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Adolescence is a fundamental period for female athletes to develop athletic performance, mitigate injury risk, and gain collegiate sport scholarships, but there is also a high incidence of sport-related injuries. Physical profiling and athlete screening can support the individualisation of training programmes; however, there is a lack of data pertaining to the reliability of athletic performance and injury surrogate measures in adolescent female athletes. The aim of this study was to quantify the between-session reliability of an athletic performance and injury mitigation testing battery in female adolescent athletes. A total of 31 post-peak height velocity (PHV) (3.00 ± 0.82 years) female athletes (age: 16.20 ± 1.20 years; standing height: 166.00 ± 6.00 cm; mass: 65.5 ± 10.70 kg) from various sports (track and field = 1; lacrosse = 2; basketball = 2; soccer = 3; softball = 11; volleyball = 12) completed two sessions of a multicomponent testing battery 48 h to 1 week apart including the assessment of 33 measures addressing lower-limb isometric strength, eccentric strength, reactive strength, linear sprint and change of direction speed, and lower limb control. Of the 33 measures, between sessions, 29 had a high to nearly perfect intraclass correlation coefficient (ICC) (0.508–0.979), and 26 measures were not statistically significantly different between sessions (p ≤ 0.05). All measures demonstrated low to acceptable coefficient variation (CV%) (0.61–14.70%). The testing battery used can be utilised for recruitment and longitudinal monitoring within sports organisations for female adolescent athletes. [ABSTRACT FROM AUTHOR]

The International Olympic Committee (IOC) recently published a framework on fairness, inclusion, and nondiscrimination on the basis of gender identity and sex variations. Although we appreciate the IOC's recognition of the role of sports science and medicine in policy development, we disagree with the assertion that the IOC framework is consistent with existing scientific and medical evidence and question its recommendations for implementation. Testosterone exposure during male development results in physical differences between male and female bodies; this process underpins male athletic advantage in muscle mass, strength and power, and endurance and aerobic capacity. The IOC's "no presumption of advantage" principle disregards this reality. Studies show that transgender women (male‐born individuals who identify as women) with suppressed testosterone retain muscle mass, strength, and other physical advantages compared to females; male performance advantage cannot be eliminated with testosterone suppression. The IOC's concept of "meaningful competition" is flawed because fairness of category does not hinge on closely matched performances. The female category ensures fair competition for female athletes by excluding male advantages. Case‐by‐case testing for transgender women may lead to stigmatization and cannot be robustly managed in practice. We argue that eligibility criteria for female competition must consider male development rather than relying on current testosterone levels. Female athletes should be recognized as the key stakeholders in the consultation and decision‐making processes. We urge the IOC to reevaluate the recommendations of their Framework to include a comprehensive understanding of the biological advantages of male development to ensure fairness and safety in female sports. [ABSTRACT FROM AUTHOR]

Purpose: Genetic polymorphisms have been associated with the adaptation to training in maximal oxygen uptake ( V ˙ O 2 max). However, the genotype distribution of selected polymorphisms in athletic cohorts is unknown, with their influence on performance characteristics also undetermined. This study investigated whether the genotype distributions of 3 polymorphisms previously associated with V ˙ O 2 max training adaptation are associated with elite athlete status and performance characteristics in runners and rugby athletes, competitors for whom aerobic metabolism is important. Methods: Genomic DNA was collected from 732 men including 165 long-distance runners, 212 elite rugby union athletes, and 355 nonathletes. Genotype and allele frequencies of PRDM1 rs10499043 C/T, GRIN3A rs1535628 G/A, and KCNH8 rs4973706 T/C were compared between athletes and nonathletes. Personal-best marathon times in runners, as well as in-game performance variables and playing position, of rugby athletes were analyzed according to genotype. Results: Runners with PRDM1 T alleles recorded marathon times ∼3 minutes faster than CC homozygotes (02:27:55 [00:07:32] h vs 02:31:03 [00:08:24] h, P =.023). Rugby athletes had 1.57 times greater odds of possessing the KCNH8 TT genotype than nonathletes (65.5% vs 54.7%, χ2 = 6.494, P =.013). No other associations were identified. Conclusions: This study is the first to demonstrate that polymorphisms previously associated with V ˙ O 2 max training adaptations in nonathletes are also associated with marathon performance (PRDM1) and elite rugby union status (KCNH8). The genotypes and alleles previously associated with superior endurance-training adaptation appear to be advantageous in long-distance running and achieving elite status in rugby union. [ABSTRACT FROM AUTHOR]

