174 research outputs found

    Effects of the 8 psia / 32% O2 Atmosphere on the Human in the Spaceflight Environment

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    Extravehicular activity (EVA) is at the core of a manned space exploration program. There are elements of exploration that may be safely and effectively performed by robots, but there are critical elements of exploration that will require the trained, assertive, and reasoning mind of a human crewmember. To effectively use these skills, NASA needs a safe, effective, and efficient EVA component integrated into the human exploration program. The EVA preparation time should be minimized and the suit pressure should be low to accommodate EVA tasks without undue fatigue, physical discomfort, or suit-related trauma. Commissioned in 2005, the Exploration Atmospheres Working Group (EAWG) had the primary goal of recommending to NASA an internal environment that allowed efficient and repetitive EVAs for missions that were to be enabled by the former Constellation Program. At the conclusion of the EAWG meeting, the 8.0 psia and 32% oxygen (O2) environment were recommended for EVA intensive phases of missions. As a result of selecting this internal environment, NASA gains the capability for efficient EVA with low risk of decompression sickness (DCS), but not without incurring additional negative stimulus of hypobaric hypoxia to the already physiologically challenging spaceflight environment. This paper provides a literature review of the human health and performance risks associated with the 8 psia/32% O2 environment. Of most concern are the potential effects on the central nervous system including increased intracranial pressure, visual impairment, sensorimotor dysfunction, and oxidative damage. Other areas of focus include validation of the DCS mitigation strategy, incidence and treatment of acute mountain sickness (AMS), development of new exercise countermeasures protocols, effective food preparation at 8 psia, assurance of quality sleep, and prevention of suit-induced injury. As a first effort, the trade space originally considered in the EAWG was re-evaluated looking for ways to decrease the hypoxic dose by further enriching the O2% or increasing the pressure. After discussion with the NASA engineering and materials community, it was determined that the O2 could be enriched from 32% to 34% and the pressure increased from 8.0 to 8.2 psia without significant penalty. These two small changes increase alveolar O2 pressure by 11 mmHg, which is expected to significantly benefit crewmembers. The 8.2/34 environment (inspired O2 pressure = 128 mmHg) is also physiologically equivalent to the staged decompression atmosphere of 10.2 psia / 26.5% O2 (inspired O2 pressure = 127 mmHg) used on 34 different shuttle missions for approximately a week each flight. Once decided, the proposed internal environment, if different than current experience, should be evaluated through appropriately simulated research studies. In many cases, the human physiologic concerns can be investigated effectively through integrated multi-discipline ground-based studies. Although missions proposing to use an 8.2/34 environment are still years away, it is recommended that these studies begin early enough to ensure that the correct decisions pertaining to vehicle design, mission operational concepts, and human health countermeasures are appropriately informed

    Acute hypoxia reduces plasma myostatin independent of hypoxic dose

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    Background: Muscle atrophy is seen ~ 25 % of patients with cardiopulmonary disorders, such as chronic obstructive pulmonary disorder and chronic heart failure. Multiple hypotheses exist for this loss, including inactivity, inflammation, malnutrition and hypoxia. Healthy individuals exposed to chronic hypobaric hypoxia also show wasting, suggesting hypoxia alone is sufficient to induce atrophy. Myostatin regulates muscle mass and may underlie hypoxic-induced atrophy. Our previous work suggests a decrease in plasma myostatin and increase in muscle myostatin following 10 hours of exposure to 12 % O2. Aims: To establish the effect of hypoxic dose on plasma myostatin concentration. Concentration of plasma myostatin following two doses of normobaric hypoxia (10.7 % and 12.3 % O2) in a randomised, single-blinded crossover design (n = 8 lowlanders, n = 1 Sherpa), with plasma collected pre (0 hours), post (2 hours) and 2 hours following (4 hours) exposure. Results: An effect of time was noted, plasma myostatin decreased at 4 hours but not 2 hours relative to 0 hours (p = 0.01; 0 hours = 3.26 [0.408] ng.mL-1, 2 hours = 3.33, [0.426] ng.mL-1, 4 hours = 2.92, [0.342] ng.mL-1). No difference in plasma myostatin response was seen between hypoxic conditions (10.7 % vs. 12.3 % O2). Myostatin reduction in the Sherpa case study was similar to the lowlander cohort. Conclusions: Decreased myostatin peptide expression suggests hypoxia in isolation is sufficient to challenge muscle homeostasis, independent of confounding factors seen in chronic cardiopulmonary disorders, in a manner consistent with our previous work. Decreased myostatin peptide may represent flux towards peripheral muscle, or a reduction to protect muscle mass. Chronic adaption to hypoxia does not appear to protect against this response, however larger cohorts are needed to confirm this. Future work will examine tissue changes in parallel with systemic effects

