Age and sex differences in microvascular responses during reactive hyperaemia.

Microvascular impairments are typical of several cardiovascular diseases. Near-infrared spectroscopy (NIRS) combined with a vascular occlusion test provides non-invasive insights into microvascular responses by monitoring skeletal muscle oxygenation changes during reactive hyperaemia. Despite increasing interest in the effects of sex and ageing on microvascular responses, evidence remains inconsistent. Therefore, the present study aimed to investigate the effects of sex and age on microvascular responsiveness. Twenty-seven participants (seven young men and seven young women; seven older men and six older women; aged 26 ± 1, 26 ± 4, 67 ± 3 and 69 ± 4 years, respectively) completed a vascular occlusion test consisting of 5 min of arterial occlusion followed by 5 min reperfusion. Oxygenation changes in the vastus lateralis were monitored by near-infrared spectroscopy. The findings revealed that both women (referring to young and older women) and older participants (referring to both men and women) exhibited lower microvascular responsiveness. Notably, both women and older participants demonstrated reduced desaturation (-38% and -59%, respectively) and reperfusion rates (-24% and -40%, respectively) along with a narrower range of tissue oxygenation (-39% and -39%, respectively) and higher minimal tissue oxygenation levels (+34% and +21%, respectively). Women additionally displayed higher values in resting (+12%) and time-to-peak (+15%) tissue oxygenation levels. In conclusion, this study confirmed decreased microvascular responses in women and older individuals. These results emphasize the importance of considering sex and age when studying microvascular responses. Further research is needed to uncover the underlying mechanisms and clinical relevance of these findings, enabling the development of tailored strategies for preserving vascular health in diverse populations.

Fitness Level- and Sex-Related Differences in Pulmonary Limitations to Maximal Exercise in Normoxia and Hypoxia.

PURPOSE: Both maximal-intensity exercise and altitude exposure challenge the pulmonary system that may reach its maximal capacities. Expiratory flow limitation (EFL) and exercise-induced hypoxemia (EIH) are common in endurance-trained athletes. Furthermore, due to their smaller airways and lung size, women, independently of their fitness level, may be more prone to pulmonary limitations during maximal-intensity exercise; particularly when performed in hypoxic conditions. The objective of this study was to investigate the impact of sex and fitness level on pulmonary limitations during maximal exercise in normoxia and their consequences in acute hypoxia. METHODS: Fifty-one participants were distributed across four different groups according to sex and fitness level. Participants visited the laboratory on three occasions to perform maximal incremental cycling tests in normoxia and hypoxia (inspired oxygen fraction = 0.14) and two hypoxic chemosensitivity tests. Pulmonary function and ventilatory capacities were evaluated at each visit. RESULTS: EIH was more prevalent (62.5% vs. 22.2%, p = 0.004) and EFL less common (37.5% vs. 70.4%, p = 0.019) in women than men. EIH prevalence was different (p = 0.004) between groups of trained men (41.7%), control men (6.7%), trained women (50.0%), and control women (75.0%). All EIH men but only 40% of EIH women exhibited EFL. EFL individuals had higher slope ratio (p = 0.029), higher ventilation (V̇E) (p < 0.001), larger ΔVO2max (p = 0.019) and lower hypoxia-related V̇E increase (p < 0.001). CONCLUSIONS: Women reported a higher EIH prevalence than men, regardless of their fitness level, despite a lower EFL prevalence. EFL seems mainly due to the imbalance between ventilatory demands and capacities. It restricts ventilation, leading to a larger performance impairment during maximal exercise in hypoxic conditions.

Women at Altitude: Sex-Related Physiological Responses to Exercise in Hypoxia.

Sex differences in physiological responses to various stressors, including exercise, have been well documented. However, the specific impact of these differences on exposure to hypoxia, both at rest and during exercise, has remained underexplored. Many studies on the physiological responses to hypoxia have either excluded women or included only a limited number without analyzing sex-related differences. To address this gap, this comprehensive review conducted an extensive literature search to examine changes in physiological functions related to oxygen transport and consumption in hypoxic conditions. The review encompasses various aspects, including ventilatory responses, cardiovascular adjustments, hematological alterations, muscle metabolism shifts, and autonomic function modifications. Furthermore, it delves into the influence of sex hormones, which evolve throughout life, encompassing considerations related to the menstrual cycle and menopause. Among these physiological functions, the ventilatory response to exercise emerges as one of the most sex-sensitive factors that may modify reactions to hypoxia. While no significant sex-based differences were observed in cardiac hemodynamic changes during hypoxia, there is evidence of greater vascular reactivity in women, particularly at rest or when combined with exercise. Consequently, a diffusive mechanism appears to be implicated in sex-related variations in responses to hypoxia. Despite well-established sex disparities in hematological parameters, both acute and chronic hematological responses to hypoxia do not seem to differ significantly between sexes. However, it is important to note that these responses are sensitive to fluctuations in sex hormones, and further investigation is needed to elucidate the impact of the menstrual cycle and menopause on physiological responses to hypoxia.

