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Physical inactivity increases cardiometabolic risk through a variety of mechanisms, among which alterations of immunological, metabolic, and autonomic control systems may play a pivotal role. Physical inactivity is frequently associated with other factors that may further worsen prognosis. The association between physical inactivity and hypoxia is particularly interesting and characterizes several conditions—whether physiological (e.g., residing or trekking at high altitude and space flights) or pathological (e.g., chronic cardiopulmonary diseases and COVID-19). In this randomized intervention study, we investigated the combined effects of physical inactivity and hypoxia on autonomic control in eleven healthy and physically active male volunteers, both at baseline (ambulatory) conditions and, in a randomized order, hypoxic ambulatory, hypoxic bedrest, and normoxic bedrest (i.e., a simple experimental model of physical inactivity). Autoregressive spectral analysis of cardiovascular variabilities was employed to assess cardiac autonomic control. Notably, we found hypoxia to be associated with an impairment of cardiac autonomic control, especially when combined with bedrest. In particular, we observed an impairment of indices of baroreflex control, a reduction in the marker of prevalent vagal control to the SA node, and an increase in the marker of sympathetic control to vasculature. [ABSTRACT FROM AUTHOR]

Acclima(tiza)tion to heat or hypoxia enhances work capacity in hot and hypoxic environmental conditions, respectively; an acclimation response is considered to be mediated by stimuli-specific molecular/systemic adaptations and potentially facilitated by the addition of exercise sessions. Promising findings at the cellular level provided the impetus for recent studies investigating whether acclimation to one stressor will ultimately facilitate whole body performance when exercise is undertaken in a different environmental condition. The present critical Mini-Review examines the theory of cross-adaptation between heat and hypoxia with particular reference to the determinants of aerobic performance. Indeed, early functional adaptations (improved exercise economy and enhanced oxyhemoglobin saturation) succeeded by later morphological adaptations (increased hemoglobin mass) might aid acclimatized humans perform aerobic work in an alternative environmental setting. Longer-term acclimation protocols that focus on the specific adaptation kinetics (and further allow for the adaptation reversal) will elucidate the exact physiological mechanisms that might mediate gains in aerobic performance or explain the lack thereof. [ABSTRACT FROM AUTHOR]

Hematological changes are commonly observed following prolonged exposure to hypoxia and bed rest. Typically, such responses have been reported as means and standard deviations, however, investigation into the responses of individuals is insufficient. Therefore, the present study retrospectively assessed individual variation in the hematological responses to severe inactivity (bed rest) and hypoxia. The data were derived from three-bed rest projects: two 10-d (LunHab project: 8 males; FemHab project: 12 females), and one 21-d (PlanHab project: 11 males). Each project comprised a normoxic bed rest (NBR; PIO2=133mmHg) and hypoxic bed rest (HBR; PIO2=91mmHg) intervention, where the subjects were confined in the Planica facility (Rateče, Slovenia). During the HBR intervention, subjects were exposed to normobaric hypoxia equivalent to an altitude of 4,000m. NBR and HBR interventions were conducted in a random order and separated by a washout period. Blood was drawn prior to (Pre), during, and post bed rest (R1, R2, R4) to analyze the individual variation in the responses of red blood cells (RBC), erythropoietin (EPO), and reticulocytes (Rct) to bed rest and hypoxia. No significant differences were found in the mean ∆(Pre-Post) values of EPO across projects (LunHab, FemHab, and PlanHab; p >0.05), however, female EPO responses to NBR (Range - 17.39, IQR – 12.97 mIU.ml−1) and HBR (Range – 49.00, IQR – 10.91 mIU.ml−1) were larger than males (LunHab NBR Range – 4.60, IQR – 2.03; HBR Range – 7.10, IQR – 2.78; PlanHab NBR Range – 7.23, IQR – 1.37; HBR Range – 9.72, IQR – 4.91 mIU.ml−1). Bed rest duration had no impact on the heterogeneity of EPO, Rct, and RBC responses (10-d v 21-d). The resultant hematological changes that occur during NBR and HBR are not proportional to the acute EPO response. The following cascade of hematological responses to NBR and HBR suggests that the source of variability in the present data is due to mechanisms related to hypoxia as opposed to inactivity alone. Studies investigating hematological changes should structure their study design to explore these mechanistic responses and elucidate the discord between the EPO response and hematological cascade to fully assess heterogeneity. [ABSTRACT FROM AUTHOR]

This retrospective study was designed to analyze the interindividual variability in the responses of different variables characterizing the skeletal muscle oxidative function to normoxic (N-BR) and hypoxic (H-BR) bed rests and to a hypoxic ambulatory confinement (H-AMB) of 10 and 21 days. We also assessed whether and how the addition of hypoxia to bed rest might influence the heterogeneity of the responses. In vivo measurements of O2 uptake and muscle fractional O2 extraction were carried out during an incremental one-leg knee-extension exercise. Mitochondrial respiration was assessed in permeabilized muscle fibers. A total of 17 subjects were included in this analysis. This analysis revealed a similar variability among subjects in the alterations induced by N-BR and H-BR both in peak O2 uptake (SD: 4.1% and 3.3% after 10 days; 4.5% and 8.1% after 21 days, respectively) and peak muscle fractional O2 extraction (SD: 5.9% and 7.3% after 10 days; 6.5% and 7.3% after 21 days), independently from the duration of the exposure. The individual changes measured in these variables were significantly related (r = 0.66, P = 0.004 after N-BR; r = 0.61, P = 0.009 after H-BR). Mitochondrial respiration showed a large variability of response after both N-BR (SD: 25.0% and 15.7% after 10 and 21 days) and H-BR (SD: 13.0% and 19.8% after 10 and 21 days); no correlation was found between N-BR and H-BR changes. When added to bed rest, hypoxia altered the individual adaptations within the mitochondria but not those intrinsic to the muscle oxidative function in vivo, both after the short- and medium-term exposures. [ABSTRACT FROM AUTHOR]

Introduction: While hypoxia is known to decrease peak oxygen uptake ( V. ⁢ o 2 max) and maximal power output in both adults and children its influence on submaximal exercise cardiorespiratory and, especially, muscle oxygenation responses remains unclear. Methods: Eight pre-pubertal boys (age = 8 ± 2 years.; body mass (BM) = 29 ± 7 kg) and seven adult males (age = 39 ± 4 years.; BM = 80 ± 8 kg) underwent graded exercise tests in both normoxic (PiO2 = 134 ± 0.4 mmHg) and hypoxic (PiO2 = 105 ± 0.6 mmHg) condition. Continuous breath-by-breath gas exchange and near infrared spectroscopy measurements, to assess the vastus lateralis oxygenation, were performed during both tests. The gas exchange threshold (GET) and muscle oxygenation thresholds were subsequently determined for both groups in both conditions. Results: In both groups, hypoxia did not significantly alter either GET or the corresponding V. ⁢ o 2 at GET. In adults, higher V. E levels were observed in hypoxia (45 ± 6 l/min) compared to normoxia (36 ± 6 l/min, p < 0.05) at intensities above GET. In contrast, in children both the hypoxic V. E and V. ⁢ o 2 responses were significantly greater than those observed in normoxia only at intensities below GET (p < 0.01 for V. E and p < 0.05 for V. ⁢ o 2). Higher exercise-related heart rate (HR) levels in hypoxia, compared to normoxia, were only noted in adults (p < 0.01). Interestingly, hypoxia per se did not influence the muscle oxygenation thresholds during exercise in neither group. However, and in contrast to adults, the children exhibited significantly higher total hemoglobin concentration during hypoxic as compared to normoxic exercise (tHb) at lower exercise intensities (30 and 60 W, p = 0.01). Conclusion: These results suggest that in adults, hypoxia augments exercise ventilation at intensities above GET and might also maintain muscle blood oxygenation via increased HR. On the other hand, children exhibit a greater change of muscle blood perfusion, oxygen uptake as well as ventilation at exercise intensities below GET. [ABSTRACT FROM AUTHOR]

