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SummaryPotassium bicarbonate was administrated to an already alkaline diet in seven male subjects during a 21-day bed rest study and was able to decrease bed rest induced increased calcium excretion but failed to prevent bed rest-induced bone resorption.IntroductionSupplementation with alkali salts appears to positively influence calcium and bone metabolism and, thus, could be a countermeasure for population groups with an increased risk for bone loss. However, the extent to which alkalization counteracts acid-induced bone resorption or whether it merely has a calcium and bone maintenance effect is still not completely understood. In the present study, we hypothesized that additional alkalization to an already alkaline diet can further counteract bed rest-induced bone loss.MethodsSeven healthy male subjects completed two parts of a crossover designed 21-day bed rest study: bed rest only (control) and bed rest supplemented with 90 mmol potassium bicarbonate (KHCO3) daily.ResultsKHCO3supplementation during bed rest resulted in a more alkaline status compared to the control intervention, demonstrated by the increase in pH and buffer capacity level (pH p = 0.023, HCO3p = 0.02, ABE p = 0.03). Urinary calcium excretion was decreased during KHCO3 supplementation (control 6.05 ± 2.74 mmol/24 h; KHCO3 4.87 ± 2.21 mmol/24 h, p = 0.03); whereas, bone formation was not affected by additional alkalization (bAP p = 0.58; PINP p = 0.60). Bone resorption marker UCTX tended to be lower during alkaline supplementation (UCTX p = 0.16).ConclusionsThe more alkaline acid-base status, achieved by KHCO3 supplementation, reduced renal calcium excretion during bed rest, but was not able to prevent immobilization-induced bone resorption. However, advantages of alkaline salts on bone metabolism may occur under acidic metabolic conditions or with respect to the positive effect of reduced calcium excretion within a longer time frame.Trial registrationTrial number: NCT01509456

Objectives The present study evaluated the effectiveness of a short and versatile daily exercise regime, named locomotion replacement training (LRT), to maintain muscle size, isometric strength, power, and endurance capacity of the leg muscles following 5 days of head-down tilt (HDT) bed rest. Methods 10 male subjects (age 29.4 ± 5.9 years; height 178.8 ± 3.7 cm; body mass 77.7 ± 4.1 kg) performed, in random order, 5 days of 6° head-down tilt bed rest (BR) with no exercise (CON), or BR with daily 25 min of upright standing (STA) or LRT. Results Knee extensor and plantar flexor cross-sectional area (CSA) were reduced by 2–3 % following bed rest ( P  < 0.01) for CON and STA, yet maintained for LRT. Knee extensor isometric strength (MVC) decreased by 8 % for CON ( P  < 0.05), was maintained for STA, and increased with 12 % for LRT ( P  < 0.05). Plantar flexor MVC remained unaltered during the study. Maximum jump height declined (~1.5 cm) for all conditions ( P  < 0.001). Neural activation and knee extensor fatigability did not change with bed rest. Bone resorption increased during BR and neither LRT nor STA was able to prevent or attenuate this increase. Conclusion LRT was adequate to maintain muscle size and to even increase knee extensor MVC, but not muscle power and bone integrity, which likely requires more intense and/or longer exercise regimes. However, with only some variables showing significant changes, we conclude that 5 days of BR is an inadequate approach for countermeasure assessments.

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.

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.

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.

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.

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.

Proper dietary intake is important for masters athletes because of the physiological changes that occur with aging and the unique nutritional needs when competing at high levels. We evaluated the dietary intake of masters athletes competing at the World Masters Athletics Championships (outdoor games, Tampere, Finland, 2022, and indoor games, Torun, Poland, 2023). A total of 43 athletes (16 females and 27 males, mean age 59.2 ± 10.3 y, height 168 ± 8 cm, and body mass 62.3 ± 10.8 kg) participating in endurance (n = 21), sprint (n = 16), jumping (2), multi-component (e.g., decathlon; n = 3), and throwing (n = 1) events provided 24 h dietary recalls while participating in the games. Carbohydrate intake was below the recommended levels for endurance athletes. Protein intake was below the recommended levels for masters athletes, except for female athletes involved in power events (i.e., sprinters and jumpers). Other nutrient intakes that were below the recommended levels included vitamins D and E, calcium, potassium, vitamin A (except for female endurance athletes), folate (except for female power athletes), vitamin C for female endurance athletes, vitamin K and fiber for males, and zinc for endurance athletes. We conclude that while competing at world championships, many athletes are not consuming the recommended levels of carbohydrates, protein, and micronutrients. Athletes attending these games would benefit from increased nutritional support.