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The impact of effective exercise against bone loss during experimental bed rest appears to be associated with increases in bone formation rather than reductions of bone resorption. Sclerostin and dickkopf-1 are important inhibitors of osteoblast activity. We hypothesized that exercise in bed rest would prevent increases in sclerostin and dickkopf-1. Twenty-four male subjects performed resistive vibration exercise (RVE; n  = 7), resistive exercise only (RE; n  = 8), or no exercise (control n  = 9) during 60 days of bed rest (2nd Berlin BedRest Study). We measured serum levels of BAP, CTX-I, iPTH, calcium, sclerostin, and dickkopf-1 at 16 time-points during and up to 1 year after bed rest. In inactive control, after an initial increase in both BAP and CTX-I, sclerostin increased. BAP then returned to baseline levels, and CTX-I continued to increase. In RVE and RE, BAP increased more than control in bed rest ( p  ≤ 0.029). Increases of CTX-I in RE and RVE did not differ significantly to inactive control. RE may have attenuated increases in sclerostin and dickkopf-1, but this was not statistically significant. In RVE there was no evidence for any impact on sclerostin and dickkopf-1 changes. Long-term recovery of bone was also measured and 6–24 months after bed rest, and proximal femur bone mineral content was still greater in RVE than control ( p  = 0.01). The results, while showing that exercise against bone loss in experimental bed rest results in greater bone formation, could not provide evidence that exercise impeded the rise in serum sclerostin and dickkopf-1 levels.

Space agencies are looking for effective and efficient countermeasures for the degrading effects of weightlessness on the human body. The aim of this study was to assess the effects of a novel jump exercise countermeasure during bed rest on vitals, body mass, body composition, and jump performance. 23 male participants (29±6 years, 181±6 cm, 77±7 kg) were confined to a bed rest facility for 90 days: a 15-day ambulatory measurement phase, a 60-day six-degree head-down-tilt bed rest phase (HDT), and a 15-day ambulatory recovery phase. Participants were randomly allocated to the jump training group (JUMP, n = 12) or the control group (CTRL, n = 11). A typical training session consisted of 4x10 countermovement jumps and 2x10 hops in a sledge jump system. The training group had to complete 5-6 sessions per week. Peak force for the reactive hops (3.6±0.4 kN) as well as jump height (35±4 cm) and peak power (3.1±0.2 kW) for the countermovement jumps could be maintained over the 60 days of HDT. Lean body mass decreased in CTRL but not in JUMP (-1.6±1.9 kg and 0±1.0 kg, respectively, interaction effect p = 0.03). Resting heart rate during recovery was significantly increased for CTRL but not for JUMP (interaction effect p<0.001). Participants tolerated the near-daily high-intensity jump training and maintained high peak forces and high power output during 60 days of bed rest. The countermeasure was effective in preserving lean body mass and partly preventing cardiac deconditioning with only several minutes of training per day.

Long-duration spaceflight imposes significant physiological stress on astronauts, including profound alterations in immune function. This study investigated epigenetic changes in immune cells following prolonged orbital spaceflight by analysing histone modifications in CD4+ and CD8+ T-cells from astronauts before, immediately after, and during recovery from spaceflight. Using Cleavage Under Targets and Tagmentation (Cut&Tag) to assess H3K27ac modifications, we identified significant alterations in chromatin accessibility, predominantly involving immune response pathways, gene regulation, and cellular adaptation mechanisms. While some epigenetic changes were transient, others persisted beyond 50 days post-return, suggesting long-term effects. These findings enhance our understanding of immune adaptation to spaceflight and have implications for mitigating spaceflight-associated health risks. Furthermore, they provide valuable insights into immune system regulation under high-stress conditions, potentially informing research on immunodeficiency disorders, cancer epigenetics, and aging-related immune decline on Earth. This study underscores the critical role of epigenetics in long-term space missions and terrestrial health applications.

Abstract Introduction: Long-term sodium balance studies show that sodium can be temporarily stored and released in tissues, mediated by circaseptan rhythms of aldosterone and cortisol. This complicates the reliability of a single 24-h urine collection to estimate individual sodium intake. We investigated whether repeated timed urine collection with and without correction for plasma aldosterone is a more accurate alternative for estimating daily sodium intake. Methods: We conducted a post hoc analysis of a metabolic ward study in which 16 healthy male adults consumed a diet with a fixed sodium content (50 or 200 mmol/day) for 7 days. Each day, urine was collected in 4 intervals (7:00–13:00 h, 13:00–19:00 h, 19:00–23:00 h, and 23:00–07:00 h). Plasma aldosterone was measured at 6:30 h, 12:30 h, and 18:30 h. Sodium intakes were estimated by various formulas using 3 timed urines of day 5–7. Results: During a 200-mmol daily sodium intake, sodium intake estimates based on three repeated timed urine samples and the Toft equation differed 10 [IQR: 3–14], 8 [6–19], 36 [16–49], and 20 [10–43] mmol from the actual intake for intervals 7:00–13:00 h, 13:00–19:00 h, 19:00–23:00 h, 23:00–7:00 h, respectively. These measurements did not significantly differ from a single 24-h urine (20 [12–55] mmol). During a 50-mmol daily sodium intake, repeated timed urine collection performed worse than a single 24-h urine collection. On both diets, correction for plasma aldosterone increased accuracy and sodium intake estimates were significantly more accurate than a single 24-h urine. Conclusion: In a controlled environment, repeated timed urine collection corrected for plasma aldosterone is more accurate than a single 24-h urine collection.