    Similar Hemoglobin Mass Response in Hypobaric and Normobaric Hypoxia in Athletes

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    Purpose: To compare hemoglobin mass (Hbmass) changes during an 18-day live high-train low (LHTL) altitude training camp in normobaric hypoxia (NH) and hypobaric hypoxia (HH). Methods: Twenty-eight well-trained male triathletes were split into three groups (NH: n = 10, HH: n = 11, control (CON): n = 7) and participated in an 18-day LHTL camp. NH and HH slept at 2250 m while CON slept and all groups trained at altitudes 0.08) and remained unchanged in CON (+0.2%, P = 0.89). Conclusion: HH and NH evoked similar Hbmass increases for the same hypoxic dose and after 18-day LHTL. The wide variability in individual Hbmass responses in HH and NH emphasize the importance of individual Hbmass evaluation of altitude training.This study was financially supported by the Federal Office of Sport (FOSPO; Switzerland) and by the Ministère des Sports, de la Jeunesse, de l’Education Populaire et de la Vie Associative (MSJEPVA)/Institut National du Sport, de l’Expertise et de la Performance (INSEP, France)

    Altitude Exposure at 1800 m Increases Haemoglobin Mass in Distance Runners

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    The influence of low natural altitudes (\u3c 2000 m) on erythropoietic adaptation is currently unclear, with current recommendations indicating that such low altitudes may be insufficient to stimulate significant increases in haemoglobin mass (Hbmass). As such, the purpose of this study was to determine the influence of 3 weeks of live high, train high exposure (LHTH) at low natural altitude (i.e. 1800 m) on Hbmass, red blood cell count and iron profile. A total of 16 elite or well-trained runners were assigned into either a LHTH (n = 8) or CONTROL (n = 8) group. Venous blood samples were drawn prior to, at 2 weeks and at 3 weeks following exposure. Hbmass was measured in duplicate prior to exposure and at 2 weeks and at 3 weeks following exposure via carbon monoxide rebreathing. The percentage change in Hb mass from baseline was significantly greater in LHTH, when compared with the CONTROL group at 2 (3.1% vs 0.4%; p = 0.01;) and 3 weeks (3.0% vs -1.1%; p \u3c 0.02, respectively) following exposure. Haematocrit was greater in LHTH than CONTROL at 2 (p = 0.01) and 3 weeks (p = 0.04) following exposure. No significant interaction effect was observed for haemoglobin concentration (p = 0.06), serum ferritin (p = 0.43), transferrin (p = 0.52) or reticulocyte percentage (p = 0.16). The results of this study indicate that three week of natural classic (i.e. LHTH) low altitude exposure (1800 m) results in a significant increase in Hbmass of elite distance runners, which is likely due to the continuous exposure to hypoxia

