[Show abstract][Hide abstract] ABSTRACT: INTRODUCTION: The emergence of normobaric devices for hypoxia awareness training makes crucial the study of physiological and cognitive effects induced by acute normobaric hypoxia (NH) exposure. Our study aimed to 1) investigate the effects of acute NH exposure on physiological variables and working memory; and 2) investigate the physiological and cognitive effects of oxygen breathing before and after acute NH exposure.
METHODS: There were 86 healthy men who were randomized into 4 groups: the Normoxia-Air group (N = 23), whose subjects were breathing air; the Hypoxia-Air group (N = 22), where NH exposure was preceded and followed by air breathing; the Normoxia-O2 group (N = 21), whose protocol was similar to the Normoxia-Air group, except with the addition of 100% O2 breathing periods; and the Hypoxia-O2 group (N = 20), whose participants were exposed to 100% O2 before and after NH exposure. Working memory was assessed with the Paced Auditory Serial Addition Test. Peripheral oxygen saturation (Spo2), heart rate (HR), and electroencephalogram (EEG) were recorded.
RESULTS: Acute NH exposure induced a classical physiological response (i.e., decreased Spo2 and increased HR), but not identical to the well-described physiological response to acute hypobaric hypoxia. Acute NH also caused a strong impairment in working memory. Oxygen breathing following NH exposure induced a slowing in the EEG associated with a worsening of working memory performance.
DISCUSSION: Acute NH exposure revealed a good surrogate for the classical hypobaric chamber for refresher hypoxia awareness training. Because the association between hypoxia and hyperoxia seems deleterious for the brain, we suggest that NH exposure should be surrounded by air breathing.
[Show abstract][Hide abstract] ABSTRACT: During an acute hypoxia exposure, impairment of memory is one of the most frequently reported symptoms, either during hypoxia awareness training of aircrews or after an in-flight hypoxic incident. However, the effects of acute hypoxia on memory have been little studied in laboratory-controlled conditions. Moreover, none of these studies were performed in hypobaric conditions. The main aim of our study was to investigate the effects of acute hypobaric hypoxia on working memory (WM). This study also aimed to find links between physiological measurements and cognitive performance during acute hypoxia exposure.
During hypoxia awareness training, 28 subjects (experimental group) were exposed to a simulated altitude level of 10,000 m (31,000 ft) in a hypobaric chamber, while 29 subjects (control group) stayed at sea level. WM was assessed in both groups with the Paced Auditory Serial Addition Test (PASAT). Peripheral oxygen saturation (SpO2) and heart rate were recorded.
WM was strongly impaired in the hypoxic group. One major finding is that hypoxia highly increased the mean error frequency rate. WM performance decreased linearly with hypoxemia, but SpO2 was weakly predictive of PASAT performance and vice versa.
WM is impaired by acute hypobaric hypoxia. Given the importance of WM in aircraft piloting and its sensitivity to hypoxia, the PASAT, in association with SpO2 and EEG recordings, could improve both hypoxia training and our understanding of the effects of hypoxia on memory.
Full-text · Article · Aug 2013 · Aviation Space and Environmental Medicine
[Show abstract][Hide abstract] ABSTRACT: To what extent can a deficit in oxygen, i.e. hypoxia, affect cerebral functioning, and particularly memory? This is the question we attempted to answer in this article. We discussed the two main types of hypoxia, high-altitude-induced hypoxia on the one hand and disease-induced hypoxia on the other hand. A review of literature of the last 30 years allowed us to highlight the main memory systems impaired by these different types of hypoxia, namely working memory and episodic memory. We also distinguished two patterns of memory impairments. Indeed, memory disorders due to high-altitude chronic exposure and to chronic diseases seem to include mostly deficits in attention and learning and/or retrieval strategies, while it is episodic memory that is directly impaired in acute hypoxia, both in cases of abrupt high-altitude exposure and after carbon monoxide poisoning. Whereas oxygen-based treatments definitely improve the outcome of memory disorders in patients submitted to chronic hypoxia, their effectiveness seems limited after acute hypoxia, probably because of the development of irreversible cerebral lesions.