Recommendations for Women in Mountain Sports and Hypoxia Training/Conditioning.

The (patho-)physiological responses to hypoxia are highly heterogeneous between individuals. In this review, we focused on the roles of sex differences, which emerge as important factors in the regulation of the body's reaction to hypoxia. Several aspects should be considered for future research on hypoxia-related sex differences, particularly altitude training and clinical applications of hypoxia, as these will affect the selection of the optimal dose regarding safety and efficiency. There are several implications, but there are no practical recommendations if/how women should behave differently from men to optimise the benefits or minimise the risks of these hypoxia-related practices. Here, we evaluate the scarce scientific evidence of distinct (patho)physiological responses and adaptations to high altitude/hypoxia, biomechanical/anatomical differences in uphill/downhill locomotion, which is highly relevant for exercising in mountainous environments, and potentially differential effects of altitude training in women. Based on these factors, we derive sex-specific recommendations for mountain sports and intermittent hypoxia conditioning: (1) Although higher vulnerabilities of women to acute mountain sickness have not been unambiguously shown, sex-dependent physiological reactions to hypoxia may contribute to an increased acute mountain sickness vulnerability in some women. Adequate acclimatisation, slow ascent speed and/or preventive medication (e.g. acetazolamide) are solutions. (2) Targeted training of the respiratory musculature could be a valuable preparation for altitude training in women. (3) Sex hormones influence hypoxia responses and hormonal-cycle and/or menstrual-cycle phases therefore may be factors in acclimatisation to altitude and efficiency of altitude training. As many of the recommendations or observations of the present work remain partly speculative, we join previous calls for further quality research on female athletes in sports to be extended to the field of altitude and hypoxia.

Mechanisms underlying the health benefits of intermittent hypoxia conditioning.

Intermittent hypoxia (IH) is commonly associated with pathological conditions, particularly obstructive sleep apnoea. However, IH is also increasingly used to enhance health and performance and is emerging as a potent non-pharmacological intervention against numerous diseases. Whether IH is detrimental or beneficial for health is largely determined by the intensity, duration, number and frequency of the hypoxic exposures and by the specific responses they engender. Adaptive responses to hypoxia protect from future hypoxic or ischaemic insults, improve cellular resilience and functions, and boost mental and physical performance. The cellular and systemic mechanisms producing these benefits are highly complex, and the failure of different components can shift long-term adaptation to maladaptation and the development of pathologies. Rather than discussing in detail the well-characterized individual responses and adaptations to IH, we here aim to summarize and integrate hypoxia-activated mechanisms into a holistic picture of the body's adaptive responses to hypoxia and specifically IH, and demonstrate how these mechanisms might be mobilized for their health benefits while minimizing the risks of hypoxia exposure.

Hypoxia and the Aging Cardiovascular System.

Older individuals represent a growing population, in industrialized countries, particularly those with cardiovascular diseases, which remain the leading cause of death in western societies. Aging constitutes one of the largest risks for cardiovascular diseases. On the other hand, oxygen consumption is the foundation of cardiorespiratory fitness, which in turn is linearly related to mortality, quality of life and numerous morbidities. Therefore, hypoxia is a stressor that induces beneficial or harmful adaptations, depending on the dose. While severe hypoxia can exert detrimental effects, such as high-altitude illnesses, moderate and controlled oxygen exposure can potentially be used therapeutically. It can improve numerous pathological conditions, including vascular abnormalities, and potentially slows down the progression of various age-related disorders. Hypoxia can exert beneficial effects on inflammation, oxidative stress, mitochondrial functions, and cell survival, which are all increased with age and have been discussed as main promotors of aging. This narrative review discusses specificities of the aging cardiovascular system in hypoxia. It draws upon an extensive literature search on the effects of hypoxia/altitude interventions (acute, prolonged, or intermittent exposure) on the cardiovascular system in older individuals (over 50 years old). Special attention is directed toward the use of hypoxia exposure to improve cardiovascular health in older individuals.