Part 1 of this genetic association series highlighted several genetic variants independently associated with elite status in rugby. However, it is highly likely that the genetic influence on elite status is polygenic due to the interaction of multiple genes. Therefore, the aim of the present study was to investigate whether polygenic profiles of elite rugby athletes differed from non-athletes utilising 13 genetic polymorphisms previously associated with tendon/ligament injury. Total genotype score (TGS) was calculated and multifactor dimensionality reduction (MDR) was used to calculate SNP-SNP epistasis interactions. Based on our elite rugby data from Part 1, mean TGS was significantly higher in elite rugby athletes (52.1 ± 10.7) than non-athletes (48.7 ± 10.8). There were more elite rugby athletes (54%) within the upper TGS quartile, and fewer (46%) within the lower quartile, compared to non-athletes (31% and 69%, respectively; P = 5·10−5), and the TGS was able to distinguish between elite rugby athletes and non-athletes (area under the curve = 0.59; 95% confidence interval 0.55-0.63; P = 9·10−7). Furthermore, MDR identified a three-SNP model of COL5A1 rs12722, COL5A1 rs3196378 and MIR608 rs4919510 that was best able to predict elite athlete status, with a greater frequency of the CC-CC-CC genotype combination in elite rugby athletes (9.8%) than non-athletes (5.3%). We propose that elite rugby athletes possess "preferable" musculoskeletal soft-tissue injury-associated polygenic profiles that have helped them achieve success in the high injury risk environment of rugby. These data may, in future, have implications for the individual management of musculoskeletal soft-tissue injury. Highlights Elite rugby athletes have preferable polygenic profiles to non-athletes in terms of genetic variants previously associated with musculoskeletal soft-tissue injury. The total genotype score was able to distinguish between elite rugby athletes and non-athletes. COL5A1 rs12722, COL5A1 rs3196378 and MIR608 rs4919510 produced the best model for predicting elite athlete status. We propose that elite rugby athletes may have an inherited advantage to achieving elite status due to an increased resistance to soft-tissue injury. [ABSTRACT FROM AUTHOR]

There is growing evidence of genetic contributions to tendon and ligament pathologies. Given the high incidence and severity of tendon and ligament injuries in elite rugby, we studied whether 13 gene polymorphisms previously associated with tendon/ligament injury were associated with elite athlete status. Participants from the RugbyGene project were 663 elite Caucasian male rugby athletes (RA) (mean (standard deviation) height 1.85 (0.07) m, mass 101 (12) kg, age 29 (7) yr), including 558 rugby union athletes (RU) and 105 rugby league athletes. Non-athletes (NA) were 909 Caucasian men and women (56% female; height 1.70 (0.10) m, mass 72 (13) kg, age 41 (23) yr). Genotypes were determined using TaqMan probes and groups compared using Χ2 and odds ratio (OR). COLGALT1 rs8090 AA genotype was more frequent in RA (27%) than NA (23%; P = 0.006). COL3A1 rs1800255 A allele was more frequent in RA (26%) than NA (23%) due to a greater frequency of GA genotype (39% vs 33%). For MIR608 rs4919510, RA had 1.7 times the odds of carrying the CC genotype compared to NA. MMP3 rs591058 TT genotype was less common in RA (25.1%) than NA (31.2%; P < 0.04). For NID1 rs4660148, RA had 1.6 times the odds of carrying the TT genotype compared to NA. It appears that elite rugby athletes have an inherited advantage that contributes to their elite status, possibly via resistance to soft tissue injury. These data may, in future, assist personalised management of injury risk amongst athletes. Highlights The elite rugby athletes we studied had differing genetic characteristics to non-athletes regarding genetic variants previously associated with soft-tissue injury risk. COLGALT1 rs8090, COL3A1 rs1800255, MIR608 rs4919510, MMP3 rs591058 and NID1 rs4660148 were all associated with elite status in rugby. We propose that elite rugby athletes might possess an inherited resistance to soft tissue injury, which has enabled them to achieve elite status despite exposure to the high-risk environment of elite rugby. [ABSTRACT FROM AUTHOR]