[Show abstract][Hide abstract] ABSTRACT: To study the effects of a 29-h total sleep deprivation (TSD) on local cold tolerance, 10 healthy men immersed their right hand for 30 min in a 5°C water bath (CWI) after a 30-min rest period in a thermoneutral environment (Control), after a normal night (NN) and after a 29-h TSD. CWI was followed by a 30-min passive rewarming (Recovery). Finger 2 and 4 skin temperatures (Tfi2, Tfi4) and finger 2 cutaneous vascular conductance (CVC) were monitored to study cold-induced vasodilation (CIVD). Rectal temperature (Tre), mean skin temperature ([Formula: see text]), heart rate (HR) and blood pressure (BP) were also measured. Blood samples were collected at the end of the Control, at the lower and at the first maximal Tfi2 values during CWI and at Recovery. Tfi2, Tfi4 and CVC did not differ after TSD at Control, whereas they were reduced during CWI (-2.6 ± 0.7°C for Tfi2; -2 ± 0.8°C for Tfi4, -79 ± 25% for relative CVC, P < 0.05) as during Recovery (-4.9 ± 1.9°C for Tfi2, -2.6 ± 1.8°C for Tfi4, -70 ± 22% for relative CVC, P < 0.05). After TSD, the lower CVC values appeared earlier during CWI (-59 ± 19.6 s, P < 0.05). After TSD at Control and CWI, plasma endothelin levels were higher and negatively correlated with Tfi2, Tfi4 and CVC. However, no effect of TSD was found on the number and amplitude of CIVD and in Tre, HR, BP and catecholamines, for all periods. We concluded that TSD induced thermal and vascular changes in the hand which impair the local cold tolerance, suggesting that TSD increases the risk of local cold injuries.
No preview · Article · Jan 2012 · Arbeitsphysiologie
[Show abstract][Hide abstract] ABSTRACT: Total sleep deprivation in humans is associated with increased daytime sleepiness, decreased performance, elevations in inflammatory cytokines, and hormonal/metabolic disturbances. To assess the effects of 40 h of total sleep deprivation (TSD) under constant and well controlled conditions, on plasma levels of TNF-α and its receptor (TNFR1), interleukin-6 (IL-6), cortisol and C-reactive protein (CRP), sleepiness and performance, 12 healthy men (29±3 years) participated in a 5-days sleep deprivation experiment (two control nights followed by a night of sleep loss and one recovery night). Between 0800 and 2300 (i.e. between 25 and 40 h of sleep deprivation), a serial of blood sampling, multiple sleep latency, subjective levels of sleepiness and reaction time tests were completed before (day 2: D2) and after (day 4: D4) one night of sleep loss. We showed that an acute sleep deprivation (i.e. after 34 and 37 h of sleep deprivation) induced a significant increase in TNF-α (P<0.01), but there were no significant changes in TNFR1, IL-6, cortisol and CRP. In conclusion, our study in which constant and controlled experimental conditions were realized with healthy subjects and in absence of psychological or physical stressors, an acute total sleep deprivation (from 34 h) was sufficient to induce secretion of pro-inflammatory cytokine such as TNF-α, a marker more described in chronic sleep restriction or deprivation and as mediators of excessive sleepiness in humans in pathological conditions.