Sex-related differences in endothelial function and blood viscosity in the elderly population.

Elderly represents a growing population and cardiovascular diseases (CVD) is one of the leading causes of mortality in this population. Sex differences are involved in CVD with middle-aged males being at higher risk than females. After menopause, females are no longer protected by hormones and the role of sex on cardiovascular parameters involved in CVD, such as endothelial function and blood viscosity, is still unclear. The purpose of this study was to investigate the effect of sex on endothelial function, blood viscosity and CVD in elderly. Clinical investigation and blood analyses were performed on 182 (93 females and 89 males) elderly participants (mean age: 75.83 ± 1.22). Health status of participants were classified. Sex differences in endothelial function, blood viscosity, high density lipoprotein (HDL), hematocrit, and red blood cell (RBC) aggregation were assessed. CVD prevalence was higher in males (27.0%) than in females (5.4%) (p < 0.001). Females had higher vasoreactivity (p = 0.014) and HDL (p < 0.001) level than males. Blood viscosity was higher in males than in females at any shear rate (p < 0.001). Hematocrit was greater in males than in females (p < 0.001) while RBC aggregation did not differ between the two populations. To conclude, females have less CVD than age-matched males that might be due to their greater vascular function and lower blood viscosity.

Hypoxia Does Not Change Performance and Psychophysiological Responses During Repeated Cycling Sprints to Exhaustion With Short Exercise-to-Rest Ratio.

PURPOSE: To compare the acute performance and psychophysiological responses of repeated cycling sprints to exhaustion with a short exercise-to-rest ratio (1:6), between different effort durations and inspired oxygen fractions. METHODS: On separate visits, 10 active participants completed 6 repeated cycling sprint exercises to exhaustion with 3 different effort durations (5, 10, and 20 s) and 2 conditions of inspired oxygen (20.9% and 13.6%). Exercise-to-rest ratio was 1:6 for all trials (ie, 5:30, 10:60, and 20:120). Vastus lateralis muscle oxygenation (near-infrared spectroscopy), blood lactate concentration, and lower-limb and breathing discomfort, using ratings of perceived exertion, were measured. RESULTS: Number of sprints and peak power output decreased while blood lactate increased (all P < .001) during 5:30 compared with 10:60 or 20:120. No condition or interaction effects were reported for blood lactate and exercise-related sensation. Muscle deoxyhemoglobin increased (P < .001) and total hemoglobin decreased (P = .002) during sprint with increasing sprint duration (no condition or interaction). CONCLUSION: During repeated-sprint exercise to exhaustion with a short exercise-to-rest ratio, the psychophysiological responses did not differ between normoxia and moderate hypoxia, probably due to an extended recovery period. It means that hypoxia did not modify repeated-sprint exercise performance with a short exercise-to-rest ratio. The sprint duration was the primary underlying factor of the observed differences in performance and muscle oxygenation reported between the repeated-sprint exercise sessions.

The Oxidative-Glycolytic Balance Influenced by Sprint Duration Is Key during Repeated Sprint in Hypoxia.