We examined the interactive effects of mild hypothermia and hypoxia on finger vasoreactivity to local cold stress. Eight male lowlanders performed, in a counterbalanced order, a normoxic and a hypoxic (partial pressure of oxygen: ~12 kPa) hand cold provocation (consisting of a 30-min immersion in 8°C water), while immersed to the chest either in 21°C [cold trials; 0.5°C fall in rectal temperature (Trec) from individual preimmersion values], or in 35.5°C water, or while exposed to 27°C air. The duration of the trials was kept constant in each breathing condition. Physiological (Trec, skin temperature, cutaneous vascular conductance, oxygen uptake) and perceptual (thermal sensation and comfort, local pain, affective valence) reactions were monitored continually. Hypoxia accelerated the drop in Trec by ~14 min (P = 0.06, d = 0.67). In the air-exposure trials, hypoxia did not alter finger perfusion during the local cooling, whereas it impaired the finger rewarming response following the cooling (P < 0.01). During the 35.5°C immersion, the finger vasomotor tone was enhanced, especially in hypoxia (P = 0.01). Mild hypothermia aggravated finger vasoconstriction instigated by local cooling (P < 0.01), but the response did not differ between the two breathing conditions (P > 0.05). Hypoxia tended to attenuate the sensation of coldness (P = 0.10, r = 0.40) and thermal discomfort (P = 0.09, r = 0.46) in the immersed hand. Both in normoxia and hypoxia, the whole body thermal state dictates the cutaneous vasomotor reactivity to localized cold stimulus. [ABSTRACT FROM AUTHOR]

Purpose: Cold-induced vasodilatation (CIVD) is a peripheral blood flow response, observed in both the hands and feet. Exercise has been shown to enhance the response, specifically by increasing mean skin temperatures (Tsk), in part due to the increased number of CIVD waves. In contrast, hypobaric hypoxia has been suggested to impair digit skin temperature responses, particularly during subsequent hand rewarming following the cold stimulus. This study examined the combined effect of exercise and hypobaric hypoxia on the CIVD response. We compared the CIVD responses in the digits of both the hands and feet of a team of alpinists (N = 5) before and after a 35-day Himalayan expedition to Broadpeak, Pakistan (8051 m).Methods: Five elite alpinists participated in hand and foot cold water immersion tests 20 days before and immediately upon return from their expedition.Results: The alpinists summited successfully without supplemental oxygen. Post-expedition, all alpinists demonstrated higher minimum Tsk in their hands (pre: 9.9 ± 1.1, post: 10.1 ± 0.7 °C, p = 0.031). Four alpinists had either greater CIVD waves, and, consequently, higher mean Tsk in their hands, or higher recovery temperatures (pre: 26.0 ± 5.5 °C post: 31.0 ± 4.1 °C, p = 0.052), or faster rewarming rate (pre: 2.6 ± 0.5 °C min-1 post: 3.1 ± 0.4 °C min-1,p = 0.052). In the feet, the responses varied: 1/5 had higher wave amplitudes and 1/5 had higher passive recovery temperatures, whereas 3/5 had lower mean toe temperatures during cold exposure.Conclusions: The results of the cold stress test suggest after a 35-day Himalayan expedition, alpinists experienced a slight cold adaptation of the hands, but not the feet. [ABSTRACT FROM AUTHOR]

Key points: Superposition of hypoxia on 21 day bed rest did not worsen the impairment of skeletal muscle oxidative function induced by bed rest alone. A significant impairment of maximal oxidative performance was identified downstream of cardiovascular O2 delivery, involving both the intramuscular matching between O2 supply and utilization and mitochondrial respiration. These chronic adaptations appear to be relevant in terms of exposure to spaceflights and reduced gravity habitats (Moon or Mars), as characterized by low gravity and hypoxia, in patients with chronic diseases characterized by hypomobility/immobility and hypoxia, as well as in ageing. Abstract: Skeletal muscle oxidative function was evaluated in 11 healthy males (mean ± SD age 27 ± 5 years) prior to (baseline data collection, BDC) and following a 21 day horizontal bed rest (BR), carried out in normoxia ( P I O 2 = 133 mmHg; N‐BR) and hypoxia ( P I O 2 = 90 mmHg; H‐BR). H‐BR was aimed at simulating reduced gravity habitats. The effects of a 21 day hypoxic ambulatory confinement ( P I O 2 = 90 mmHg; H‐AMB) were also assessed. Pulmonary O2 uptake ( V ̇ O 2), vastus lateralis fractional O2 extraction (changes in deoxygenated haemoglobin + myoglobin concentration, Δ[deoxy(Hb + Mb)]; near‐infrared spectroscopy) and femoral artery blood flow (ultrasound Doppler) were evaluated during incremental one‐leg knee‐extension exercise (reduced constraints to cardiovascular O2 delivery) carried out to voluntary exhaustion in a normoxic environment. Mitochondrial respiration was evaluated ex vivo by high‐resolution respirometry in permeabilized vastus lateralis fibres. V ̇ O 2 peak decreased (P < 0.05) after N‐BR (0.98 ± 0.13 L min−1) and H‐BR (0.96 ± 0.17 L min−1) vs. BDC (1.05 ± 0.14 L min−1). In the presence of a decreased (by ∼6–8%) thigh muscle volume, V ̇ O 2 peak normalized per unit of muscle mass was not affected by both interventions. Δ[deoxy(Hb + Mb)]peak decreased (P < 0.05) after N‐BR (65 ± 13% of limb ischaemia) and H‐BR (62 ± 12%) vs. BDC (73 ± 13%). H‐AMB did not alter V ̇ O 2 peak or Δ[deoxy(Hb + Mb)]peak. An overshoot of Δ[deoxy(Hb + Mb)] was evident during the first minute of unloaded exercise after N‐BR and H‐BR. Arterial blood flow to the lower limb during both unloaded and peak knee extension was not affected by any intervention. Maximal ADP‐stimulated mitochondrial respiration decreased (P < 0.05) after all interventions vs. control. In 21 day N‐BR, a significant impairment of oxidative metabolism occurred downstream of cardiovascular O2 delivery, affecting both mitochondrial respiration and presumably the intramuscular matching between O2 supply and utilization. Superposition of H on BR did not worsen the impairment induced by BR alone. [ABSTRACT FROM AUTHOR]