[Show abstract][Hide abstract] ABSTRACT: Points essentiels ■ Le conflit actuel en Afghanistan, pays de montagne, est l'occasion de faire la revue des pathologies et des contraintes médicales liées à l'altitude en opérations extérieures. ■ L'exposition progressive à l'hypoxie hypobare en montagne est à distinguer des accidents hypoxiques aigus par décompression en vol. ■ Aucun cas de pathologie lié à l'altitude n'a été rapporté chez les soldats acclimatés près de Kaboul (1 800 mètres) et évoluant à des altitudes généralement inférieures à 2 500 mètres. ■ Les équipages des avions de transport, contraints à des niveaux de vol de sécurité élevés en Afghanistan, sont exposés aux effets de l'altitude. ■ Si les lésions thoraciques sont devenues moins fréquentes (6 %), les pneumothorax compressifs restent à l'origine de décès évitables et leur exsufflation s'impose pour l'évacuation aérienne. ■ Le diagnostic échographique des pneumothorax est performant et trouve sa place au cours des évacuations aériennes. Chapitre 74 Pathologies et contraintes médicales liées à l'altitude au cours du conflit en Afghanistan
[Show abstract][Hide abstract] ABSTRACT: Sleep disorders are associated with inflammation and sympathetic activation, which are suspected to induce endothelial dysfunction, a key factor in the increased risk of cardiovascular disease. Less is known about the early effects of acute sleep deprivation on vascular function. We evaluated microvascular reactivity and biological markers of endothelial activation during continuous 40 h of total sleep deprivation (TSD) in 12 healthy men (29 +/- 3 yr). The days before [day 1 (D1)] and during TSD (D3), at 1200 and 1800, endothelium-dependent and -independent cutaneous vascular conductance was assessed by iontophoresis of acetylcholine and sodium nitroprusside, respectively, coupled to laser-Doppler flowmetry. At 0900, 1200, 1500, and 1800, heart rate (HR) and instantaneous blood pressure (BP) were recorded in the supine position. At D1, D3, and the day after one night of sleep recovery (D4), markers of vascular endothelial cell activation, including soluble intercellular adhesion molecule-1, vascular cell adhesion molecule-1, E-selectin, and interleukin-6 were measured from blood samples at 0800. Compared with D1, plasma levels of E-selectin were raised at D3, whereas intercellular adhesion molecule-1 and interleukin-6 were raised at D4 (P < 0.05). The endothelium-dependent and -independent CVC were significantly decreased after 29 h of TSD (P < 0.05). By contrast, HR, systolic BP, and the normalized low-frequency component of HR variability (0.04-0.15 Hz), a marker of the sympathetic activity, increased significantly within 32 h of TSD (P < 0.05). In conclusion, acute exposure to 40 h of TSD appears to cause vascular dysfunction before the increase in sympathetic activity and systolic BP.
Full-text · Article · Nov 2009 · Journal of Applied Physiology
[Show abstract][Hide abstract] ABSTRACT: This study investigated effects of a high protein (PROT) versus a high carbohydrate (CHO) diet on performance and physiological responses during an ultraendurance climbing race at moderate altitude. On two different periods, in a randomised crossover design, ten climbers (30.0+/-0.9 years) participated in the race (duration 29 h approximately, energy expenditure 43.6+/-1.2 MJ.day (-1)) and were fed either with the PROT (30% protein content) or the CHO diet (68% carbohydrate) each providing 16.74 MJ. Mental performance was assessed by the Stroop test and we estimated maximal voluntary strength of quadriceps muscle. We quantified metabolic and hormonal circulating concentrations. Mental performance was unaffected after the two races, while muscular performance and body weight were decreased (both p<0.01) with no diet effects. Decreases were measured for IGF-I concentration and its binding protein IGFBP-3 (p<0.001), and increases for cortisol and norepinephrine (p<0.01) with no diet effects. Glucose concentration decreased (p<0.05) without diet effects, while amino acids (leucine, isoleucine, valine, and tyrosine) decreased in CHO group (p<0.001). Leptin concentration decreased (p<0.001) without diet effects, whereas total ghrelin increased in CHO group (p<0.01). Our results showed that a high PROT or high CHO intake during physical exertion at moderate altitude maintained mental performance, but did not limit muscle force reduction and body weight loss. There was decreased glucose availability, and hormonal responses indicated both catabolism and extreme energy deficiency induced by exercise with opposite responses of ghrelin and leptin. The ghrelin response was additionally indicative of macronutrient intake during the race.
Full-text · Article · Oct 2009 · Hormone and Metabolic Research
[Show abstract][Hide abstract] ABSTRACT: Accurate reports of energy expenditure (EE) during prolonged mountaineering activity are sparse. The purpose of this study was to estimate EE during a winter ultraendurance climbing race and individual mountaineering activities in Mont Blanc, France.