PURPOSE: This study investigates the effects of normobaric hypoxia on repeated sprint exercise (RSE) with different balance between oxidative (phosphocreatine and oxidative pathway) and glycolytic contributions. Therefore, performance and psychophysiological responses were compared during RSE to exhaustion with the same exercise-to-rest ratio (1:2) but different sprint durations (5, 10, or 20 s) either in normoxic (RSN) or hypoxic (RSH; F io2 = 0.13) conditions. METHODS: On separate visits, 10 active participants completed in random order three cycling RSN (5:10; 10:20 and 20:40) and three similar RSH sessions to exhaustion. Vastus lateralis muscle oxygenation was recorded by near-infrared spectroscopy. Blood lactate concentration, limb and breathing discomfort, and ratings of perceived exertion were measured. RESULTS: Total sprint number was smaller in hypoxia than in normoxia for 5:10 (20.8 ± 8.6 vs 14.7 ± 3.4; P = 0.014) and 10:20 (13.7 ± 6.3 vs 8.8 ± 2.5; P = 0.018) but not 20:40 (5.6 ± 1.9 vs 5.6 ± 2.5). The fatigue index was larger in hypoxia only for 5:10 (-43.5%, P < 0.001). Irrespective of condition, blood lactate concentration increased with the sprint duration with higher values for 20:40 than 5:10 (13.1 ± 2.7 vs 11.5 ± 2.2 mmoL·L -1 ; P = 0.027). Limb and breathing discomfort and ratings of perceived exertion did not differ in all RSE. Muscle oxygenation was mainly impacted by sprint duration (i.e., main effect of sprint duration on [HHb] min, [tHb] max, Δ[HHb], and Δ[tHb]) but not by hypoxia. The normoxia-to-hypoxia percentage decrease for total sprint number for 5:10 was correlated with the highest power output over 5 s ( R2 = 0.55; P = 0.013) and 10 s ( R2 = 0.53; P = 0.016). CONCLUSIONS: Hypoxia impairs repeated sprint ability when the oxidative but not the glycolytic contribution is substantial. The oxidative-glycolytic balance, influenced partly by sprint duration, is key during repeated sprint in hypoxia.

Hypoxia and hemorheological properties in older individuals.

Hypoxia is caused by insufficient oxygen availability for the organism leading to reduced oxygen delivery to tissues and cells. It has been regarded as a severe threat to human health and it is indeed implicated in pathophysiological mechanisms involved in the development and progression of many diseases. Nevertheless, the potential of controlled hypoxia interventions (i.e. hypoxia conditioning) for improving cardio-vascular health is gaining increased attention. However, blood rheology is often a forgotten factor for vascular health while aging and hypoxia exposure are both suspected to alter hemorheological properties. These changes in blood rheology may influence the benefits-risks balance of hypoxia exposure in older individuals. The benefits of hypoxia exposure for vascular health are mainly reported for healthy populations and the combined impact of aging and hypoxia on blood rheology could therefore be deleterious in older individuals. This review discusses evidence of hypoxia-related and aging-related changes in blood viscosity and its determinants. It draws upon an extensive literature search on the effects of hypoxia/altitude and aging on blood rheology. Aging increases blood viscosity mainly through a rise in plasma viscosity, red blood cell (RBC) aggregation and a decrease in RBC deformability. Hypoxia also causes an increase in RBC aggregation and plasma viscosity. In addition, hypoxia exposure may increase hematocrit and modulate RBC deformability, depending on the hypoxic dose, i.e, beneficial effect of intermittent hypoxia with moderate dose vs deleterious effect of chronic continuous or intermittent hypoxia or if the hypoxic dose is too high. Special attention is directed toward the risks vs. benefits of hemorheological changes during hypoxia exposure in older individuals, and its clinical relevance for vascular disorders.

Implication of Blood Rheology and Pulmonary Hemodynamics on Exercise-Induced Hypoxemia at Sea Level and Altitude in Athletes.

This study aimed to investigate the changes in blood viscosity, pulmonary hemodynamics, nitric oxide (NO) production, and maximal oxygen uptake (V˙O2max) during a maximal incremental test conducted in normoxia and during exposure to moderate altitude (2,400 m) in athletes exhibiting exercise-induced hypoxemia at sea level (EIH). Nine endurance athletes with EIH and eight without EIH (NEIH) performed a maximal incremental test under three conditions: sea level, 1 day after arrival in hypoxia, and 5 days after arrival in hypoxia (H5) at 2,400 m. Gas exchange and oxygen peripheral saturation (SpO2) were continuously monitored. Cardiac output, pulmonary arterial pressure, and total pulmonary vascular resistance were assessed by echocardiography. Venous blood was sampled before and 3 min after exercise cessation to analyze blood viscosity and NO end-products. At sea level, athletes with EIH exhibited an increase in blood viscosity and NO levels during exercise while NEIH athletes showed no change. Pulmonary hemodynamics and aerobic performance were not different between the two groups. No between-group differences in blood viscosity, pulmonary hemodynamics, and V˙O2max were found at 1 day after arrival in hypoxia. At H5, lower total pulmonary vascular resistance and greater NO concentration were reported in response to exercise in EIH compared with NEIH athletes. EIH athletes had greater cardiac output and lower SpO2 at maximal exercise in H5, but no between-group differences occurred regarding blood viscosity and V˙O2max. The pulmonary vascular response observed at H5 in EIH athletes may be involved in the greater cardiac output of EIH group and counterbalanced the drop in SpO2 in order to achieve similar V˙O2max than NEIH athletes.

