Suchergebnisse

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.

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.