Explore the vast range of titles available.

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.

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.

OBJECTIVE Epidemioiogical studies show an increased number and impact of serious knee and ankle injuries that occur not only in the field of high level senior soccer but also with dramatically rising figures in youth soccer. There-fore, the German Federal Institute of Sport Science (BISp) promotes a several years lasting interdisciplinary project in close cooperation with the German Soccer Federation (DFB). Injuries of the lower extremities or the proneness to cer-tain knee and/or ankle injuries are thought to be caused by many factors. Therefore the aim of this study was to optimize prevention, rehabilitation and reinjury-prophylaxis of knee and ankle injuries in soccer and get information about the coherences of physical, psychological and biomechanical data concerning injury frequency. METHODS Diagnosis variables include the individual knee and ankle stability, coordinative and psychological abili-ties. Thus, a manifold of research disciplines (biomechanics, training science, psychology, medicine) worked together. Five elite male youth soccer teams (U 17, U 19) of five 1st division clubs (n=157 players) participated at eight diagno-sis sessions throughout two seasons. RESULTS Data of the coordinative abilities showed gradual increase during the observed period as well as increased values of knee stability, whereas maximum isometric strength did not improve. Psychological data suggested that the measured mood status correlated with training intensity and injury in single cases. A multivariate analysis was con-ducted for all variables and for all measurements is in progress. CONCLUSION First results indicated a positive influence of the proprioceptive training concerning knee stability and coordinative ability, even though there seemed to be no structural changes. Psychological data would be very useful for coaches to modify the training process, as well as provide increased awareness of the body perceptions of the soccer players.

While observational studies show an association between 25(OH)vitamin D concentrations and depressive symptoms, intervention studies, which examine the preventive effects of vitamin D supplementation on the development of depression, are lacking. To estimate the role of lowered 25(OH)vitamin D concentrations in the etiology of depressive disorders, we conducted a two-sample Mendelian randomization (MR) study on depression, i.e., “depressive symptoms” (DS, n = 161,460) and “broad depression” (BD, n = 113,769 cases and 208,811 controls). Six single nucleotide polymorphisms (SNPs), which were genome-wide significantly associated with 25(OH)vitamin D concentrations in 79,366 subjects from the SUNLIGHT genome-wide association study (GWAS), were used as an instrumental variable. None of the six SNPs was associated with DS or BD (all p > 0.05). MR analysis revealed no causal effects of 25(OH)vitamin D concentration, either on DS (inverse variance weighted (IVW); b = 0.025, SE = 0.038, p = 0.52) or on BD (IVW; b = 0.020, SE = 0.012, p = 0.10). Sensitivity analyses confirmed that 25(OH)vitamin D concentrations were not significantly associated with DS or BD. The findings from this MR study indicate no causal relationship between vitamin D concentrations and depressive symptoms, or broad depression. Conflicting findings from observational studies might have resulted from residual confounding or reverse causation.

Purpose While observational studies revealed inverse associations between serum vitamin D levels [25(OH)D] and depression, randomized controlled trials (RCT) in children and adolescents are lacking. This RCT examined the effect of an untreated vitamin D deficiency compared to an immediate vitamin D 3 supplementation on depression scores in children and adolescents during standard day and in-patient psychiatric treatment. Methods Patients with vitamin D deficiency [25(OH)D ≤ 30 nmol/l] and at least mild depression [Beck Depression Inventory II (BDI-II) > 13] ( n  = 113) were 1:1 randomized into verum (VG; 2640 IU vitamin D 3 /d) or placebo group (PG) in a double-blind manner. During the intervention period of 28 days, both groups additionally received treatment as usual. BDI-II scores were assessed as primary outcome, DISYPS-II (Diagnostic System for Mental Disorders in Childhood and Adolescence, Self- and Parent Rating) and serum total 25(OH)D were secondary outcomes. Results At admission, 49.3% of the screened patients ( n  = 280) had vitamin D deficiency. Although the intervention led to a higher increase of 25(OH)D levels in the VG than in the PG (treatment difference: + 14 ng/ml; 95% CI 4.86–23.77; p  = 0.003), the change in BDI-II scores did not differ (+ 1.3; 95% CI − 2.22 to 4.81; p  = 0.466). In contrast, DISYPS parental ratings revealed pronounced improvements of depressive symptoms in the VG (− 0.68; 95% CI − 1.23 to − 0.13; p  = 0.016). Conclusion Whereas this study failed to show a vitamin D supplementation effect on self-rated depression in adolescent in- or daycare patients, parents reported less depressive symptoms in VG at the end of our study. Future trials should consider clinician-rated depressive symptoms as primary outcome. Trial registration “German Clinical Trials Register” ( https://www.drks.de ), registration number: DRKS00009758