Exercise-Induced Hypoxemia in Endurance Athletes: Consequences for Altitude Exposure.

Exercise-induced hypoxemia (EIH) is well-described in endurance-trained athletes during both maximal and submaximal exercise intensities. Despite the drop in oxygen (O2) saturation and provided that training volumes are similar, athletes who experience EIH nevertheless produce the same endurance performance in normoxia as athletes without EIH. This lack of a difference prompted trainers to consider that the phenomenon was not relevant to performance but also suggested that a specific adaptation to exercise is present in EIH athletes. Even though the causes of EIH have been extensively studied, its consequences have not been fully characterized. With the development of endurance outdoor activities and altitude/hypoxia training, athletes often train and/or compete in this stressful environment with a decrease in the partial pressure of inspired O2 (due to the drop in barometric pressure). Thus, one can reasonably hypothesize that EIH athletes can specifically adapt to hypoxemic episodes during exercise at altitude. Although our knowledge of the interactions between EIH and acute exposure to hypoxia has improved over the last 10 years, many questions have yet to be addressed. Firstly, endurance performance during acute exposure to altitude appears to be more impaired in EIH vs. non-EIH athletes but the corresponding physiological mechanisms are not fully understood. Secondly, we lack information on the consequences of EIH during chronic exposure to altitude. Here, we (i) review research on the consequences of EIH under acute hypoxic conditions, (ii) highlight unresolved questions about EIH and chronic hypoxic exposure, and (iii) suggest perspectives for improving endurance training.

Pro-Oxidant/Antioxidant Balance during a Prolonged Exposure to Moderate Altitude in Athletes Exhibiting Exercise-Induced Hypoxemia at Sea-Level.

This study examined to what extent athletes exhibiting exercise-induced hypoxemia (EIH) possess an altered redox status at rest, in response to exercise at sea level (SL) and during moderate altitude exposure. EIH was defined as a fall in arterial O2 saturation of at least 4% during exercise. Nine endurance athletes with EIH and ten without (NEIH) performed a maximal incremental test under three conditions: SL, one (H1) and five (H2) days after arrival to 2400 m. Gas exchange and peripheral capillary oxygen saturation (SpO2) were continuously monitored. Blood was sampled before exercise and after exercise cessation. Advanced oxidation protein products (AOPP), catalase, ferric-reducing antioxidant power, glutathione peroxidase, superoxide dismutase (SOD) and nitric oxide metabolites (NOx) were measured in plasma by spectrophotometry. EIH athletes had higher AOPP and NOx concentrations at pre- and post-exercise stages compared to NEIH at SL, H2 but not at H1. Only the EIH group experienced increased SOD activity between pre- and post-exercise exercise at SL and H2 but not at H1. EIH athletes had exacerbated oxidative stress compared to the NEIH athletes at SL and H2. These differences were blunted at H1. Oxidative stress did not alter the EIH groups' aerobic performance and could lead to higher minute ventilation at H2. These results suggest that higher oxidative stress response EIH athletes could be involved in improved aerobic muscle functionality and a greater ventilatory acclimatization during prolonged hypoxia.

Role of Gender and Physical Activity Level on Cardiovascular Risk Factors and Biomarkers of Oxidative Stress in the Elderly.