Seven days before the race, resting metabolic rate (RMR) and maximal oxygen consumption (Vo2(max)) were measured in 10 experienced male climbers (30.0 +/- 0.9 years). Three days before (reference period) and during the race, heart rate (HR) was recorded for estimation of total daily EE (TDEE), and the type and duration of all activities were collected through questionnaires. Total DEE was calculated by adding DEE during sleep (DEE sleep), sedentary (DEE sedentary), and during exercise (DEE exercise). Daily energy expenditure during exercise was determined through assumption of the rectilinear relationship between heart rate (HR) and Vo2. Anthropometric measurements were performed 7 days before, just before, and immediately after the race.
Total time of the race averaged approximately 29 hours and 29 minutes, including 11 hours and 24 minutes in the hut, plus 18 hours and 5 minutes dedicated to climbing. During the race, TDEE was 43.6 +/- 1.2 MJ x d(-1). Energy expenditures for cross-country skiing and alpine climbing were similar (57.3 +/- 2.1 kJ x min(-1) and 54.0 +/- 2.9 kJ x min(-1), respectively). An energy deficit of 33.5 +/- 2.3 MJ resulted after the race, with a mean weight loss of 1.52 +/- 0.31 kg (P < .001).
Experienced climbers expended a high level of energy during a winter ultraendurance alpine climbing race at moderate altitude under high degrees of difficulty and risk exposure. These results provide comparative data on the energy cost of the main mountaineering activities during a race: cross-country skiing and alpine climbing.
No preview · Article · Sep 2009 · Wilderness and Environmental Medicine
[Show abstract][Hide abstract] ABSTRACT: Assessment of individual susceptibility to altitude illnesses and more particularly to acute mountain sickness (AMS) by means of tests performed in normobaric hypoxia (NH) or in hypobaric hypoxia (HH) is still debated. Eighteen subjects were submitted to HH and NH tests (PIO2=120 hPa, 30 min) before an expedition. Maximal and mean acute mountain sickness scores (AMSmax and mean) were determined using the self-report Lake Louise questionnaire scored daily. Cardio-ventilatory (f, V(T), PetO2 and PetCO2, HR and finger pulse oxymetry SpO2) were measured at times 5 and 30 min of the tests. Arterial (PaO2, PaCO2, pH, SaO2) and capillary haemoglobin (Hb) measurements were performed at times 30 min. Hypoxic ventilatory (HVR) and cardiac (HCR) responses, peripheral O2 blood content (CpO2) were calculated. A significant time effect is found for DeltaSpO2 (P = 0.04). Lower PaCO2 (P = 0.005), SaO2 (P = 0.07) and higher pH (P = 0.02) are observed in HH compared to NH. AMSmax varied from 3 to12 and AMSmean between 0.6 and 3.5. In NH at 30 min, AMSmax is related to PetO2 (R = 0.61, P = 0.03), CpO2 (R = -0.53, P = 0.02) and in HH to CpO2 (R = -0.57, P = 0.01). In NH, AMSmean is related to Deltaf (R = 0.46, P = 0.05), HCR (R = 0.49, P = 0.04), CpO2 (R = -0.51, P = 0.03) and, in HH at 30 min, to V(T) (R = 0.69, P = 0.01) and a tendency for CpO2 (R = -0.43, P = 0.07). We conclude that HH and NH tests are physiologically different and they must last 30 min. CpO2 is an important variable to predict AMS. For practical considerations, NH test is proposed to quantify AMS individual susceptibility using the formulas: AMSmax = 9.47 + 0.104PetO2(hPa)-0.68CpO2 (%), (R = 0.77, P = 0.001); and AMSmean = 3.91 + 0.059Deltaf + 0.438HCR-0.135CpO2 (R = 0.71, P = 0.017).
