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Human extravehicular activity (EVA) is essential to space exploration and involves risk of decompression sickness (DCS). On Earth, the effect of microgravity on physiological systems is simulated in an experimental model where subjects are confined to a 6° head-down bed rest (HDBR). This model was used to investigate various resting and exercise regimen on the formation of venous gas emboli (VGE), an indicator of decompression stress, post-hyperbaric exposure. Eight healthy male subjects participating in a bed rest regimen also took part in this study, which incorporated five different hyperbaric exposure (HE) interventions made before, during and after the HDBR. Interventions i–iv were all made with the subjects lying in 6° HD position. They included (C1) resting control, (C2) knee-bend exercise immediately prior to HE, (T1) HE during the fifth week of the 35-day HDBR period, (C3) supine cycling exercise during the HE. In intervention (C4), subjects remained upright and ambulatory. The HE protocol followed the Royal Navy Table 11 with 100 min spent at 18 m (280 kPa), with decompression stops at 6 m for 5 min, and at 3 m for 15 min. Post-HE, regular precordial Doppler audio measurements were made to evaluate any VGE produced post-dive. VGE were graded according to the Kisman Masurel scale. The number of bubbles produced was low in comparison to previous studies using this profile [Kisman integrated severity score (KISS) ranging from 0–1], and may be because subjects were young, and lay supine during both the HE and the 2 h measurement period post-HE for interventions i–iv. However, the HE during the end of HDBR produced significantly higher maximum bubble grades and KISS score than the supine control conditions (p < 0.01). In contrast to the protective effect of pre-dive exercise on bubble production, a prolonged period of bed rest prior to a HE appears to promote the formation of post-decompression VGE. This is in contrast to the absence of DCS observed during EVA. Whether this is due to a difference between hypo- and hyperbaric decompression stress, or that the HDBR model is a not a good model for decompression sensitivity during microgravity conditions will have to be elucidated in future studies. [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]

Prolonged inactivity, such as bed rest induces several detrimental changes within a short timeframe. Impaired postural balance and responses of trunk muscles to (un)expected perturbations were both shown to be impaired after bed rest. Certain populations (e.g., astronauts) are exposed to hypoxic environment in addition to inactivity, similar to bed rest. While the isolated negative effects of hypoxia on postural balance have been observed before, no study to date has examined the combined effects of hypoxia and bed rest on postural balance or trunk muscle responses. In this study, we examined the effects of 21-day exposure to three conditions: (i) bed rest in hypoxic environment (HBR), (ii) bed rest in normoxic environment (NBR), and (iii) ambulatory hypoxic environment (HAMB). Fourteen healthy male subjects crossed over between conditions in a randomized order, with a 4-month break between conditions to ensure full recovery. Most body sway parameters indicated a similar deterioration of postural balance following both HBR and NBR. Similarly, both anticipatory and reactive responses of the trunk muscles (m. erector spinae and m. multifidus) were impaired after HBR and NBR to a similar degree and mostly unchanged after HAMB. Certain body sway parameters were impaired after HAMB, confirming that hypoxia alone can undermine postural balance. On the other hand, some trunk responses were improved after HAMB. In conclusion, the results of our study confirmed previous findings on negative effects of bed rest, but showed little or no additional effect of hypoxia during bed rest. Physical activity during bed rest is encouraged to preserve neuromuscular functions of the trunk. While the HBR condition in our study resembled conditions during space missions, our results could be relevant to other populations, such as patients with pulmonary diseases exposed to bed rest. [ABSTRACT FROM AUTHOR]