BACKGROUND: Cardiovascular diseases remain as the leading cause of morbidity and mortality in industrialized countries. Ageing and gender strongly modulate the risk to develop cardiovascular diseases but very few studies have investigated the impact of gender on cardiovascular diseases in the elderly, which represents a growing population. The purpose of this study was to test the impact of gender and physical activity level on several biochemical and clinical markers of cardiovascular risk in elderly individuals. METHODS: Elderly individuals (318 women (75.8 ± 1.2 years-old) and 227 men (75.8 ± 1.1 years-old)) were recruited. Physical activity was measured by a questionnaire. Metabolic syndrome was defined using the National Cholesterol Education Program Expert Panel's definition. Polysomnography and digital tonometry were used to detect obstructive sleep apnea and assess vascular reactivity, respectively. Blood was sampled to measure several oxidative stress markers and adhesion molecules. RESULTS: The frequency of cardiovascular diseases was significantly higher in men (16.4%) than in women (6.1%) (p < 0.001). Body mass index (25.0 ± 4.3 vs. 25.8 ± 3.13 kg.m-2) and glycaemia (94.9 ± 16.5 vs. 101.5 ± 22.6 mg.dL-1) were lower, and High Density Lipoprotein (HDL) (74.6 ± 17.8 vs. 65.0 ± 17.2 mg.dL-1) was higher in women compared to men (p < 0.05). Oxidative stress was lower in women than in men (uric acid: 52.05 ± 13.78 vs. 59.84 ± 13.58, advanced oxidation protein products: 223 ± 94 vs. 246 ± 101 µmol.L-1, malondialdehyde: 22.44 ± 6.81 vs. 23.88 ± 9.74 nmol.L-1). Physical activity was not associated with lower cardiovascular risk factors in both genders. Multivariate analyses showed an independent effect of gender on acid uric (ß = 0.182; p = 0.020), advanced oxidation protein products (ß = 0.257; p < 0.001), and HDL concentration (ß = -0.182; p = 0.026). CONCLUSION: These findings suggest that biochemical cardiovascular risk factors are lower in women than men which could explain the lower cardiovascular disease proportion observed in women in the elderly.

Muscle and cerebral oxygenation during exercise in athletes with exercise-induced hypoxemia: A comparison between sea level and acute moderate hypoxia.

The objective of the present study was to evaluate the influence of exercise-induced hypoxemia (EIH) on muscle and cerebral oxygenation responses during maximal exercise in normoxia and in acute moderate hypoxia (fraction of inspired oxygen: 15.3%, 2400 m). EIH was defined as a drop in hemoglobin saturation of at least 4% for at least three consecutive minutes during maximal exercise at sea level. Twenty-five athletes performed incremental treadmill tests to assess maximal oxygen consumption (VO2max) in normoxia and in hypoxia. Oxygenation of the vastus lateralis muscle and the left prefrontal cortex of the brain was monitored using near-infrared spectroscopy. During the normoxic test, 15 athletes exhibited EIH; they displayed a larger change in muscle levels of oxyhemoglobin (ΔO2Hb) (p = 0.04) and a greater change in cerebral levels of deoxyhemoglobin (ΔHHb) (p = 0.02) than athletes without EIH (NEIH group). During the hypoxic test, muscle ΔO2Hb was lower in the EIH group than in the NEIH group (p = 0.03). At VO2max, hypoxia was associated with a smaller cerebral ΔO2Hb in both groups, and a greater cerebral ΔHHb compared to normoxia in the NEIH group only (p = 0.02). No intergroup differences in changes in muscle oxygenation were observed. The severity of O2 arterial desaturation was negatively correlated with changes in total muscle hemoglobin in normoxia (r = -0.48, p = 0.01), and positively correlated with the cerebral ΔHHb in normoxia (r = 0.45, p = 0.02). The occurrence of EIH at sea level was associated with specific muscle and cerebral oxygenation responses to exercise under both normoxia and moderate hypoxia.

Evolution of blood rheology and its relationship to pulmonary hemodynamic during the first days of exposure to moderate altitude.

Blood rheology and hemodynamic parameters have never been explored together during acclimatization to altitude. This study aimed to investigate changes in blood rheology parameters and pulmonary hemodynamics during the first days of real moderate altitude exposure.Seventeen athletes were tested at sea-level, 20 hours after their arrival at 2,400 meters of altitude (H1) and five days later (H2). Blood was sampled to analyze red blood cell (RBC) aggregation, blood viscosity and hematocrit. Pulmonary arterial pressure (PAP), pulmonary capillary pressure (Pcap) and pulmonary vascular resistance (PVR) were assessed by echocardiography.We observed a rise in hematocrit, blood viscosity, RBC aggregation, PAP, Pcap and PVR between sea-level and H1. In H2, RBC aggregation, hematocrit, PAP, Pcap and PVR remained different compared to sea-level and no difference was observed between H1 and H2. Blood viscosity decreased in H2 and returned to sea-level values.Our results suggest that hemoconcentration occurring within the first hours of altitude exposure increased blood viscosity, which contributed to the changes in pulmonary hemodynamic. When blood viscosity decreased in H2, no change occurred in pulmonary hemodynamic parameters suggesting that hypoxic pulmonary vasoconstriction was still present. The elevated RBC aggregation observed after in H2 could participate in the increase of Pcap.