Dines, HR, Nixon, J, Lockey, SJ, Herbert, AJ, Kipps, C, Pedlar, CR, Day, SH, Heffernan, SM, Antrobus, MR, Brazier, J, Erskine, RM, Stebbings, GK, Hall, ECR, and Williams, AG. Collagen gene polymorphisms previously associated with resistance to soft-tissue injury are more common in competitive runners than nonathletes. J Strength Cond Res 37(4): 799–805, 2023—Single-nucleotide polymorphisms (SNPs) of collagen genes have been associated with soft-tissue injury and running performance. However, their combined contribution to running performance is unknown. We investigated the association of 2 collagen gene SNPs with athlete status and performance in 1,429 Caucasian subjects, including 597 competitive runners (354 men and 243 women) and 832 nonathletes (490 men and 342 women). Genotyping for COL1A1 rs1800012 (C > A) and COL5A1 rs12722 (C > T) SNPs was performed by a real-time polymerase chain reaction. The numbers of "injury-resistant" alleles from each SNP, based on previous literature (rs1800012 A allele and rs12722 C allele), were combined as an injury-resistance score (RScore, 0–4; higher scores indicate injury resistance). Genotype frequencies, individually and combined as an RScore, were compared between cohorts and investigated for associations with performance using official race times. Runners had 1.34 times greater odds of being rs12722 CC homozygotes than nonathletes (19.7% vs. 15.5%, p = 0.020) with no difference in the rs1800012 genotype distribution (p = 0.659). Fewer runners had an RScore 0 of (18.5% vs. 24.7%) and more had an RScore of 4 (0.6% vs. 0.3%) than nonathletes (p < 0.001). Competitive performance was not associated with the COL1A1 genotype (p = 0.933), COL5A1 genotype (p = 0.613), or RScore (p = 0.477). Although not associated directly with running performance among competitive runners, a higher combined frequency of injury-resistant COL1A1 rs1800012 A and COL5A1 rs12722 C alleles in competitive runners than nonathletes suggests these SNPs may be advantageous through a mechanism that supports, but does not directly enhance, running performance. [ABSTRACT FROM AUTHOR]

Background: Eumenorrheic women experience cyclic variations in sex hormones attributed to the menstrual cycle (MC) which can impact anterior cruciate ligament (ACL) properties, knee laxity, and neuromuscular function. This systematic review aimed to examine the effects of the MC on ACL neuromuscular and biomechanical injury risk surrogates during dynamic tasks, to establish whether a particular MC phase predisposes women to greater ACL injury risk. Methods: PubMed, Medline, SPORTDiscus, and Web of Science were searched (May-July 2021) for studies that investigated the effects of the MC on ACL neuromuscular and biomechanical injury risk surrogates. Inclusion criteria were: 1) injury-free women (18–40 years); 2) verified MC phases via biochemical analysis and/or ovulation kits; 3) examined neuromuscular and/or biomechanical injury risk surrogates during dynamic tasks; 4) compared ≥1 outcome measure across ≥2 defined MC phases. Results: Seven of 418 articles were included. Four studies reported no significant differences in ACL injury risk surrogates between MC phases. Two studies showed evidence the mid-luteal phase may predispose women to greater risk of non-contact ACL injury. Three studies reported knee laxity fluctuated across the MC; two of which demonstrated MC attributed changes in knee laxity were associated with changes in knee joint loading (KJL). Study quality (Modified Downs and Black Checklist score: 7–9) and quality of evidence were low to very low (Grading of Recommendations Assessment Development and Evaluation: very low). Conclusion: It is inconclusive whether a particular MC phase predisposes women to greater non-contact ACL injury risk based on neuromuscular and biomechanical surrogates. Practitioners should be cautious manipulating their physical preparation, injury mitigation, and screening practises based on current evidence. Although variable (i.e., magnitude and direction), MC attributed changes in knee laxity were associated with changes in potentially hazardous KJLs. Monitoring knee laxity could therefore be a viable strategy to infer possible ACL injury risk. [ABSTRACT FROM AUTHOR]

Background: The aim of the study was to provide an isotemporal substitution model to predict how changes in physical behavior may affect the cardiovascular parameters (CVPs) of older adults. Methods: Participants wore a thigh-mounted accelerometer for 7 days. Phenotype of the carotid, brachial, and popliteal artery was conducted using ultrasound. Isotemporal substitution was used to simulate the degree to which replacing 1 hour of physical behavior with another would affect CVP. Results: Substitution of sedentary behavior with Standing and sporadic moderate- to vigorous-intensity physical activity (MVPA accumulated in bouts <10 min) would reduce resting heart rate [-6.20 beats per minute (-12.1 to -0.22) and -3.72 beats per minute (-7.01 to -0.44), respectively]. Substitution of sedentary behavior with light-intensity physical activity would reduce carotid artery diameter [-0.54 mm (-1.00 to -0.07)]. Substitution of Standing with sporadic MVPA would increase popliteal artery diameter [1.31 mm (0.11 to 2.51)]. Conclusions: Our modeling suggests that an accumulation of MVPA bouts that are shorter than the recommended 10-minute minimum may still improve CVP, with lower intensity physical activity also influencing CVP. Our findings are a promising avenue for lifestyle interventions in older adults to reduce the aging effects on CVP for those who cannot engage or sustain sufficient MVPA. [ABSTRACT FROM AUTHOR]