We explored the assembly of intestinal microbiota in healthy male participants during the run-in (5 day) and experimental phases [21-day normoxic bed rest (NBR), hypoxic bedrest (HBR)], and hypoxic ambulation (HAmb) in a strictly controlled laboratory environment, balanced fluid, and dietary intakes, controlled circadian rhythm, microbial ambiental burden, and 24/7 medical surveillance. The fraction of inspired O2 (FiO2) and partial pressure of inspired O2 (PiO2) were 0.209 and 133.1 ± 0.3 mmHg for NBR and 0.141 ± 0.004 and 90.0 ± 0.4 mmHg for both hypoxic variants (HBR and HAmb; ~4,000m simulated altitude), respectively. A number of parameters linked to intestinal transit spanning Bristol Stool Scale, defecation rates, zonulin, α1-antitrypsin, eosinophil derived neurotoxin, bile acids, reducing sugars, short chain fatty acids, total soluble organic carbon, water content, diet composition, and food intake weremeasured (167 variables). The abundance, structure, and diversity of butyrate producing microbial community were assessed using the two primary bacterial butyrate synthesis pathways, butyryl-CoA: acetate CoA-transferase (but) and butyrate kinase (buk) genes. Inactivity negatively affected fecal consistency and in combination with hypoxia aggravated the state of gut inflammation (p < 0.05). In contrast, gut permeability, various metabolic markers, the structure, diversity, and abundance of butyrate producing microbial community were not significantly affected. Rearrangements in the butyrate producing microbial community structure were explained by experimental setup (13.4%), experimentally structured metabolites (12.8%), and gut metabolite-immunological markers (11.9%), with 61.9% remaining unexplained. Many of the measured parameters were found to be correlated and were hence omitted from further analyses. The observed progressive increase in two immunological intestinal markers suggested that the transition from healthy physiological state toward the developed symptoms of low magnitude obesity-related syndromes was primarily driven by the onset of inactivity (lack of exercise in NBR) that were exacerbated by systemic hypoxia (HBR) and significantly alleviated by exercise, despite hypoxia (HAmb). Butyrate producing community in colon exhibited apparent resilience toward short-term modifications in host exercise or hypoxia. Progressive constipation (decreased intestinal motility) and increased local inflammation marker suggest that changes in microbial colonization and metabolism were taking place at the location of small intestine. [ABSTRACT FROM AUTHOR]

Purpose: High G tolerance is based on the capacity to maintain a sufficient level of arterial pressure (AP) during G load; therefore, we hypothesized that subjects with high G tolerance (H group) would have stronger arterial baroreflex responses compared to subjects with low G tolerance (L group). The carotid baroreflex was evaluated using the neck pressure method (NP), which assesses open-loop responses.Methods: The carotid baroreflex was tested in 16 subjects, n = 8 in the H and L group, respectively, in the supine and upright posture. Heart rate and AP were measured.Results: There were no differences between groups in the maximum slopes of the carotid baroreflex curves. However, the H group had a larger systolic and mean AP (SAP, MAP) increase to the initial hypotensive stimuli of the NP sequence in the upright position compared to the L group, 7.5 ± 6.6 vs 2.0 ± 2.4 and 4.1 ± 3.4 vs 1.1 ± 1.1 mmHg for SAP and MAP, respectively. Furthermore, the L group exhibited an increased latency between stimuli and response in AP in the upright compared to supine position, 4.1 ± 1.0 vs 3.1 ± 0.9 and 4.7 ± 1.1 vs 3.6 ± 0.9 s, for SAP and MAP. No differences in chronotropic responses were observed between the groups.Conclusions: It is concluded that the capacity for reflexive vasoconstriction and maintained speed of the vascular baroreflex during orthostatic stress are coupled to a higher relaxed GOR tolerance. [ABSTRACT FROM AUTHOR]

