order to achieve an equivalent intensity compared to exercise in normoxia.     

Exercise with the intensity of the individual anaerobic threshold in acute hypoxia

PURPOSE: The aim of the present study was to find out if the determination of the individual anaerobic threshold (IAT) during incremental treadmill tests in normoxia and acute normobaric hypoxia (FiO2 0.15) defines equivalent relative submaximal intensities in these environmental conditions. METHODS: 11 male middle and long distance runners performed a 1-h treadmill run in normoxia and hypoxia at the intensity of the IAT determined in the respective environment with measurement of lactate, glucose, heart rate, catecholamines, ventilatory parameters, and rate of perceived exertion (RPE). RESULTS: During the 1-h treadmill runs, speed was significantly reduced in hypoxia compared with normoxia (12.8 +/- 0.7 vs 14.7 +/- 0.7 km x h(-1)). Relative intensity expressed as a percentage of VO(2max) was similar in both environments (82-83% on the average) and elicited comparable lactate steady states [LaSS, 2.5 +/- 0.7 - 3.4 +/- 1.1 mmol x L(-1) (normoxia), 2.7 +/- 0.8 - 3.6 +/- 1.0 mmol x L(-1) (hypoxia) after 10 and 60 min, respectively] and glucose levels, but significantly reduced heart rate in hypoxia by 5 beats x min(-1) on the average. A steady state was also found for the ventilatory parameters. Plasma epinephrine and norepinephrine levels were similar in both environments. RPE was significantly lower after 40-60 min of exercise in hypoxia. CONCLUSIONS: Relative intensities in normoxia and acute hypoxia are equivalent when endurance exercise is performed with the running speed at the IAT determined in the respective environment. The heart rate-blood lactate relationship, however, is changed in hypoxia and relative submaximal exercise intensity is higher in acute hypoxia when training is performed with similar heart rate as in normoxia.     

Fluid-regulatory hormone responses during cycling exercise in acute hypobaric hypoxia

PURPOSE: This study was designed to describe the responses of fluid-regulating hormones during exercise in acute hypobaric hypoxia and to test the hypothesis that they would be dependent on the relative intensity of exercise rather than the absolute workload. METHODS: Thirteen men cycled for 60 min on four occasions in the same individual hydration status: in normoxia at 55% and 75% of normoxia maximal aerobic power (N55 and N75, respectively), in hypoxia (PB = 594 hPa) at the same absolute workload and at the same relative intensity as N55 (H75 and H55, respectively). VO2, heart rate, and rectal and mean skin temperatures were recorded during exercise. The total water loss was measured by the difference in nude body mass adjusted for metabolic losses. Venous blood samples were drawn before and 15, 30, 45, and 60 min after the beginning of exercise to measure variations in plasma volume, osmolality, and concentrations in arginine vasopressin (AVP), atrial natriuretic factor (ANF), plasma renin activity (ARP), aldosterone (Aldo), and noradrenaline (NA). RESULTS: During N55 and H55, AVP, Aldo and ARP did not change, whereas ANF increased slightly. Increases in AVP, Aldo, ARP, and NA were greater during N75 than during H75, whereas the increase in ANF was greater during H75 than N75. CONCLUSION: Plasma levels of AVP, Aldo, and ARP increase during exercise when a threshold is reached and thereafter are dependent on the absolute workload, without any specific effect of hypoxia. The time course of ANF appears to be different from that of the other hormones.     

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.     

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.     

Atrial natriuretic factor during hypoxia and mild exercise

The effect of hypoxia on plasma atrial natriuretic factor (ANF), plasma renin activity (PRA), and plasma aldosterone concentration (PAC) was evaluated during 2 h of treadmill exercise at 2 km/h, 0 grade at sea level. Six male subjects exercised on 2 separate days during normoxia (21% O2) and hypoxia (13.3 +/- 0.3% O2). No significant changes in ANF or PRA occurred during either normoxic or hypoxic exercise. However, PAC fell significantly during normoxic exercise (17.5 +/- 3.6 vs. 12.7 +/- 2.6 ng/dl, p less than 0.05) but not during hypoxic exercise. Serum potassium concentration fell during hypoxic exercise (5.0 +/- 0.1 vs. 4.4 +/- 0.1 mmol/l, p less than 0.05) along with bicarbonate (27.8 +/- 0.7 vs. 25.8 +/- 0.6 mmol/l, p less than 0.01). Between normoxic and hypoxic studies there was a significantly higher heart rate during hypoxic exercise (78 +/- 5 vs. 90 +/- 6 b/min, p less than 0.01). The major conclusion of this study is that hypoxia resulting in arterial oxygen saturations of 81 +/- 0.7% does not affect plasma atrial natriuretic factor levels during mild exercise in normal male subjects.     

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.     

缺氧对肺腺癌细胞生长特性及血管形成的影响

目的探讨缺氧对肺腺癌肿瘤生长及血管形成的影响。方法人肺腺癌细胞株A549暴露于常氧(空气，5%CO2)、缺氧(1％O2，5％CO2，94%N2)、无氧(95％N2，5%CO2)环境48h后，将细胞接种于裸鼠皮下，观察其生长情况。通过免疫组化染色计数微血管密度，测定移植瘤组织中血管内皮细胞生长因子(VEGF)及碱性成纤维细胞生长因子(bFGF)的表达水平。结果移植10天后，缺氧组肿瘤体积显著大于常氧组。移植25天后缺氧组肿瘤体积、重量、微血管密度以及瘤组织中VEGF、bFGF水平均显著高于常氧组，而无氧组显著低于常氧组。结论适度缺氧可以刺激肺癌细胞VEGF、bFGF等生长因子的表达，促进移植瘤血管形成，提高肿瘤的生长能力；而严重缺氧损伤癌细胞，影响生长因子合成表达，阻碍血管形成，抑制肿瘤的生长。     