No preview · Article · Jun 2007 · Arbeitsphysiologie
[Show abstract][Hide abstract] ABSTRACT: Suggested mechanisms for the systemic, circulating cytokinemia observed during heavy physical exertion include inflammation and energy demand. We compared cytokine levels and examined the underlying physiological mechanisms between a long-distance triathlon and a 100-km run, two endurance races of similar duration but characterized by differences in muscle strain. Blood samples were collected from 12 triathletes (34.8 +/- 1.4 yr) and 11 runners (42.4 +/- 2.2 yr) the day before and at the end of races (T1, R1), and 24 h and 7 days post-race (R2, R3). At R1, significant race-related differences were observed, with greater increases in plasma levels of interleukins (IL)-6, IL-1ra, and IL-10 in the triathletes than in the runners, while levels of the chemokine IL-8 increased solely in the runners (P < 0.05, P < 0.05, P < 0.01, and P < 0.001, respectively). At R1, free fatty acid (FFA) levels were 119% higher in the triathletes than in the runners, who were the most liable to muscle damage in view of increased levels of the muscle-specific enzyme, creatine kinase (CK), loss of muscle flexibility and decreased physical performance. At R1, levels of heat shock protein (HSP)72 increased in the two groups but were 173% higher in the runners. For the two groups, all parameters had returned to pre-race levels by seven days post-race. Positive correlations were noted between IL-6 and FFA in the triathletes and between IL-8 and CK and HSP72 in the runners. The differences between cytokine responses after a long distance triathlon and a 100-km run suggested that IL-6 and IL-8 could be employed as respective markers of the intensity of the muscular activity required for substrate availability and vascular inflammation.
Full-text · Article · Jun 2006 · European cytokine network
[Show abstract][Hide abstract] ABSTRACT: This investigation examined the impact of a multistressor situation on salivary immunoglobulin A (sIgA) levels, and incidence of upper respiratory tract infection (URTI) during the French commando training (3 weeks of training followed by a 5-day combat course). For the URTI, the types of symptoms were classified according to the anatomical location of the infection. Saliva samples were collected (8 a.m.) from 21 males [21 (2) years] before entry into the commando training, the morning following the 3 weeks of training, after the 5-day combat course, and after 1 week of recovery. sIgA, protein and cortisol concentrations were measured. Symptoms of URTI were recorded during the study from health logs and medical examinations. After the 3 weeks of training, the sIgA concentration was not changed, although it was reduced after the 5-day course [from 120 (14) mg l(-1) to 71 (9) mg l(-1), P<0.01]. It returned to pre-training levels within a week of recovery. The incidence of URTI increased during the trial (chi(2)=53.48; P<0.01), but was not related to sIgA. Among the 30 episodes of URTI reported, there were 12 rhino-pharyngitis, 6 bronchitis, 5 tonsillitis, 4 sinusitis and 3 otitis. Cortisol levels were raised after the 3-week training (P<0.01), dropping below baseline after the combat course (P<0.01). Stressful situations have an adverse effect on mucosal immunity and incidence of URTI. However, the relationship between sIgA and illness remained unclear. The large proportion of rhino-pharyngitis indicated that the nasopharyngeal cavity is at a higher risk of infection.
Full-text · Article · Feb 2005 · Arbeitsphysiologie
[Show abstract][Hide abstract] ABSTRACT: The aim of this study was to examine hormonal and metabolic changes in a group of 18 professional male cyclists ((.)VO(2)max 69.9 [95 % CI 64.9 to 74.9] mL x kg(-1) x min(-1) ) during two successive periods of adapted intensive training. The second training period included 4 days of cycling competition. Intensity was increased while volume was decreased in the second training. Anthropometric data were collected before and at the end of the two training periods. Venous blood samples were taken in a basal state before the two training sessions and after each training session. Serum concentrations of cortisol (C), testosterone (T), dehydroepiandrosterone sulfate (DHEAs), and catecholamines were determined as well as branched-chain amino acids (valine, leucine, isoleucine) (BCAA) and free fatty acids (FFAs). At the end of the two training periods, the subjects lost fat mass whereas mean body mass was unchanged. The T/C ratio was reduced transiently after the first training session (45.90 %), while DHEAs/C remained unchanged. T/C and DHEAs/C were significantly increased after the second training session compared to the first (48.40 and 97.18 %, respectively). Catecholamines and FFAs were unchanged. The significant increase in BCAA levels after the second training session was of note as it might constitute a "store shape" of amino acids in anticipation of future intense training loads. Based on the responses of testosterone, DHEAs, and cortisol, and on the training-induced increase in BCAA, there appeared to be hormonal and metabolic adaptation despite the inherent psychological stress of competition.
Full-text · Article · Jan 2005 · Canadian journal of applied physiology = Revue canadienne de physiologie appliquée