Purpose: This study tested the hypothesis that hypoxia exacerbates reductions in body mass observed during unloading. Methods: To discern the separate and combined effects of simulated microgravity and hypoxia, 11 healthy males underwent three 21-day campaigns in a counterbalanced fashion: (1) normoxic bed rest (NBR; FO = 0.209; PO = 133.1 ± 0.3); (2) hypoxic ambulatory confinement (HAMB; FO = 0.141 ± 0.004; PO = 90.0 ± 0.4; ~4,000 m); and (3) hypoxic bed rest (HBR; FO = 0.141 ± 0.004; PO = 90.0 ± 0.4). The same dietary menu was applied in all campaigns. Targeted energy intakes were estimated individually using the Harris-Benedict equation taking into account whether the subjects were bedridden or ambulatory. Body mass and water balance were assessed throughout the campaigns. Whole body and regional body composition was determined before and after the campaigns using dual-energy X-ray absorptiometry. Before and during the campaigns, indirect calorimetry and visual analogue scores were employed to assess the resting energy expenditure (REE) and perceived appetite sensations, respectively. Results: Energy intakes were lower than targeted in all campaigns (NBR: −5 %; HAMB: −14 %; HBR: −6 %; P < 0.01). Body mass significantly decreased following all campaigns (NBR: −3 %; HAMB: −4 %; HBR: −5 %; P < 0.01). While fat mass was not significantly altered, the whole body fat free mass was reduced (NBR: −4 %; HAMB: −5 %; HBR: −5 %; P < 0.01), secondary to lower limb fat-free mass reduction. Water balance was comparable between the campaigns. No changes were observed in REE and perceived appetite. Conclusions: Exposure to simulated altitude of ~4,000 m does not seem to worsen the whole body mass and fat-free mass reductions or alter resting energy expenditure and appetite during a 21-day simulated microgravity. [ABSTRACT FROM AUTHOR]

Introduction: Future planetary habitats will be hypobaric and hypoxic to reduce the risk of decompression sickness during preparation for extra-vehicular activities. This study was part of a research programme investigating the combined effects of hypoxia and microgravity on physiological systems. Purpose: We tested the hypothesis that hypoxia-induced peripheral vasoconstriction persists at night and is aggravated by bed rest. Since sleep onset has been causally linked to nocturnal vasodilatation, we reasoned that hypoxia-induced vasoconstriction at night may explain sleep disturbances at altitude. Peripheral perfusion alterations as a consequence of bed rest may explain poor sleep quality reported during sojourns on the International Space Station. Methods: Eleven males underwent three 10-day interventions in a randomised order: (1) hypoxic ambulatory confinement; (2) hypoxic bed rest; (3) normoxic bed rest. During each intervention we conducted 22-h monitoring of peripheral perfusion, as reflected by the skin temperature gradient. Measurements were conducted on the first (D 1) and last day (D 10) of each intervention. Results: All interventions resulted in a decrease in daytime toe perfusion from D 1 to D 10. There was no difference in the magnitude of the daytime reduction in toe perfusion between the three interventions. There was a significant vasodilatation of the toes in all interventions by 11 pm. The fingertips remained well perfused throughout. Conclusions: Daytime vasoconstriction induced by hypoxia and/or bed rest is abolished at night, lending further support to the theory that changes in peripheral skin temperature may be functionally linked to sleep onset. [ABSTRACT FROM AUTHOR]

Purpose: The objective was to determine the separate and combined effects of hypoxia and inactivity/unloading on sleep architecture during a 10-day period of confinement. Methods: Ten subjects participated in three 10-day trials in random order: hypoxic ambulatory (HAMB), hypoxic bedrest (HBR), and normoxic bedrest (NBR). During the HAMB and HBR trials, subjects were confined to a hypoxic facility. The hypoxia profile was: simulated altitude of 2,990 m on day 1, 3,380 m on day 2, and 3,881 m on day 3. In the NBR and HBR trials, subjects maintained a horizontal position throughout the confinement period. During each trial, sleep polysomnography was conducted one night prior to (baseline; altitude of facility is 940 m) and on the first (NT1, altitude 2,990 m) and tenth (NT10, altitude 3,881 m) night of the 10-day intervention. Results: Average time in sleep stage 1 decreased from NT1 to NT10 irrespective of trial. Overall incidence and time spent in periodic breathing increased from NT1 to NT10 in both HAMB and HBR. During NT1, both HAMB and HBR reduced slow-wave sleep and increased light sleep, whereas NBR and HBR increased the number of awakenings/night. There were fewer awakenings during HAMB than NBR. Conclusions: Acute exposure to both hypoxia and bedrest (HBR) results in greater sleep fragmentation due to more awakenings attributed to bedrest, and lighter sleep as a result of reduced slow wave sleep caused by the hypoxic environment. [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]