高原肺水肿大鼠模型的建立与研究

 目的 模拟高原环境,研究大鼠急性低氧复合运动高原肺水肿的发生及低氧习服后的改变.方法 健康SD-大鼠分为常氧对照组(n=10)、5 000 m急性低氧组(n=10)及3 000 m低氧习服组(n=10).对比研究大鼠的肺血流动力学、肺水肿程度及肺组织病理形态学改变.结果 与常氧对照组相比,急性低氧组大鼠动脉血氧分压及氧饱合度显著降低,肺体指数及肺含水率升高,病理学显示肺间质充血,肺泡隔增宽等间质性肺水肿表现.低氧习服组明显改善.结论 成功建立高原间质性肺水肿模型及低氧习服模型,有利于进一步研究高原肺水肿低氧习服机制.     

Effects of maximal and submaximal exercise under normoxic and hypoxic conditions on serum erythropoietin level.

This study was carried out to investigate the influence of different exercise regimens on serum immunoreactive erythropoietin concentration (EPO). The same untrained male subjects performed bouts of maximal and submaximal exercise (60 min at 60% of maximal performance) under normoxia (n = 10) and normobaric hypoxia (PIO2 92 mmHg, n = 9). Five of them were exposed to hypoxia for 90 min under resting conditions (RTH). [EPO] was unchanged up to five hours after maximal (MEN) and submaximal (SEN) exercise under normoxia. After RTH, [EPO] increased after 3 hours by 5.0 mU/ml (p less than 0.01). Submaximal exercise under hypoxia (SEH) led to a similar increase in [EPO] (after 3 hours: + 5.5 mU/ml), which remained elevated the following days (after 24 h: + 6.1 mU/ml, 48 h: + 5.3 mU/ml; ANOVA p less than 0.001). Maximal exercise under hypoxia (MEH) had no significant effect. The results indicate that exercise has no immediate effect on serum [EPO], whereas the higher EPO level one and two days after SEH could result from the occurring hemodilution as is indicated by a slight negative correlation between [EPO] and Hct (r = 0.59, p less than 0.001). The number of reticulocytes increased after all hypoxic experiments and after MEN without any correlation to [EPO].     

Oxygen uptake response during maximal cycling in hyperoxia, normoxia and hypoxia

BACKGROUND: Oxygen uptake (VO2) on-kinetics is decelerated in acute hypoxia and accelerated in hyperoxia in comparison with normoxia during submaximal exercise. However, the effects of fraction of oxygen in inspired air (FIO2) on VO2 kinetics during maximal exercise are unknown. HYPOTHESIS: The effects of FIO2 on VO2 on-kinetics during maximal exercise are similar to submaximal exercise. METHODS: There were 11 endurance athletes who were studied during maximal 7-min cycle ergometer exercise in hyperoxia (FIO2 0.325), hypoxia (FIO2 0.166) and normoxia (FIO2 0.209). The individual VO2 data were fit to a curve by using a three exponential model. RESULTS: In hypoxia, VO2 on-response amplitude during Phase 2 (approximately 20-100 s from the beginning of exercise) was lower (p < 0.05) when compared with hyperoxia; time constant of VO2 Phase 3 (beyond approximately 100 s after beginning of exercise) was shorter (p < 0.05) when compared with hyperoxia; and mean response time (MRT, O-63%) for VO2peak was shorter (p < 0.05) when compared with normoxia and hyperoxia. VO2peak was higher in hyperoxia (4.80 +/- 0.48 L x min(-1), p < 0.05) and lower in hypoxia (4.03 +/- 0.46 L x min(-1), p < 0.05) than in normoxia (4.36 +/- 0.44 L x min(-1)). CONCLUSIONS: Moderate hypoxia or hyperoxia do not affect VO2 time constants at the onset of maximal exercise. However, MRT for VO2peak is shortened in hypoxia. It is suggested that the differences in VO2peak and power output during the latter half of the test and the point that FIO2 was modified only moderately might explain most of the discrepancy with the previous studies.     

Cardiorespiratory dynamics to hypoxia at the onset of cycling exercise in male endurance subjects

AIM: It is well established that altering O2 delivering to contracting skeletal muscle affects human performance. In this respect, a reduced O2 supply (e.g., hypoxia) increases the rate of muscle fatigue. This study aimed to determine the effects of moderate hypoxia and exercise intensity on oxygen uptake (VO2) and cardiac output (CO) kinetics during moderate [below the ventilatory threshold (VT)] and heavy (above VT) constant work rate cycling exercises. METHODS: Eight trained males (age, mean+/-SD, 22+/-3 years; height 182+/-5 cm; body mass 71+/-12 kg) performed at the same relative intensity in normoxic (FIO2=0.21) and hypoxic (FIO2=0.13) conditions moderate and heavy exercises during which pulmonary gas exchange was determined breath-by-breath and CO was monitored beat-by-beat with Doppler echocardiography. RESULTS: The rate of increase (t63%, corresponding to time constant and time delay of a monoexponential response) in CO was significantly faster than that of VO2 in 3 out of 4 experimental conditions (p<0.05). Moreover VO2 kinetics were significantly slowed by hypoxia and speeded by exercise intensity, while CO responses were unaffected by such conditions. A slowed CO response was apparent in hypoxia compared to normoxia (p>0.05) in heavy exercise. CONCLUSIONS: These results suggest an absence of coupling between CO and VO2 kinetics, and that cardiorespiratory O2 delivery is likely different at exercise onset as a function of exercise intensity and FIO2.     

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.