Poor musculoskeletal state is commonly observed in numerous clinical populations such as chronic obstructive pulmonary disease (COPD) and heart failure patients. It, however, remains unresolved whether systemic hypoxemia, typically associated with such clinical conditions, directly contributes to muscle deterioration. We aimed to experimentally elucidate the effects of systemic environmental hypoxia upon inactivity-related muscle wasting. For this purpose, fourteen healthy, male participants underwent three 21-day long interventions in a randomized, cross-over designed manner: (i) bed rest in normoxia (NBR; PiO2 = 133.1 ± 0.3 mmHg), (ii) bed rest in normobaric hypoxia (HBR; PiO2 = 90.0 ± 0.4 mmHg) and ambulatory confinement in normobaric hypoxia (HAmb; PiO2 = 90.0 ± 0.4 mmHg). Peripheral quantitative computed tomography and vastus lateralis muscle biopsies were performed before and after the interventions to obtain thigh and calf muscle cross-sectional areas and muscle fiber phenotype changes, respectively. A significant reduction of thigh muscle size following NBR (- 6.9%, SE 0.8%; P < 0.001) was further aggravated following HBR (-9.7%, SE 1.2%; P = 0.027). Bed rest-induced muscle wasting in the calf was, by contrast, not exacerbated by hypoxic conditions (P = 0.47). Reductions in both thigh (-2.7%, SE 1.1%, P = 0.017) and calf (-3.3%, SE 0.7%, P < 0.001) muscle size were noted following HAmb. A significant and comparable increase in type 2× fiber percentage of the vastus lateralis muscle was noted following both bed rest interventions (NBR = C3.1%, SE 2.6%, HBR = C3.9%, SE 2.7%, P < 0.05). Collectively, these data indicate that hypoxia can exacerbate inactivity-related muscle wasting in healthy active participants and moreover suggest that the combination of both, hypoxemia and lack of activity, as seen in COPD patients, might be particularly harmful for muscle tissue. [ABSTRACT FROM AUTHOR]

Previous research, although limited, suggests that both hypoxia and bed rest influence psychological responses by exaggerating negative psychological responses and attenuating positive emotions. The present study investigated the effect of a 21-day prolonged exposure to normobaric hypoxia and bed rest on affective responses and fatigue. Eleven healthy participants underwent three 21-day interventions using a cross-over design: (1) normobaric hypoxic ambulatory confinement (HAMB), (2) normobaric hypoxic bed rest (HBR) and (3) normoxic bed rest (NBR). Affective and fatigue responses were investigated using the Activation Deactivation Adjective Check List, and the Multidimensional Fatigue Inventory, which were completed before (Pre), during (Day 7, Day 14, and Day 21) and after (Post) the interventions. The most negative psychological profile appeared during the HBR intervention. Specifically, tiredness, tension, general and physical fatigue significantly increased on days 7, 14, and 21, as well as at Post. After the HBR intervention, general and physical fatigue remained higher compared to Pre values. Additionally, a deterioration of psychological responses was also noted following HAMB and NBR. In particular, both hypoxia and BR per se induced subjective fatigue and negative affective responses. BR seems to exert a moderate negative effect on the sensation of fatigue, whereas exercise attenuates the negative effects of hypoxia as noted during the HAMB condition. In conclusion, our data suggest that the addition of hypoxia to bed rest-induced inactivity significantly worsens affective responses and feeling of fatigue. [ABSTRACT FROM AUTHOR]

Hypoxia and confinement have both been shown to influence emotional state. It is envisaged that the inhabitants of future planetary habitats will be exposed to concomitant confinement, reduced gravity and hypoxia. We examined the independent and combined effects of a 21-day inactivity/unloading and normobaric hypoxia under confined conditions on various psychological factors. Eleven healthy men participated in three 21-day experimental campaigns designed in a cross-over manner: (1) Normobaric hypoxic ambulatory confinement, (2) Normobaric hypoxic bed rest and (3) Normobaric normoxic bed rest. The Profile of Mood States, and the Positive and Negative Affect Schedule were employed to assess the participants' psychological responses before (Pre), during (Day 7, Day 14, and Day 21) and after (Post) the confinements. The most negative psychological profile appeared on days 14 and 21 of the hypoxic bed rest campaign. A significant increase in depression, tension, and confusion was noted on days 14 and 21 of the hypoxic bed rest condition. Concomitantly, a decrease, albeit not statistically significant, in positive psychological responses was observed. The psychological profile returned to the initial level at Post following all confinements. These data suggest that the combined effect of hypoxia and bed rest induced themost negative effects on an individual's mood. However, significant intra- and inter-individual differences in psychological responses were noted and should be taken into consideration. [ABSTRACT FROM AUTHOR]

Dipeptidyl peptidase 4 (DPP4) is a transmembrane glycoprotein involved in protein degradation. Due to its action on incretins, which increase insulin secretion, DPP4 is considered a therapeutic target for type 2 diabetes. Here we have studied the role of single and combined effects of hypoxia and inactivity on the expression of DPP4 in human adipose tissue of 12 adult normalweight males. Fat biopsies were obtained at baseline and after each of three experimental campaigns. The results revealed that in isolated human preadipocytes the expression of DPP4 was significantly increased by exposure of participants to hypoxia. Physical inactivity per se had no apparent effect on the DPP4 expression. It is concluded that DPP4 may be a marker to monitor indirectly tissue hypoxia, as occurs in obese subjects. [ABSTRACT FROM AUTHOR]

We aimed to elucidate potential differential effects of hypoxia on cardiorespiratory responses during submaximal cycling and simulated skiing exercise between adults and pre-pubertal children. Healthy, low-altitude residents (adults, N = 13, Age = 40 ± 4yrs.; children, N = 13, age = 8 ± 2yrs.) were tested in normoxia (Nor: PiO2 = 134 ± 0.4 mmHg; 940 m) and normobaric hypoxia (Hyp: PiO2 = 105 ± 0.6 mmHg; ~3 000 m) following an overnight hypoxic acclimation ( ≥ 12-hrs). On both days, the participants underwent a graded cycling test and a simulated skiing protocol. Minute ventilation (VE), oxygen uptake (VO2), heart rate (HR) and capillary-oxygen saturation (SpO2) were measured throughout both tests. The cycling data were interpolated for 2 relative workload levels (1 W · kg-1 & 2 W · kg-1). Higher resting HR in hypoxia, compared to normoxia was only noted in children (Nor:78 ± 17; Hyp:89 ± 17 beats · min-1; p < 0.05), while SpO2 was significantly lower in hypoxia (Nor:97 ± 1 %; Hyp:91 ± 2 %; p < 0.01) with no betweengroup differences. The VE, VO2 and HR responses were higher during hypoxic compared to normoxic cycling test in both groups (p < 0.05). Except for greater HR during hypoxic compared to normoxic skiing in children (Nor:155 ± 19; Hyp:167 ± 13 (beats · min-1); p < 0.05), no other significant between-group differences were noted during the cycling and skiing protocols. In summary, these data suggest similar cardiorespiratory responses to submaximal hypoxic cycling and simulated skiing in adults and children. [ABSTRACT FROM AUTHOR]

