Suchergebnisse

Purpose: Few human studies have reported early structural adaptations of bone to weight-bearing exercise, which provide a greater contribution to improved bone strength than increased density. This prospective study examined site- and regional-specific adaptations of the tibia during arduous training in a cohort of male military (infantry) recruits to better understand how bone responds in vivo to mechanical loading. Methods: Tibial bone density and geometry were measured in 90 British Army male recruits (ages 21 + 3 y, height 1.78 ± 0.06 m, body mass 73.9 + 9.8 kg) in weeks 1 (Baseline) and 10 of initial military training. Scans were performed at the 4%, 14%, 38% and 66% sites, measured from the distal end plate, using pQCT (XCT2000L, Stratec Pforzheim, Germany). Customised software (BAMPack, L-3 ATI) was used to examine whole bone cross-section and regional sectors. T-tests determined significant differences between time points (P<0.05). Results: Bone density of trabecular and cortical compartments increased significantly at all measured sites. Bone geometry (cortical area and thickness) and bone strength (i, MMi and BSI) at the diaphyseal sites (38 and 66%) were also significantly higher in week 10. Regional changes in density and geometry were largely observed in the anterior, medial-anterior and anterior-posterior sectors. Calf muscle density and area (66% site) increased significantly at week 10 (P<0.01). Conclusions: In vivo mechanical loading improves bone strength of the human tibia by increased density and periosteal expansion, which varies by site and region of the bone. These changes may occur in response to the nature and distribution of forces originating from bending, torsional and shear stresses of military training. These improvements are observed early in training when the osteogenic stimulus is sufficient, which may be close to the fracture threshold in some individuals.

We examined the relationship between football-specific training and changes in bone structural properties across a 12-week period in 15 male football players aged 16 years (Mean ± 1 SD = 16.6 ± 0.3 years) that belonged to a professional football academy. Tibial scans were performed at 4%, 14% and 38% sites using peripheral quantitative computed tomography immediately before and 12 weeks after increased football-specific training. Training was analysed using GPS to quantify peak speed, average speed, total distance and high-speed distance. Analyses were conducted with bias-corrected and accelerated bootstrapped 95% confidence intervals (BCa 95% CI). There were increases in bone mass at the 4% (mean ∆ = 0.15 g, BCa 95% CI = 0.07, 0.26 g, g = 0.72), 14% (mean ∆ = 0.04 g, BCa 95% CI = 0.02, 0.06 g, g = 1.20), and 38% sites (mean ∆ = 0.03 g, BCa 95% CI = 0.01, 0.05 g, g = 0.61). There were increases in trabecular density (4%), (mean ∆ = 3.57 mg·cm−3, BCa 95% CI = 0.38, 7.05 mg·cm−3, g = 0.53), cortical dentsity (14%) (mean ∆ = 5.08 mg·cm−3, BCa 95% CI = 0.19, 9.92 mg·cm−3, g = 0.49), and cortical density (38%) (mean ∆ = 6.32 mg·cm−3, BCa 95% CI = 4.31, 8.90 mg·cm−3, g = 1.22). Polar stress strain index (mean ∆ = 50.56 mm3, BCa 95% CI = 10.52, 109.95 mm3, g = 0.41), cortical area (mean ∆ = 2.12 mm2, BCa 95% CI = 0.09, 4.37 mm2, g = 0.48) and thickness (mean ∆ = 0.06 mm, BCa 95% CI = 0.01, 0.13 mm, g = 0.45) increased at the 38% site. Correlations revealed positive relationships between total distance and increased cortical density (38%) (r = 0.39, BCa 95% CI = 0.02, 0.66), and between peak speed and increased trabecular density (4%) (r = 0.43, BCa 95% CI = 0.03, 0.73). There were negative correlations between total (r = −0.21, BCa 95% CI = −0.65, −0.12) and high-speed distance (r = −0.29, BCa 95% CI = −0.57, −0.24) with increased polar stress strain index (38%). Results suggest that despite football training relating to increases in bone characteristics in male academy footballers, the specific training variables promoting adaptation over a 12-week period may vary. Further studies conducted over a longer period are required to fully elucidate the time-course of how certain football-specific training characteristics influence bone structural properties.