The present study investigated whether neuromuscular electrical stimulation for 20 min twice a day with an electrode placed over the soleus muscle and nutritional supplementation with 19 g of protein rich lupin seeds can reduce the loss in volume and strength of the human calf musculature during long term unloading by wearing an orthotic unloading device. Thirteen healthy male subjects (age of 26.4 ± 3.7 years) wore a Hephaistos orthosis one leg for 60 days during all habitual activities. The leg side was randomly chosen for every subject. Six subjects only wore the orthosis as control group, and 7 subjects additionally received the countermeasure consisting of neuromuscular electrical stimulation of the soleus and lateral gastrocnemius muscles and lupin protein supplementation. Twenty-eight days before and on the penultimate day of the intervention cross-sectional images of the calf muscles were taken by magnetic resonance imaging (controls n = 5), and maximum voluntary torque (controls n = 6) of foot plantar flexion was estimated under isometric (extended knee, 90° knee flexion) and isokinetic conditions (extended knee), respectively. After 58 days of wearing the orthosis the percentage loss of volume in the entire triceps surae muscle of the control subjects (-11.9 ± 4.4%, mean ± standard deviation) was reduced by the countermeasure (-3.5 ± 7.2%, p = 0.032). Wearing the orthosis generally reduced plantar flexion torques values, however, only when testing isometric contraction at 90° knee ankle the countermeasure effected a significantly lower percentage decrease of torque (-9.7 ± 7.2%, mean ± SD) in comparison with controls (-22.3 ± 11.2%, p = 0.032). Unloading of calf musculature by an orthotic device resulted in the expected loss of muscle volume and maximum of plantar flexion torque. Neuromuscular electrical muscle stimulation and lupin protein supplementation could significantly reduce the process of atrophy. ClinicalTrials.gov, identifier NCT02698878.

Astronauts on the International Space Station are exposed to levels of atmospheric carbon dioxide (CO2) above typical terrestrial levels. We explored the possibility that increased levels of ambient CO2 further stimulate bone resorption during bed rest. We report here data from 2 ground-based spaceflight analog studies in which 12 male and 7 female subjects were placed in a strict 6° head-down tilt (HDT) position for either 30 days at 0.5% ambient CO2 or 60 days with nominal environmental exposure to CO2. Bone mineral density (BMD) and bone mineral content (BMC) were determined using dual-energy X-ray absorptiometry (DXA). Blood and urine were collected before and after HDT for biochemical analysis. No change was detected in either BMD or BMC, as expected given the study duration. Bone resorption markers increased after bed rest as expected; however, elevated CO2 had no additive effect. Elevated CO2 did not affect concentrations of minerals in serum and urine. Serum parathyroid hormone and 1,25-dihydroxyvitamin D were both reduced after bed rest, likely secondary to calcium efflux from bone. In summary, exposure to 0.5% CO2 for 30 days did not exacerbate the typical bone resorption response observed after HDT bed rest. Furthermore, results from these strict HDT studies were similar to data from previous bed rest studies, confirming that strict 30–60 days of HDT can be used to evaluate changes in bone metabolism. This is valuable in the continuing effort to develop and refine efficacious countermeasure protocols to mitigate bone loss during spaceflight in low-Earth orbit and beyond.

Aim. We hypothesized that 4 days of normal daily activity after 21 days of experimental bed rest (BR) will not reverse BR induced impaired glucose tolerance. Design. Glucose tolerance of seven male, healthy, untrained test subjects (age: 27.6 (3.3) years (mean (SD)); body mass: 78.6 (6.4) kg; height: 1.81 (0.04) m; VO2 max: 39.5 (5.4) ml/kg body mass/min) was studied. They stayed twice in the metabolic ward (crossover design), 21 days in bed and 7 days before and after BR each. Oral glucose tolerance tests were applied before, on day 21 of BR, and 5 and 14 days after BR. Results. On day 21 of BR, AUC120 min of glucose concentration was increased by 28.8 (5.2)% and AUC120 min of insulin by 35.9 (10.2)% (glucose: P < 0.001 ; insulin: P = 0.02 ). Fourteen days after BR, AUC120 min of serum insulin concentrations returned to pre-bed-rest concentrations ( P = 0.352 ) and AUC120 min of glucose was still higher ( P = 0.038 ). Insulin resistance did not change, but sensitivity index was reduced during BR ( P = 0.005 ). Conclusion. Four days of light physical workload does not compensate inactivity induced impaired glucose tolerance. An individually tailored and intensified training regime is mandatory in patients being in bed rest to get back to normal glucose metabolism in a reasonable time frame.