Objective: Despite over 50 years of research on the physiological effects of sustained bed rest, data characterizing its effects on sleep macrostructure and breathing stability in humans are scarce. This study was conducted to determine the effects of continuous exposure to hypoxia and sustained best rest, both individually and combined, on nocturnal sleep and breathing stability. Methods: Eleven participants completed three randomized, counter-balanced, 21-days trials of: (1) normoxic bed rest (NBR, PIO2 = 133.1 ± 0.3), (2) hypoxic ambulatory confinement (HAMB, PIO2 = 90.0 ± 0.4) and (3) hypoxic bed rest (HBR, PIO2 = 90.0 ± 0.4; ~4,000m equivalent altitude). Full objective polysomnography was performed at baseline, on Night 1 and Night 21 in each condition. Results: In NBR Night 1, more time was spent in light sleep (10 ± 2%) compared to baseline (8 ± 2%; p = 0.028); Slow-wave sleep (SWS) was reduced from baseline in the hypoxic-only trial by 18%(HAMB Night 21, p = 0.028) and further reduced by 33% (HBR Night 1, p = 0.010), and 36% (HBR Night 21, p = 0.008) when combined with bed rest. The apnea-hypopnea index doubled from Night 1 to Night 21 in HBR (32-62 events·h-1) and HAMB (31-59 events·h-1; p = 0.002). Those who experienced greatest breathing instability from Night 1 to Night 21 (NBR) were correlated to unchanged or higher (+1%) night SpO2 concentrations (R² = 0.471, p = 0.020). Conclusion: Bed rest negatively affects sleep macrostructure, increases the apnea-hypopnea index, and worsens breathing stability, each independently exacerbated by continuous exposure to hypoxia. [ABSTRACT FROM AUTHOR]

New Findings What is the central question of this study? What are the distinct and interactive effects of a 10 day exposure to hypoxia and horizontal bedrest on the whole-body peak oxygen uptake and on the regional cerebral and skeletal muscle tissue oxygenation during upright cycle ergometry in male lowlanders?, What is the main finding and its importance? A 10 day sustained exposure to hypoxia aggravates the bedrest-induced reduction in peak oxygen uptake during dynamic exercise engaging large muscle groups, but mitigates the skeletal muscle oxidative capacity impairment elicited by bedrest., The study examined the interactive effects of a 10 day exposure to hypoxia and bedrest on the whole-body peak oxygen uptake ( [ABSTRACT FROM AUTHOR]

Purpose: Acute hypoxia alters the threshold for sensation of cutaneous thermal stimuli. We hypothesised that hypoxia-induced alterations in cutaneous temperature sensation may lead to modulation of the perception of temperature, ultimately influencing behavioural thermoregulation and that the magnitude of this effect could be influenced by daily physical training.Methods: Fourteen men were confined 10 days to a normobaric hypoxic environment (PIO2 = 88.2 ± 0.6 mmHg, corresponding to 4175 m elevation). Subjects were randomly assigned to a non-exercising (Live-high, LH, N = 6), or exercising group (Live-high Train-high, LH-TH, N = 8) comprised of 1-h bouts of cycle ergometry, twice daily, at a work-rate equivalent to 50% hypoxic peak power output. A subset of subjects (N = 5) also completed a control trial under normoxic conditions. The thermal comfort zone (TCZ) was determined in normoxia, and during hypoxic confinement days 2 (HC2) and 10 (HC10) in both groups using a water-perfused suit in which water temperature was regulated by the subjects within a range, they deemed thermally comfortable. Mean skin temperature and proximal-distal temperature gradients (two sites: forearm-fingertip, calf-toe) were recorded each minute throughout the 60-min protocol.Results: The average width of the TCZ did not differ between the control group (9.0 ± 6.9 °C), and the LH and LH-TH groups on days HC2 (7.2 ± 4.2 °C) and HC10 (10.2 ± 7.5 °C) of the hypoxic exposure (p = 0.256). [Formula: see text] was marginally higher on HC2 (35.9 ± 1.0 °C) compared to control (34.9 ± 0.8 °C, p = 0.040), but not on HC10 (35.6 ± 1.0 °C), reflecting the responses of hand perfusion.Conclusion: There was a little systematic effect of hypoxia or exercise training on TCZ magnitude or boundary temperatures. [ABSTRACT FROM AUTHOR]

The study examined the effects of hypoxia and horizontal bed rest, separately and in combination, on peak oxygen uptake (VO2 peak) during upright cycle ergometry. Ten male lowlanders underwent three 21-day confinement periods in a counterbalanced order: 1) normoxic bed rest [NBR; partial pressure of inspired O2 (PIO2) = 133.1 ± 0.3 mmHg]; 2) hypoxic bed rest (HBR; PIO2 = 90.0 ± 0.4 mmHg), and 3) hypoxic ambulation (HAMB; PIO2 = 90.0 ± 0.4 mmHg). Before and after each confinement, subjects performed two incremental-load trials to exhaustion, while inspiring either room air (AIR), or a hypoxic gas (HYPO; PIO2 = 90.0 ± 0.4 mmHg). Changes in regional oxygenation of the vastus lateralis muscle and the frontal cerebral cortex were monitored with nearinfrared spectroscopy. Cardiac output (CO) was recorded using a bioimpedance method. The AIR VO2 peak was decreased by both HBR (~13.5%; P = 0.001) and NBR (~8.6%; P ≥ 0.001), with greater drop after HBR (P = 0.01). The HYPO VO2 peak was also reduced by HBR (-9.7%; P = 0.001) and NBR (-6.1%; P ≤ 0.001). Peak CO was lower after both bed-rest interventions, and especially after HBR (HBR: ~13%, NBR: ~7%; P ≤ 0.05). Exercise-induced alterations in muscle and cerebral oxygenation were blunted in a similar manner after both bed-rest confinements. No changes were observed in HAMB. Hence, the bed-rest-induced decrease in VO2 peak was exaggerated by hypoxia, most likely due to a reduction in convective O2 transport, as indicated by the lower peak values of CO. [ABSTRACT FROM AUTHOR]

To assess the effect of normobaric hypoxia on metabolism, gut hormones, and body composition, 11 normal weight, aerobically trained (VO2peak: 60.6 ± 9.5ml·kg-1·min-1) men (73.0 ± 7.7 kg; 23.7 ± 4.0 years, BMI 22.2 ± 2.4 kg·m-2) were confined to a normobaric (altitude ≃ 940 m) normoxic (NORMOXIA; PIO2 ≃ 133.2mmHg) or normobaric hypoxic (HYPOXIA; PIO was reduced from 105.6 to 97.7mmHg over 10 days) environment for 10 days in a randomized cross-over design. The wash-out period between confinements was 3 weeks. During each 10-day period, subjects avoided strenuous physical activity and were under continuous nutritional control. Before, and at the end of each exposure, subjects completed a meal tolerance test (MTT), during which blood glucose, insulin, GLP-1, ghrelin, peptide-YY, adrenaline, noradrenaline, leptin, and gastro-intestinal blood flow and appetite sensations were measured. There was no significant change in body weight in either of the confinements (NORMOXIA: -0.7±0.2 kg; HYPOXIA: -0.9 ± 0.2 kg), but a significant increase in fat mass in NORMOXIA (0.23 ± 0.45 kg), but not in HYPOXIA (0.08 ± 0.08 kg). HYPOXIA confinement increased fasting noradrenaline and decreased energy intake, the latter most likely associated with increased fasting leptin. The majority of all other measured variables/responses were similar in NORMOXIA and HYPOXIA. To conclude, normobaric hypoxic confinement without exercise training results in negative energy balance due to primarily reduced energy intake. [ABSTRACT FROM AUTHOR]