Abstract
Apolipoprotein ɛ4 (APOE ɛ4) may be a genetic risk factor for reduced bone mineral density (BMD) and muscle function, which could have implications for fall and fracture risk. We examined the association between APOE ɛ4 status and long-term fall- and fracture-related hospitalization risk in older women. A total of 1 276 community-dwelling women from the Perth Longitudinal Study of Aging Women (mean age ± SD = 75.2 ± 2.7 years) were included. At baseline, women underwent APOE genotyping and detailed phenotyping for covariates including prevalent falls and fractures, as well as health and lifestyle factors. The association between APOE ɛ4 and fall-, any fracture-, and hip fracture-related hospitalizations, obtained over 14.5 years from linked health records, was examined using multivariable-adjusted Cox-proportional hazard models. Over 14.5 years, 507 (39.7%) women experienced a fall-related hospitalization and 360 (28.2%) women experienced a fracture-related hospitalization, including 143 (11.2%) attributed to a hip fracture. In multivariable-adjusted models, compared to noncarriers, APOE ɛ4 carriers (n = 297, 23.3%) had greater risk for a fall- (hazard ratio [HR] 1.48, 95% CI: 1.22–1.81), fracture- (HR 1.28, 95% CI: 1.01–1.63), or hip fracture-related hospitalization (HR 1.83, 95% CI: 1.29–2.61). The estimates remained similar when specific fall and fracture risk factors (fear of falling, plasma 25-hydroxyvitamin D, grip strength, timed up-and-go, hip BMD, vitamin K status, prevalent diabetes, HbA1c, cholesterol, and abbreviated mental test score) were added to the multivariable model. In conclusion, APOE ɛ4 is a potential risk factor for fall- and fracture-related hospitalization in community-dwelling older women. Screening for APOE ɛ4 could provide clinicians an opportunity to direct higher-risk individuals to appropriate intervention strategies.

Purpose. To determine vitamin D metabolites and vitamin D receptor (VDR) single-nucleotide polymorphisms (SNPs) relationships with physical performance. Methods. In 1205 men and 322 women (94.8% white Caucasian, 22.0 ± 2.8 years) commencing military training, we measured: serum vitamin D metabolites (25-hydroxyvitamin D (25(OH)D) and 24,25-dihydroxyvitamin D (24,25(OH)2D) by high-performance liquid chromatography tandem mass spectrophotometry, and 1,25-dihydroxyvitamin D (1,25(OH)2D) by immunoassay); VDR SNPs (rs2228570, rs4516035, and rs7139166 by polymerase chain reaction genotyping); and endurance performance by 2.4 km run, muscle strength by maximal dynamic lift, and muscle power by maximal vertical jump. Results. Serum 25(OH)D was negatively associated with 2.4 km run time and positively associated with muscle power (β = –12.0 and 90.1), 1,25(OH)2D was positively associated with run time and negatively associated with strength and muscle power (β = 5.6, –1.06, and –38.4), and 24,25(OH)2D was negatively associated with run time (β = –8.9; P < 0.01), after controlling for age, sex, smoking, alcohol, physical activity, time outdoors, season, and BMI. Vitamin D metabolites (25(OH)D, 1,25(OH)2D, and 24,25(OH)2D) together explained variances of 5.0% in run time, 0.7% in strength, and 0.9% in muscle power (ΔF P < 0.001). All performance measures were superior with low 1,25(OH)2D:24,25(OH)2D ratio (P < 0.05). VDR SNPs were not associated with physical performance (ΔF P ≥ 0.306). Conclusion. Vitamin D metabolites accounted for a small portion of variance in physical performance. Associations between vitamin D metabolites and run time were the most consistent. VDR SNPs explained no variance in performance. Greater conversion of 25(OH)D to 24,25(OH)2D, relative to 1,25(OH)2D (i.e., low 1,25(OH)2D:24,25(OH)2D ratio), was favourable for performance, indicating 24,25(OH)2D may have a role in optimising physical performance.

Military recruits and elite athletes are susceptible to stress fracture injuries. Genetic predisposition has been postulated to have a role in their development. The P2X7 receptor (P2X7R) gene, a key regulator of bone remodelling, is a genetic candidate that may contribute to stress fracture predisposition. The aim of this study is to evaluate the putative contribution of P2X7R to stress fracture injury in two separate cohorts, military personnel and elite athletes. In 210 Israeli Defense Forces (IDF) military conscripts, stress fracture injury was diagnosed (n = 43) based on symptoms and a positive bone scan. In a separate cohort of 518 elite athletes, self-reported medical imaging scan-certified stress fracture injuries were recorded (n = 125). Non-stress fracture controls were identified from these cohorts who had a normal bone scan or no history or symptoms of stress fracture injury. Study participants were genotyped for functional SNPs within the P2X7R gene using proprietary fluorescence-based competitive allele-specific PCR assay. Pearson's chi-squared (χ2) tests, corrected for multiple comparisons, were used to assess associations in genotype frequencies. The variant allele of P2X7R SNP rs3751143 (Glu496Ala—loss of function) was associated with stress fracture injury, whilst the variant allele of rs1718119 (Ala348Thr—gain of function) was associated with a reduced occurrence of stress fracture injury in military conscripts (P < 0.05). The association of the variant allele of rs3751143 with stress fractures was replicated in elite athletes (P < 0.05), whereas the variant allele of rs1718119 was also associated with reduced multiple stress fracture cases in elite athletes (P < 0.05). The association between independent P2X7R polymorphisms with stress fracture prevalence supports the role of a genetic predisposition in the development of stress fracture injury.