Immobilization and space flight are causes of disuse osteoporosis. Increasing calcium intake may counteract this disuse-induced bone loss. We conducted two bedrest experiments (crossover design: bedrest versus ambulatory control) in a metabolic ward, studying the effect of 1000 mg/d of calcium intake (study A, length of intervention 14 d) compared with that of a high calcium intake of 2000 mg/d (study B, 6 d) on markers of bone turnover. Both studies were randomized, controlled studies with the subjects staying under well-controlled environmental conditions (study A, 9 male subjects, age 23.6 ± 3.0 y; study B, 8 male subjects, age 25.5 ± 2.9 y). Blood was drawn to analyze serum calcium, parathyroid hormone, procollagen type I C-terminal propeptide, and bone alkaline phosphatase. Urine (24-h) was collected for analysis of calcium, C-terminal telopeptide of collagen type I, and N-terminal telopeptide of collagen type I. In both studies, serum calcium levels remained unchanged. Procollagen type I C-terminal propeptide was lower ( P = 0.03) in the bedrest phase than in the ambulatory phase in study A and tended to be lower ( P = 0.08) in bedrest in study B, whereas bone alkaline phosphatase was not affected in either study. Urinary calcium excretion was greater during bedrest than during the ambulatory phase (study A, P = 0.005; study B, P = 0.002). C-terminal telopeptide of collagen type I excretion was also greater during bedrest in both studies (study A, P < 0.001; study B, P < 0.001). Doubling calcium intake to 2000 mg/d does not prevent increased bone resorption induced by bedrest.

Background Space motion sickness (SMS) is the most relevant medical problem during the first days in microgravity. Studies addressing pathophysiology in space face severe technical challenges and microgravity is frequently simulated using the 6° head-down tilt bed rest test (HDT). Aim We were aiming to test whether SMS could be simulated by HDT, identify related changes in gastrointestinal physiology and test for beneficial effects of exercise interventions. Methods HDT was performed in ten healthy individuals. Each individual was tested in three study campaigns varying by a 30-min daily exercise intervention of either standing, an upright exercise regimen, or no intervention. Gastrointestinal symptoms, stool characteristics, gastric emptying time, and small intestinal transit were assessed using standardized questionnaires, 13 C octanoate breath test, and H 2 lactulose breath test, respectively, before and at day 2 and 5 of HDT. Results Individuals described no or minimal gastrointestinal symptoms during HDT. Gastric emptying remained unchanged relative to baseline data collection (BDC). At day 2 of HDT the H 2 peak of the lactulose test appeared earlier (mean ± standard error for BDC-1, HDT2, HDT5: 198 ± 7, 139 ± 18, 183 ± 10 min; p : 0.040), indicating accelerated small intestinal transit. Furthermore, during HDT, stool was softer and stool mass increased (BDC: 47 ± 6, HDT: 91 ± 12, recovery: 53 ± 8 g/day; p : 0.014), indicating accelerated colonic transit. Exercise interventions had no effect. Conclusion HDT did not induce symptoms of SMS. During HDT, gastric emptying remained unchanged, but small and large intestinal transit was accelerated.

The absence of mechanical loading leads to a prompt increase in bone resorption measured by bone resorption markers. There is high potential that vibration training can positively influence bone metabolism in immobilized subjects, reduce the increase in osteoclastic activity and increase bone formation processes. We investigated whether vibration training at 20 Hz with an amplitude of 2–4 mm influences bone metabolism during immobilization. Eight male subjects (26.4 ± 4.9 years; 78.1 ± 9.5 kg) performed a 14 day bed rest in 6°-head down tilt (HDT). Subjects received vibration training for 2 × 5 min/day or a control intervention without vibration (crossover design). Calcium excretion and bone resorption markers C-telopeptide (CTX) and N-telopeptide (NTX) were analyzed from 24 h urine samples. Bone formation markers, bone alkaline phosphatase (bAP) and procollagen-N propeptide (PINP) were analyzed from fasting blood samples. Our results show an increase in bone resorption very early during HDT bed rest in both interventions (CTX: p  < 0.01; NTX: p  < 0.001). Vibration training did not have any different effect on bone resorption markers (CTX: p  = 0.10; NTX: p  = 0.58), bone formation markers (PINP: p  = 0.21; bAP: p  = 0.12) and calcium excretion ( p  < 0.64) compared to the control condition. Mere vibration training with 20 Hz for 2 × 5 min/day does not prevent increase in bone resorption as measured with the described methods in our short-term HDT bed rest.