To gain insights into microgravity-induced ophthalmic changes (microgravity ocular syndrome), and as part of a project investigating effects of future planetary habitats, we investigated the effect of acute hypercapnia following 10-day bed rest and hypoxia on posterior eye structures. Female subjects (N = 7) completed three 10-day experimental interventions: 1) normoxic bed rest [NBR; partial pressure of inspired O2 (PIO2) 132.9 ± 0.3 Torr]; 2) hypoxic ambulatory confinement (HAMB; PIO2 =90.4 ± 0.3 Torr); and 3) hypoxic bed rest (HBR; n = 12; PIO2 = 90.4 ± 0.3 Torr). Before and on the last day of each intervention, optical coherence tomography (OCT) of the optic disk was performed, and the thicknesses of the retinal nerve fiber layer (RNFL), retina, and choroid were measured. OCT examinations were conducted with the subjects breathing the prevailing normocapnic breathing mixture (either normoxic or hypoxic) and then following a 10-min period of breathing the same gas mixture, but with the addition of 1% CO2. Choroidal thickness was greater during both bed-rest conditions (NBR and HBR) compared with the ambulatory (HAMB) condition (ANOVA, P < 0.001). Increases in RNFL thickness compared with baseline were observed in the hypoxic trials (HBR, P < 0.001; and HAMB, P = 0.021), but not the normoxic trial (NBR). A further increase in RNFL thickness (P = 0.019) was observed after the 10-min hypercapnic trial in the NBR condition only. The fact that choroidal thickness was not affected by PO2 or PCO2, but increased by bed rest, suggests a hydrostatic rather than a vasoactive effect. The increments in RNFL thickness were most likely associated with local hypoxia and hypercapnia-induced dilatation of the retinal blood vessels. [ABSTRACT FROM AUTHOR]

Background and objective Hypoxic exercise exacerbates periodic breathing in otherwise healthy, awake humans. Interactions between sleep, exercise and hypoxic exposure have not been fully elucidated. Methods Fourteen men were confined 10 days to a simulated altitude of 4175 m ( FIO2 = 0.139; PIO2 = 88 mm Hg). They were randomly assigned to an exercise intervention of 2 × 60-min cycle exercise/day at 50% of their hypoxia-specific peak power output (exercise, n = 8), or they completed no exercise (control, n = 6, random order). Sleep and breathing were objectively assessed via full polysomnography on night 1, after 14-h acute exposure ( N1), and again on night 10 ( N10). Results The exercise group spent more time in light sleep than control on N10 (95% confidence interval ( CI): 8.5-15.0%; P = 0.013) and experienced more stage shifts ( CI: 13-44; P = 0.023) on both nights compared with control. The exercise group experienced more apnoea-hypopnoea ( AH) events per hour compared with control ( CI: 1-110; P = 0.046); AH events that were associated with night desaturations were also higher on N1 (exercise: 397 ± 320, control: 124 ± 205, P = 0.047) and N10 (exercise: 375 ± 229, control: 110 ± 138, P = 0.028, CI: 49-489 total events; P = 0.020). The length of hyperpnoea was increased from 12.8 ± 2.2 s on N1 to 14.6 ± 2.7 s on N10 ( P = 0.008), and thus, total cycle length also increased ( P = 0.002) in both cohorts. Mean pooled duty ratios were 0.68 ± 0.02 on N1 and 0.69 ± 0.02 on N10 (group effect P = 0.617). Conclusion Daily, moderate-intensity exercise in normobaric hypoxia equivalent to 4175 m exacerbated AH events, and negatively affected sleep architecture in exercisers compared with matched controls. [ABSTRACT FROM AUTHOR]

The study concerns effects of 21 days of sustained bedrest and hypoxia, alone and in combination, on skeletal muscle micro RNA (mi RNA) expression. It is expected that astronauts undertaking long-duration missions will be exposed not only to microgravity but also to a hypoxic environment. The molecular machinery underlying microgravity-induced alterations in skeletal muscle structure and function is still largely unknown. One possible regulatory mechanism is altered expression of mi RNAs, a group of noncoding RNAs which down-regulate many different target genes through increased degradation or translation of their messenger RNA. Thirteen healthy men underwent three 21-day interventions, interspersed by 4-month washout periods: horizontal bedrest in normoxia, bedrest in hypoxia, ambulation in hypoxia. The level of hypoxia corresponded to 4000 m altitude. mi RNAs from v. lateralis muscle biopsies were analyzed using a microarray covering ≈4000 human mi RNAs. Sixteen mature mi RNAs were up-regulated and three down-regulated after bedrest. The magnitudes of these changes were small and a large portion of the mi RNAs affected by bedrest was also differentially expressed after washout periods. In fact, the number of differentially expressed probe sets over time was substantially larger than what could be detected after bedrest. Still, the majority of the mi RNAs (let-7, miR-15, miR-25, miR-199, miR-133) that were differentially expressed following bedrest, belong to mi RNA families previously reported in the context of muscle physiology, in particular to respond to changes in mechanical loading. Since only minor changes in mi RNA expression could be detected after bedrest, our data indicate mi RNA to play only a minor role in the substantial change in muscle phenotype seen with unloading. [ABSTRACT FROM AUTHOR]

Independently, both inactivity and hypoxia augment oxidative stress. This study, part of the FemHab project, investigated the combined effects of bed rest-induced unloading and hypoxic exposure on oxidative stress and antioxidant status. Healthy, eumenorrheic women were randomly assigned to the following three 10-day experimental interventions: normoxic bed rest (NBR; n = 11; PIO2 = 133 mmHg), normobaric hypoxic bed rest (HBR; n = 12; PIO2 = 90 mmHg), and ambulatory hypoxic confinement (HAMB; n = 8: PIO2 = 90 mmHg). Plasma samples, obtained before (Pre), during (D2, D6), immediately after (Post) and 24 h after (Post+1) each intervention, were analyzed for oxidative stress markers [advanced oxidation protein products (AOPP), malondialdehyde (MDA), and nitrotyrosine], antioxidant status [superoxide dismutase (SOD), catalase, ferric-reducing antioxidant power (FRAP), glutathione peroxidase (GPX), and uric acid (UA)], NO metabolism end-products (NOx), and nitrites. Compared with baseline, AOPP increased in NBR and HBR on D2 (+14%; +12%; P < 0.05), D6 (+19%; +15%; P < 0.05), and Post (+22%; +21%;P < 0.05), respectively. MDA increased at Post+1 in NBR (+116%; P < 0.01) and D2 in HBR (+114%; P < 0.01) and HAMB (+95%; P < 0.05). Nitrotyrosine decreased (-45%; P < 0.05) and nitrites increased (+46%; P < 0.05) at Post+1 in HAMB only. Whereas SOD was higher at D6 (+82%) and Post+1 (+67%) in HAMB only, the catalase activity increased on D6 (128%) and Post (146%) in HBR and HAMB, respectively (P < 0.05). GPX was only reduced on D6 (-20%; P < 0.01) and Post (-18%; P < 0.05) in HBR. No differences were observed in FRAP and NOx. UA was higher at Post in HBR compared with HAMB (P < 0.05). These data indicate that exposure to combined inactivity and hypoxia impairs prooxidant/antioxidant balance in healthy women. Moreover, habitual activity levels, as opposed to inactivity, seem to blunt hypoxia-related oxidative stress via antioxidant system upregulation. [ABSTRACT FROM AUTHOR]