Fighter pilots are commonly recommended strength training as a means of improving the tolerance to withstand high gravitoinertial (G) loads. Previous studies on the effect of short-term strength-training regimens on G-endurance show equivocal results, with a majority of the studies suggesting improved G-endurance. The mechanisms underlying such improvement are unknown. Presumably, any change in G-tolerance induced by physical training habits should be manifest following long-term training. We also reasoned that during repeated straining maneuvers-as during certain G-endurance protocols-the relaxed G-tolerance and the exercise pressure response may play a significant role in maintaining adequate arterial pressure, and hence that different training modalities might alter G-endurance, by altering the exercise pressor response. Three groups of males were studied, long-term (>6 months) endurance-trained (E; n = 17), strength-trained (S; n = 16) and untrained (U; n = 17) individuals. The pressor response was studied during sustained (40 s) isometric knee extensions at 50 % of the maximal contraction level. Relaxed gradual onset-rate G-tolerance was determined. G-tolerance was similar in the E (4.6 ± 0.5 G), S (4.9 ± 0.8 G) and U (4.6 ± 0.8 G) groups. The mean arterial pressure increase during isometric exercise was higher in the S (36 ± 7 mmHg = mean ± SD) and U (35 ± 16 mmHg) groups than in the E group (28 ± 8 mmHg). The results suggest that relaxed G-tolerance is unaffected by physical training habits, and that the training modality affects the magnitude of the exercise pressor response. However, it seems that the response is blunted by endurance training rather than enhanced by strength training. [ABSTRACT FROM AUTHOR]

We hypothesized that exposure to prolonged recumbency (bedrest), and thus reductions of intravascular pressure gradients, increases pressure distension in arteries/arterioles in the legs. Ten subjects underwent 5 wk of horizontal bedrest. Pressure distension was investigated in arteries and arterioles before and after the bedrest, with the subject seated or supine in a hyperbaric chamber with either one arm or a lower leg protruding through a hole in the chamber door. Increased pressure in the vessels of the arm/leg was accomplished by increasing chamber pressure. Vessel diameter and flow were measured in the brachial and posterior tibial arteries using Doppler ultrasonography. Electrical tissue impedance was measured in the test limb. Bedrest increased (P < 0.01) pressure distension threefold in the tibial artery (from 8 ± 7% to 24 ± 11%) and by a third (P < 0.05) in the brachial artery (from 15 ± 9% to 20 ± 10%). The pressure-induced increase in tibial artery flow was more pronounced (P < 0.01) after (50 ± 39 ml/min) than before (13 ± 23 mI/min) bedrest, whereas the brachial artery flow response was unaffected by bedrest. The pressure-induced decrease in tissue impedance in the leg was more pronounced (P < 0.01) after (16 ± 7%) than before (10 ± 6%) bedrest, whereas bedrest did not affect the impedance response in the arm. Thus, withdrawal of the hydrostatic pressure gradients that act along the blood vessels in erect posture markedly increases pressure distension in dependent arteries and arterioles. [ABSTRACT FROM AUTHOR]

Assesses the effects of increased gravity in the head-to-foot direction and anti-G suit pressurization on functional residual capacity, the volume of trapped gas, and ventilation distribution by using inert-gas washout. Use of normalized phase III slope analysis to determine the effects on inter- and intraregional ventilation inhomogeneity.

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]