    Approximate Simulation of Acute Hypobaric Hypoxia with Normobaric Hypoxia

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    INTRODUCTION. Some manufacturers of reduced oxygen (O2) breathing devices claim a comparable hypobaric hypoxia (HH) training experience by providing F(sub I) O2 < 0.209 at or near sea level pressure to match the ambient O2 partial pressure (iso-pO2) of the target altitude. METHODS. Literature from investigators and manufacturers indicate that these devices may not properly account for the 47 mmHg of water vapor partial pressure that reduces the inspired partial pressure of O2 (P(sub I) O2). Nor do they account for the complex reality of alveolar gas composition as defined by the Alveolar Gas Equation. In essence, by providing iso-pO2 conditions for normobaric hypoxia (NH) as for HH exposures the devices ignore P(sub A)O2 and P(sub A)CO2 as more direct agents to induce signs and symptoms of hypoxia during acute training exposures. RESULTS. There is not a sufficient integrated physiological understanding of the determinants of P(sub A)O2 and P(sub A)CO2 under acute NH and HH given the same hypoxic pO2 to claim a device that provides isohypoxia. Isohypoxia is defined as the same distribution of hypoxia signs and symptoms under any circumstances of equivalent hypoxic dose, and hypoxic pO2 is an incomplete hypoxic dose. Some devices that claim an equivalent HH experience under NH conditions significantly overestimate the HH condition, especially when simulating altitudes above 10,000 feet (3,048 m). CONCLUSIONS. At best, the claim should be that the devices provide an approximate HH experience since they only duplicate the ambient pO2 at sea level as at altitude (iso-pO2 machines). An approach to reduce the overestimation is to at least provide machines that create the same P(sub I)O2 (iso-P(sub I)O2 machines) conditions at sea level as at the target altitude, a simple software upgrade

    Prooxidant/Antioxidant Balance in Hypoxia: A Cross-Over Study on Normobaric vs. Hypobaric “Live High-Train Low”

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    “Live High-Train Low” (LHTL) training can alter oxidative status of athletes. This study compared prooxidant/antioxidant balance responses following two LHTL protocols of the same duration and at the same living altitude of 2250 m in either normobaric (NH) or hypobaric (HH) hypoxia. Twenty-four well-trained triathletes underwent the following two 18-day LHTL protocols in a cross-over and randomized manner: Living altitude (PIO2 = 111.9 ± 0.6 vs. 111.6 ± 0.6 mmHg in NH and HH, respectively); training “natural” altitude (~1000–1100 m) and training loads were precisely matched between both LHTL protocols. Plasma levels of oxidative stress [advanced oxidation protein products (AOPP) and nitrotyrosine] and antioxidant markers [ferric-reducing antioxidant power (FRAP), superoxide dismutase (SOD) and catalase], NO metabolism end-products (NOx) and uric acid (UA) were determined before (Pre) and after (Post) the LHTL. Cumulative hypoxic exposure was lower during the NH (229 ± 6 hrs.) compared to the HH (310 ± 4 hrs.; P<0.01) protocol. Following the LHTL, the concentration of AOPP decreased (-27%; P<0.01) and nitrotyrosine increased (+67%; P<0.05) in HH only. FRAP was decreased (-27%; P<0.05) after the NH while was SOD and UA were only increased following the HH (SOD: +54%; P<0.01 and UA: +15%; P<0.01). Catalase activity was increased in the NH only (+20%; P<0.05). These data suggest that 18-days of LHTL performed in either NH or HH differentially affect oxidative status of athletes. Higher oxidative stress levels following the HH LHTL might be explained by the higher overall hypoxic dose and different physiological responses between the NH and HH.The study was funded by grants from the Ministère des Sports, de la Jeunesse, de l’Education Populaire et de la Vie Associative (MSJEPVA; France; to L.S. and G.P.M.), Institut National du Sport, de l’Expertise et de la Performance (INSEP; France; to L.S. and G.P.M.) and Institut Universitaire de France (IUF; France; to V.P.)

    Hypoxic Exposure to Optimise Altitude Training Adaptations in Elite Endurance Athletes