The study examined the distinct and synergistic effects of hypoxia and bed rest on the erythropoietin ( EPO) concentration and relative changes in plasma volume ( PV). Eleven healthy male lowlanders underwent three 21-day confinement periods, in a counterbalanced order: (1) normoxic bed rest ( NBR; PIO2: 133.1 ± 0.3 mmHg); (2) hypoxic bed rest ( HBR; PIO2: 90.0 ± 0.4 mmHg, ambient simulated altitude of ~4000 m); and (3) hypoxic ambulation ( HAMB; PIO2: 90.0 ± 0.4 mmHg). Blood samples were collected before, during (days 2, 5, 14, and 21) and 2 days after each confinement to determine EPO concentration. Qualitative differences in PV changes were also estimated by changes in hematocrit and hemoglobin concentration along with concomitant changes in plasma renin concentration. NBR caused an initial reduction in EPO by ~39% ( P = 0.04). By contrast, HBR enhanced EPO ( P = 0.001), but the increase was less than that induced by HAMB ( P < 0.01). All three confinements caused a significant reduction in PV ( P < 0.05), with a substantially greater drop in HBR than in the other conditions ( P < 0.001). Thus, present results suggest that hypoxia prevents the EPO suppression, whereas it seems to exaggerate the PV reduction induced by bed rest. [ABSTRACT FROM AUTHOR]

Background: Both exposure to hypoxia and exercise training have the potential to modulate appetite and induce beneficial metabolic adaptations. The purpose of this study was to determine whether daily moderate exercise training performed during a 10-day exposure to normobaric hypoxia alters hormonal appetite regulation and augments metabolic health. Methods: Fourteen healthy, male participants underwent a 10-day hypoxic confinement at ∼4000 m simulated altitude (FIO2 = 0.139±0.003%) either combined with daily moderate intensity exercise (Exercise group; N = 8, Age = 25.8±2.4 yrs, BMI = 22.9±1.2 kg·m−2) or without any exercise (Sedentary group; N = 6 Age = 24.8±3.1 yrs, BMI = 22.3±2.5 kg·m−2). A meal tolerance test was performed before (Pre) and after the confinement (Post) to quantify fasting and postprandial concentrations of selected appetite-related hormones and metabolic risk markers. 13C-Glucose was dissolved in the test meal and 13CO2 determined in breath samples. Perceived appetite ratings were obtained throughout the meal tolerance tests. Results: While body mass decreased in both groups (−1.4 kg; p = 0.01) following the confinement, whole body fat mass was only reduced in the Exercise group (−1.5 kg; p = 0.01). At Post, postprandial serum insulin was reduced in the Sedentary group (−49%; p = 0.01) and postprandial plasma glucose in the Exercise group (−19%; p = 0.03). Fasting serum total cholesterol levels were reduced (−12%; p = 0.01) at Post in the Exercise group only, secondary to low-density lipoprotein cholesterol reduction (−16%; p = 0.01). No differences between groups or testing periods were noted in fasting and/or postprandial concentrations of total ghrelin, peptide YY, and glucagon-like peptide-1, leptin, adiponectin, expired 13CO2 as well as perceived appetite ratings (p>0.05). Conclusion: These findings suggest that performing daily moderate intensity exercise training during continuous hypoxic exposure does not alter hormonal appetite regulation but can improve the lipid profile in healthy young males. [ABSTRACT FROM AUTHOR]

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Abstract: This study investigated the effects of four exposures to normobaric hypoxia (SIH group; N =10) or placebo-control normoxia (Control group; N =9) on cardio-respiratory responses to hypoxic exercise. Before and after the exposures all subjects performed a constant power test (CP) to exhaustion in hypoxia at a work load corresponding to 75% of previously determined normoxic . Arterial oxygen saturation and minute ventilation were measured continuously. NIRS was used to monitor regional changes in oxygenated, de-oxygenated and total hemoglobin concentrations of the frontal cortex, vastus lateralis and serratus anterior. Although neither group improved CP time, the SIH group exhibited increases in both (+15%; P <0.05) and (+4%; P <0.05) after intermittent hypoxia. No physiologically significant differences were observed during exercise in vastus lateralis, serratus anterior and cerebral oxygenation between groups and testing periods. These data suggest that normobaric SIH enhances hypoxic exercise and without affecting regional oxygenation or time to exhaustion. [Copyright &y& Elsevier]

The effect of acute and 23 days of intermittent exposures to normobaric hypoxia on the forehead sweating response during steady-state exercise was investigated. Eight endurance athletes slept in a normobaric hypoxic room for a minimum of 8 h per day at a simulated altitude equivalent to 2,700 m for 23 days (sleep high–train low regimen). Peak oxygen uptake $$ {\left( {\ifmmode\expandafter\dot\else\expandafter\.\fi{V}{\text{O}}_{{2{\text{peak}}}} } \right)} $$ and peak work rate (WRpeak) were determined under normoxic (20.9%O2) and hypoxic (13.5%O2) conditions prior to (pre-IHE), and immediately after (post-IHE) the intermittent hypoxic exposures (IHE). Also, each subject performed three 30-min cycle-ergometry bouts: (1) normoxic exercise at 50% WRpeak attained in normoxia (control trial; CT); (2) hypoxic exercise at 50% WRpeak attained in hypoxia (hypoxic relative trial; HRT) and (3) hypoxic exercise at the same absolute work rate as in CT (hypoxic absolute trial; HAT). Exposure to hypoxia induced a 33 and 37% decrease ( P < 0.001) in $$ \ifmmode\expandafter\dot\else\expandafter\.\fi{V}{\text{O}}_{{2{\text{peak}}}} $$ pre-IHE and post-IHE, respectively. Despite similar relative oxygen uptake during HAT pre-IHE and post-IHE, the ratings of perceived whole-body exertion decreased substantially ( P < 0.05) post-IHE. Pre-IHE the sweat secretion on the forehead $$ {\left( {\ifmmode\expandafter\dot\else\expandafter\.\fi{m}_{{{\text{sw}}}} f} \right)} $$ was greater ( P < 0.01) in the HAT (2.60 (0.80) mg cm−2 min−1) compared to the other two trials (CT = 1.87 (1.09) mg cm−2 min−1; HRT = 1.57 (0.82) mg cm−2 min−1) despite a similar exercise-induced elevation in body temperatures, resulting in an augmented ( P < 0.01) gain of the sweating response $$ {\left( {\ifmmode\expandafter\dot\else\expandafter\.\fi{m}_{{{\text{sw}}}} f/\Delta T_{{{\text{re}}}} } \right)}. $$ The augmented $$ \ifmmode\expandafter\dot\else\expandafter\.\fi{m}_{{{\text{sw}}}} f $$ and $$ \ifmmode\expandafter\dot\else\expandafter\.\fi{m}_{{{\text{sw}}}} f/\Delta T_{{{\text{re}}}} $$ during the HAT were no longer evident post-IHE. Thus, it appears that exercise sweating on the forehead is potentiated by acute exposure to hypoxia, an effect which can be abolished by 23 days of intermittent hypoxic exposures. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented in response to the article about the effect of five nights under normobaric hypoxia on sleep quality by M. Hoshikawa et al. in the previous issue.