Muscular dystrophy (MD) is an umbrella term for muscle wasting conditions, for which longitudinal changes in function and body composition are well established in children with Duchenne (DMD), however, changes in adults with DMD and Beckers (BMD), respectively, remain poorly reported. This study aims to assess 12-month changes in lower-limb strength, muscle size, body composition and physical activity in adults with Muscular Dystrophy (MD). Adult males with Duchenne MD (DMD; N = 15) and Beckers MD (BMD; N = 12) were assessed at baseline and 12-months for body composition (Body fat and lean body mass (LBM)), Isometric maximal voluntary contraction (Knee-Extension (KEMVC) and Plantar-Flexion (PFMVC)) and physical activity (tri-axial accelerometry). 12-Month change in strength was found as −19% (PFMVC) and −14% (KEMVC) in DMD. 12-Month change in strength in BMD, although non-significant, was explained by physical activity (R2=0.532–0.585). Changes in LBM (DMD) and body fat (BMD) were both masked by non-significant changes in body mass. 12-Month changes in adults with DMD appear consistent with paediatric populations. Physical activity appears important for muscle function maintenance. Specific monitoring of body composition, and potential co-morbidities, within adults with MD is highlighted. Quantitative muscle strength assessment shows progressive muscle weakness in adults with Duchenne Muscular Dystrophy is comparable to paediatric reports (−14 to −19%). Physical activity should be encouraged in adults with Beckers Muscular Dystrophy, anything appears better than nothing. Body composition, rather than body mass, should be monitored closely to identify any increase in body fat. [ABSTRACT FROM AUTHOR]

Exercise-induced muscle damage (EIMD) is associated with transient reductions in strength and athletic performance. Muscle microvascular damage and disruption of blood flow are believed to be among the causes. Previous researchers reported modulations in muscle blood flow, oxygenation, and strength with vibration therapy (VT). To observe whether local VT alleviated the impairments and hemodynamic changes associated with EIMD. Controlled laboratory study. Laboratory and public gymnasium. A total of 10 healthy participants (6 men and 4 women; age = 38 ± 15 years; height = 1.72 ± 0.48 m; mass = 72.0 ± 10.4 kg) were randomized into experimental (VT) and control groups. Both groups performed 10 sets of 10 eccentric wrist flexions at 70% of their 1-repetition maximum to induce muscle damage. Subsequent assessment of flexor carpus ulnaris muscle oxygen saturation and wrist-flexor strength occurred at 1, 24, and 48 hours postexercise. The experimental group underwent 10 minutes of local VT (45 Hz) starting 1 hour postexercise and applied twice daily (separated by 8 hours) for 48 hours during habitual waking hours. The control group received no local VT. Resting muscle oxygen saturation (SmO2), grip strength, and muscle oxygen desaturation and resaturation rates. No difference in SmO2 resaturation was evident over time (P >.05), but the VT group had a greater resaturation rate than the control group at 1 hour (P =.007, d = 2.6), 24 hours (P =.001, d = 3.1), and 48 hours (P =.035, d = 1.7) post-EIMD. No difference in grip strength was observed pre-EIMD, but the VT group demonstrated greater strength at 1 hour (P =.004), 24 hours (P =.031), and 48 hours (P =.021) post-EIMD than did the control group. Local VT successfully attenuated the effects of EIMD and increased SmO2 resaturation in flexor carpus ulnaris muscles. Including local VT as part of a recovery protocol post-EIMD could be beneficial for rehabilitation and strength training purposes. [ABSTRACT FROM AUTHOR]

Skeletal muscle echo intensity (EI) is affected by ageing and physical activity; however, the effects of nutrition are less understood. The aim of this study was to explore whether habitual nutrient intake may be associated with ultrasound-derived EI. Partial least squares regression (PLSR) models were trained on an initial sample (n=100, M=45; F=55; 38±15 years) to predict EI of two quadriceps muscles from 19 variables, using the 'jack-knife' function within the 'pls' package (RStudio), which was then tested in an additional dataset (n= 30, M=13; F=17; 38±16 years). EI was determined using B-mode ultrasonography of the rectus femoris (RF) and vastus lateralis (VL) and nutritional intake determined via three-day weighed food diaries. Mean daily intake of specific nutrients were included as predictor variables with age, sex and self-reported physical activity. PLSR training model 1 explained ~52% and model 2 ~46% of the variance in RF and VL EI, respectively. Model 1 also explained ~35% and model 2 ~30% of the variance in RF and VL EI in the additional testing dataset. Age and biological sex were associated with EI in both models (P<0.025). Dietary protein (RF: β=-7.617,VL: β=-7.480), and selenium (RF: β=-7.144,VL: β=-4.775) were associated with EI in both muscles (P<0.05), whereas fibre intake (RF: β=-5.215) was associated with RF EI only and omega-3 fatty acids (n-3/ω-3 FAs, RF: β=3.145) with VL EI only (P<0.05). Therefore, absolute protein, selenium, fibre and n-3 FAs may be associated with skeletal muscle EI, although further mechanistic work is required before claiming causal inference.