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    The purpose of this thesis was to examine the physiological and haematological responses to altitude training and hypoxic exposures. Furthermore to investigate if additional hypoxic exposure around a “live high-train high” altitude training camp could maximise adaptations. Study one provided a detailed insight into the current practices and perceptions of elite British endurance athletes and coaches to altitude training. A survey found that the athletes and support staff’s concerns included maintaining training load at altitude, reducing the acclimatisation period, maximising haematological adaptations and when to compete on return to sea level. These challenges were prioritised and investigated further in the thesis. Confidence in the optimised carbon monoxide (CO) rebreathing method (oCOR-method) is paramount when assessing haematological adaptations. Study two found that Radiometer ABL80 hemoximeter provided a more valid and reliable determination of percent carboxyhaemoglobin (%HbCO) with a minimum of three replicate blood samples to obtain an error of ≤1%. Study three found that administering different boluses of CO produced significantly different haemoglobin mass (tHbmass) results (0.6 mL·kg−1 = 791 ± 149 g; 1.0 mL·kg−1 = 788 ± 149 g; and 1.4 mL·kg−1 = 776 ± 148 g). A bolus of 0.6 to 1.0 mL·kg−1 provided sufficient precision and safety to determine %HbCO with the ABL80 hemoximeter. Additional hypoxic exposures have been identified as a strategy to maintain altitude haematological adaptations gained from altitude training camps. Study four investigated the time course of erythropoietin (EPO) and inflammatory markers after acute (2 h passive rest) hypoxic exposures (FiO2: 0.135, 0.125, 0.115, and 0.209). [EPO] increased in all hypoxic conditions 2 h post-exposure, being maintained until 4 h post-exposure, however, the largest increase came from the FiO2: 0.115 condition increasing by ~50% (P &lt; 0.001). There were no differences found between hypoxic exposures in IL-6 or TNFα. Study five investigated the effect of acute hypoxia as a priming tool, by measuring the effect of increased circulating EPO on endurance performance. A 10 min pre-loaded treadmill running time trial (TT10) was preceded by 2 h normobaric hypoxia (HYPO; FiO2: 0.115), hyperoxia (HYPER; FiO2: 0.395) or normoxia (CON; FiO2: 0.209) 3.5 h prior to the TT10. No differences (P = 0.082) were found in distance covered during TT10 (HYPO: 2726 ± 277 vs. CON: 2724 ± 279 vs. HYPER: 2742 ± 281 m). Study six monitored physiological and haematological variables of elite endurance runners completing four weeks of live high-training high (LHTH; ~2,300 m) altitude training (ALT) compared to a control group (CON). A hypoxic sensitivity test (HST) was completed pre (PRE) and post-altitude (POST-2), alongside a treadmill test and oCOR-method. From PRE to POST-2 a difference in average lactate threshold (LT) (6.1 ± 4.6% vs. 1.8 ± 4.5%) and lactate turnpoint (LTP) (5.4 ± 3.8% vs. 1.1 ± 3.2%) was found within ALT, but not CON. Mean V̇O2max increased by 2.7 ± 3.5% in ALT, and decreased by 3.3 ± 6.3% in the CON group (P = 0.042). Total Hbmass increased by 1.9 ± 2.9% and 0.1 ± 3.3% (P &gt; 0.05) from PRE to POST-2 in the ALT and CON group, respectively. No changes were found in mean tHbmass post-LHTH; however, EPO was lower at POST-1. The HST revealed desaturation at rest and hypoxic ventilatory response at exercise predicted individual changes in tHbmass and hypoxic cardiac response at rest predicted changes in V̇O2max. The evidence reported supports the notion that additional hypoxic exposures around an altitude training camp can maximise physiological and haematological adaptation via a prior understanding of an athlete’s response to hypoxia and therefore the optimisation the athlete’s altitude training needs

    Altitude training and endurance and ultra-endurance performance

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    Background. Altitude training has been shown to improve endurance and ultra-en-durance performance at altitude, whereas the possible benefits from altitude/hypoxic training for competing at sea level have been, and still are, a matter for debate. Reasons for this discrepancy may result from the variety of protocols utilized in terms of alti-tude, natural or simulated, to which the athletes were exposed, and amount of the time spent at altitude. In order to conciliate previous findings and provide practical recommendations to athletes, the concept of optimal “hypoxic dose” has been defined. Methods. To perform a review of the literature concerning the effects of altitude training on athletic performance. Results. The dominant paradigm is that the improved performance at sea level is due primarily to an accelerated erythropoiesis due to the reduced oxygen available at alti-tude, leading to an increase in red cell mass. Indeed, in recent years it has become evident that other non-hematological factors (improved muscle efficiency, greater muscle buffering capacity, etc.), may contribute to improve athletic performance. Conclusions. Despite more than fifty years of research and studies, altitude training remains a controversial issue and yet, there are many unanswered questions
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