Environmental hypoxia and inactivity have both been shown to modulate appetite. To elucidate the independent and combined effects of hypoxia and bed rest-induced inactivity on appetite-related hormones and subjective appetite, eleven healthy, non-obese males underwent three experimental interventions in a cross-over and randomized fashion: 1) Hypoxic confinement combined with daily moderate-intensity exercise (HAMB, FiO2 = 0.141 ± 0.004; PiO2 = 90.0 ± 0.4 mmHg) 2) Bed rest in normoxia (NBR, FiO2 = 0.209; PiO2 = 133.1 ± 0.3 mmHg) and 3) Bed rest in hypoxia (HBR, FiO2 = 0.141 ± 0.004; PiO2 = 90.0 ± 0.4 mmHg). A mixed-meal tolerance test (MTT), followed by an ad libitum meal were performed before (Pre) and after 16-days (Post) of each intervention. Composite satiety scores (CSS) during the MTT were calculated from visual analogue scores, while fasting and postprandial concentrations of total ghrelin, peptide YY (PYY), glucagon-like peptide-1 (GLP-1) and leptin were quantified from arterialized-venous samples. Postprandial CSS were significantly lower at Post compared to Pre in NBR only (P < 0.05) with no differences observed in ad libitum meal intakes. Postprandial concentrations and incremental area under the curve (AUC) for total ghrelin and PYY were unchanged following all interventions. Postprandial GLP-1 concentrations were only reduced at Post following HBR (P < 0.05) with resulting AUC changes being significantly lower compared to HAMB (P < 0.01). Fasting leptin was reduced following HAMB (P < 0.05) with no changes observed following NBR and HBR. These findings suggest that independently, 16-day of simulated altitude exposure (∼4000 m) and bed rest-induced inactivity do not significantly alter subjective appetite or ad libitum intakes. The measured appetite-related hormones following both HAMB and HBR point to a situation of hypoxia-induced appetite stimulation, although this did not reflect in higher ad libitum intakes.Clinical Trial Registration Number: NCT02293772. [ABSTRACT FROM AUTHOR]

Future Lunar and Mars habitats will maintain a hypobaric hypoxic environment to minimise the risk of decompression sickness during the preparation for extra-vehicular activity. This study was part of a larger study investigating the separate and combined effects of inactivity associated with reduced gravity and hypoxia, on the cardiovascular, musculoskeletal, neurohumoural, and thermoregulatory systems. Eleven healthy normothermic young male subjects participated in three trials conducted on separate occasions: (1) Normobaric hypoxic ambulatory confinement, (2) Normobaric hypoxic bedrest and (3) Normobaric normoxic bedrest. Normobaric hypoxia was achieved by reduction of the oxygen fraction in the air (F i O 2 =0.141±0.004) within the facility, while the effects of reduced gravity were simulated by confining the subjects to a horizontal position in bed, with all daily routines performed in this position for 21 days. The present study investigated the effect of the interventions on behavioural temperature regulation. The characteristics of the thermal comfort zone (TCZ) were assessed by a water-perfused suit, with the subjects instructed to regulate the sinusoidally varying temperature of the suit within a range considered as thermally comfortable. Measurements were performed 5 days prior to the intervention (D-5), and on days 10 (D10) and 20 (D20) of the intervention. no statistically significant differences were found in any of the characteristics of the TCZ between the interventions (HAMB, HBR and NBR), or between different measurement days (D-5, D10, D20) within each intervention. rectal temperature remained stable, whereas skin temperature ( T sk ) increased during all interventions throughout the one hour trial. no difference in T sk between D-5, D10 and D20, and between HAMB, HBR and NBR were revealed. subjects perceived the regulated temperature as thermally comfortable, and neutral or warm. we conclude that regulation of thermal comfort is not compromised by hypoxic inactivity. [ABSTRACT FROM AUTHOR]

Keramidas, Michail E, Roger Kölegård, Igor B. Mekjavic, and Ola Eiken. Acute effects of normobaric hypoxia on hand-temperature responses during and after local cold stress. High Alt Med Biol. 15:183-191, 2014.-The purpose was to investigate acute effects of normobaric hypoxia on hand-temperature responses during and after a cold-water hand immersion test. Fifteen males performed two right-hand immersion tests in 8°C water, during which they were inspiring either room air (Fi o2: 0.21; AIR), or a hypoxic gas mixture (Fi o2: 0.14; HYPO). The tests were conducted in a counterbalanced order and separated by a 1-hour interval. Throughout the 30-min cold-water immersion (CWI) and the 15-min spontaneous rewarming (RW) phases, finger-skin temperatures were measured continuously with thermocouple probes; infrared thermography was also employed during the RW phase to map all segments of the hand. During the CWI phase, the average skin temperature (Tavg) of the fingers did not differ between the conditions (AIR: 10.2±0.5°C, HYPO: 10.0±0.5°C; p=0.67). However, Tavg was lower in the HYPO than the AIR RW phase (AIR: 24.5±3.4°C; HYPO: 22.0±3.8°C; p=0.002); a response that was alike in all regions of the immersed hand. Accordingly, present findings suggest that acute exposure to normobaric hypoxia does not aggravate the cold-induced drop in hand temperature of normothermic males. Still, hypoxia markedly impairs the rewarming responses of the hand. [ABSTRACT FROM AUTHOR]

Purpose: Both acute hypoxia and physical exercise are known to increase oxidative stress. This randomized prospective trial investigated whether the addition of moderate exercise can alter oxidative stress induced by continuous hypoxic exposure. Methods: Fourteen male participants were confined to 10-d continuous normobaric hypoxia (F1O2 = 0.139 ± 0.003, P1O2 = 88.2 ± 0.6 mm Hg, ~4000-m simulated altitude) either with (HCE, n = 8, two training sessions per day at 50% of hypoxic maximal aerobic power) or without exercise (HCS, n = 6). Plasma levels of oxidative stress markers (advanced oxidation protein products [AOPP], nitrotyrosine, and malondialdehyde), antioxidant markers (ferric-reducing antioxidant power, Superoxide dismutase, glutathione peroxidase, and catalase), nitric oxide end-products, and erythropoietin were measured before the exposure (Pre), after the first 24 h of exposure (Dl), after the exposure (Post) and after the 24-h reoxygenation (Post + 1). In addition, graded exercise test in hypoxia was perfotmed before and after the protocol. Results: Maximal aerobic power increased after the protocol in HCE only (+6.8%, P < 0.05). Compared with baseline, AOPP was higher at Post + 1 (+28%, P < 0.05) and nitrotyrosine at Post (+81%, P < 0.05) in HCS only. Superoxide dismutase (+30%, P < 0.05) and catalase (+53%, P < 0.05) increased at Post in HCE only. Higher levels of ferric-reducing antioxidant power (+41%, P < 0.05) at Post and lower levels of AOPP (-47%, P < 0.01) at Post + 1 were measured in HCE versus HCS. Glutathione peroxidase (+31%, P < 0.01) increased in both groups at Post + 1. Similar erythropoietin kinetics was noted in both groups with an increase at Dl (+143%, P < 0.01), a return to baseline at Post, and a decrease at Post + 1 (-56%, P < 0.05). Conclusions: These data provide evidence that 2 h of moderate daily exercise training can attenuate the oxidative stress induced by continuous hypoxic exposure. [ABSTRACT FROM AUTHOR]

The study examined the effects of a 10-day normobaric hypoxic confinement on the finger and toe temperature responses to local cooling. Eight male lowlanders underwent a normoxic (NC) and, in a separate occasion, a normobaric hypoxic confinement (HC; FO 2 : 0.154; simulated altitude ~3400 m). Before and after each confinement, subjects immersed for 30 min their right hand and, in a different session, their right foot in 8 °C water, while breathing either room air (AIR) or a hypoxic gas mixture (HYPO). Throughout the cold-water immersion tests, thermal responses were monitored with thermocouples on fingers and toes. Neither confinement influenced thermal responses in the fingers during the AIR or HYPO test. In the foot, by contrast, HC, but not NC, reduced the average toe temperature by ~1.5 °C (p=0.03), both during the AIR and HYPO test. We therefore conclude that a 10-day confinement to normobaric hypoxia per se augments cold-induced vasoconstriction in the toes, but not in the fingers. The mechanism underlying this dissimilarity remains to be established. [ABSTRACT FROM AUTHOR]

Bone losses are common as a consequence of unloading and also in patients with chronic obstructive pulmonary disease (COPD). Although hypoxia has been implicated as an important factor to drive bone loss, its interaction with unloading remains unresolved. The objective therefore was to assess whether human bone loss caused by unloading could be aggravated by chronic hypoxia. In a cross-over designed study, 14 healthy young men underwent 21-day interventions of bed rest in normoxia (NBR), bed rest in hypoxia (HBR), and hypoxic ambulatory confinement (HAmb). Hypoxic conditions were equivalent to 4000 m altitude. Bone metabolism (NTX, P1NP, sclerostin, DKK1) and phospho-calcic homeostasis (calcium and phosphate serum levels and urinary excretion, PTH) were assessed from regular blood samples and 24-hour urine collections, and tibia and femur bone mineral content was assessed by peripheral quantitative computed tomography (pQCT). Urinary NTX excretion increased ( P < 0.001) to a similar extent in NBR and HBR ( P = 0.69) and P1NP serum levels decreased ( P = 0.0035) with likewise no difference between NBR and HBR ( P = 0.88). Serum total calcium was increased during bed rest by 0.059 (day D05, SE 0.05 mM) to 0.091 mM (day D21, P < 0.001), with no additional effect by hypoxia during bed rest ( P = 0.199). HAmb led, at least temporally, to increased total serum calcium, to reduced serum phosphate, and to reduced phosphate and calcium excretion. In conclusion, hypoxia did not aggravate bed rest-induced bone resorption, but led to changes in phospho-calcic homeostasis likely caused by hyperventilation. Whether hyperventilation could have mitigated the effects of hypoxia in this study remains to be established. [ABSTRACT FROM AUTHOR]

The post-exercise emotional response is mainly dependent on the intensity of the exercise performed; moderate exercise causes positive feelings, whereas maximal exercise may prompt negative affects. Acute hypoxia impairs peak O 2 uptake ( V ̇ O 2 peak ), resulting in a shift to a lower absolute intensity at the point of exhaustion. Hence, the purpose of the study was to examine whether a severe hypoxic stimulus would influence the post-exercise affective state in healthy lowlanders performing an incremental exercise to exhaustion. Thirty-six male lowlanders performed, in a counter-balanced order and separated by a 48-h interval, two incremental exercise trials to exhaustion to determine their V ̇ O 2 peak , while they were breathing either room air (AIR; FiO 2 : 0.21), or a hypoxic gas mixture (HYPO; FiO 2 : 0.12). Before and immediately after each trial, subjects were requested to complete two questionnaires, based on how they felt at that particular moment: ( i ) the Profile of Mood States-Short Form, and ( ii ) the Activation Deactivation Adjective Check List. During the post-exercise phase, they also completed the Multidimensional Fatigue Inventory. V ̇ O 2 peak was significantly lower in the HYPO than the AIR trial (~ 15%; p < 0.001). Still, after the HYPO trial, energy, calmness and motivation were markedly impaired, whereas tension, confusion, and perception of physical and general fatigue were exaggerated ( p ≤ 0.05). Accordingly, present findings suggest that an incremental exercise to exhaustion performed in severe hypoxia provokes negative post-exercise emotions, induces higher levels of perceived fatigue and decreases motivation; the affective responses coincide with the comparatively lower V ̇ O 2 peak than that achieved in normoxic conditions. [ABSTRACT FROM AUTHOR]

Keramidas, Michail E., Stylianos N. Kounalakis, Ola Eiken, and Igor B. Mekjavic. Effects of two short-term, intermittent hypoxic training protocols on the finger temperature response to local cold stress. High Alt Med Biol 16:251-260, 2015.-The study examined the effects of two short-term, intermittent hypoxic training protocols, namely exercising in hypoxia and living in normoxia (LL-TH; n=8), and exercising in normoxia preceded by a series of brief intermittent hypoxic exposures at rest (IHE+NOR; n=8), on the finger temperature response during a sea-level local cold test. In addition, a normoxic group was assigned as a control group (NOR; n=8). All groups trained on a cycle-ergometer 1 h/day, 5 days/week for 4 weeks at 50% of peak power output. Pre, post, and 11 days after the last training session, subjects immersed their right hand for 30 min in 8°C water. In the NOR group, the average finger temperature was higher in the post (+2.1°C) and 11-day after (+2.6°C) tests than in the pre-test ( p≤0.001). Conversely, the fingers were significantly colder immediately after both hypoxic protocols (LL-TH: −1.1°C, IHE+NOR: −1.8°C; p=0.01). The temperature responses returned to the pre-training level 11 days after the hypoxic interventions. Ergo, present findings suggest that short-term intermittent hypoxic training impairs sea-level local cold tolerance; yet, the hypoxic-induced adverse responses seem to be reversible within a period of 11 days. [ABSTRACT FROM AUTHOR]

The aim was to assess the effect of a 10-day exposure to the environmental stressors anticipated in future lunar habitats on indices of psychological strain. In addition to the reduced gravity of the Moon, future habitats on the Moon will likely maintain a hypobaric hypoxic environment. The hypobaric environment will eliminate the need for long decompression profiles prior to each extra-vehicular activity. We investigated the indices of psychological strain during three 10-day conditions, designed to assess the separate and combined effects of inactivity/unloading and normobaric hypoxia on several physiological systems. Eleven male participants underwent three 10-day campaigns in a randomised manner: 1) normobaric normoxic bed rest (NBR), 2) normobaric hypoxic bed rest (HBR) and 3) normobaric hypoxic ambulatory confinement (HAMB). The most negative psychological profile appeared on day 10 of the HBR and HAMB (hypoxic) conditions. Concomitantly, a decrease in positive emotions was observed from baseline to day 10 of the HBR and NBR conditions. Thus, confinement in a hypoxic environment seems to exert a negative effect on an individual's psychological mood. [ABSTRACT FROM AUTHOR]