This article reviews tendon and ligament injury incidence and severity within elite rugby union and rugby league. Furthermore, it discusses the biological makeup of tendons and ligaments and how genetic variation may influence this and predisposition to injury. Elite rugby has one of the highest reported injury incidences of any professional sport. This is likely due to a combination of well-established injury surveillance systems and the characteristics of the game, whereby high-impact body contact frequently occurs, in addition to the high intensity, multispeed and multidirectional nature of play. Some of the most severe of all these injuries are tendon and ligament/joint (non-bone), and therefore, potentially the most debilitating to a player and playing squad across a season or World Cup competition. The aetiology of these injuries is highly multi-factorial, with a growing body of evidence suggesting that some of the inter-individual variability in injury susceptibility may be due to genetic variation. However, little effort has been devoted to the study of genetic injury traits within rugby athletes. Due to a growing understanding of the molecular characteristics underpinning the aetiology of injury, investigating genetic variation within elite rugby is a viable and worthy proposition. Therefore, we propose several single nucleotide polymorphisms within candidate genes of interest; COL1A1, COL3A1, COL5A1, MIR608, MMP3, TIMP2, VEGFA, NID1 and COLGALT1 warrant further study within elite rugby and other invasion sports.

Elite rugby league and union have some of the highest reported rates of concussion (mild traumatic brain injury) in professional sport due in part to their full-contact high-velocity collision-based nature. Currently, concussions are the most commonly reported match injury during the tackle for both the ball carrier and the tackler (8–28 concussions per 1000 player match hours) and reports exist of reduced cognitive function and long-term health consequences that can end a playing career and produce continued ill health. Concussion is a complex phenotype, influenced by environmental factors and an individual’s genetic predisposition. This article reviews concussion incidence within elite rugby and addresses the biomechanics and pathophysiology of concussion and how genetic predisposition may influence incidence, severity and outcome. Associations have been reported between a variety of genetic variants and traumatic brain injury. However, little effort has been devoted to the study of genetic associations with concussion within elite rugby players. Due to a growing understanding of the molecular characteristics underpinning the pathophysiology of concussion, investigating genetic variation within elite rugby is a viable and worthy proposition. Therefore, we propose from this review that several genetic variants within or near candidate genes of interest, namely APOE, MAPT, IL6R, COMT, SLC6A4, 5-HTTLPR, DRD2, DRD4, ANKK1, BDNF and GRIN2A, warrant further study within elite rugby and other sports involving high-velocity collisions.

Objective: Concussions are common match injuries in elite rugby, and reports exist of reduced cognitive function and long-term health consequences that can interrupt or end a playing career and produce continued ill health. The aim of this study was to investigate the association between elite rugby status and 8 concussion-associated risk polymorphisms. We hypothesized that concussion-associated risk genotypes and alleles would be underrepresented in elite rugby athletes compared with nonathletes. Design: A case–control genetic association study. Setting: Institutional (university). Participants: Elite White male rugby athletes [n = 668, mean (SD) height 1.85 (0.07) m, mass 102 (12) kg, and age 29 (7) years] and 1015 nonathlete White men and women (48% men). Interventions: Genotype was the independent variable, obtained by PCR of genomic DNA using TaqMan probes. Main Outcome Measure: Elite athlete status with groups compared using χ² and odds ratio (OR). Results: The COMT rs4680 Met/Met (AA) genotype, Met allele possession, and Met allele frequency were lower in rugby athletes (24.8%, 74.6%, and 49.7%, respectively) than nonathletes (30.2%, 77.6%, and 54.0%; P < 0.05). The Val/Val (GG) genotype was more common in elite rugby athletes than nonathletes (OR 1.39, 95% confidence interval 1.04-1.86). No other polymorphism was associated with elite athlete status. Conclusions: Elite rugby athlete status is associated with COMT rs4680 genotype that, acting pleiotropically, could affect stress resilience and behavioral traits during competition, concussion risk, and/or recovery from concussion. Consequently, assessing COMT rs4680 genotype might aid future individualized management of concussion risk among athletes.

Due to the high-velocity collision-based nature of elite rugby league and union, the risk of sustaining a concussion is high. Occurrence of and outcomes following a concussion are probably affected by the interaction of multiple genes in a polygenic manner. This study investigated whether suspected concussion-associated polygenic profiles of elite rugby athletes differed from non-athletes and between rugby union forwards and backs. We hypothesised that a total genotype score (TGS) using eight concussion-associated polymorphisms would be higher in elite rugby athletes than non-athletes, indicating selection for protection against incurring or suffering prolonged effects of, concussion in the relatively high-risk environment of competitive rugby. In addition, multifactor dimensionality reduction was used to identify genetic interactions. Contrary to our hypothesis, TGS did not differ between elite rugby athletes and non-athletes (p ≥ 0.065), nor between rugby union forwards and backs (p = 0.668). Accordingly, the TGS could not discriminate between elite rugby athletes and non-athletes (AUC ~0.5), suggesting that, for the eight polymorphisms investigated, elite rugby athletes do not have a more ‘preferable’ concussion-associated polygenic profile than non-athletes. However, the COMT (rs4680) and MAPT (rs10445337) GC allele combination was more common in rugby athletes (31.7%; p < 0.001) and rugby union athletes (31.8%; p < 0.001) than non-athletes (24.5%). Our results thus suggest a genetic interaction between COMT (rs4680) and MAPT (rs10445337) assists rugby athletes in achieving elite status. These findings need exploration vis-à-vis sport-related concussion injury data and could have implications for the management of inter-individual differences in concussion risk.

Background: Concussion is the most common neurological disorder affecting millions of people globally each year. Identifying epigenetic mechanisms influencing concussion incidence, severity and recovery could provide diagnostic and prognostic insight into this injury. Objectives: This systematic review aims to identify the epigenetic mechanisms underpinning concussion. Methods: Seven electronic databases; PubMed, MEDLINE, CINAHL, Cochrane library, SPORTDiscus, Scopus and Web of Science were searched for studies that investigated the epigenetic mechanisms of concussion and its underlying neuropathology. Results: Based on inclusion and exclusion criteria, 772 titles were independently analysed by two of the authors to a final list of 28 studies that totaled 3042 participants. We observed separate associations between sncRNAs, methylation, histone modification and concussion. Overall, 204 small non-coding RNAs were significantly dysregulated between concussed participants and controls or between concussion participants with no postconcussive symptoms and those with post-concussive symptoms. From these, 37 were reported in more than one study and 23 of these were expressed in a consistent direction with at least one further study. Ingenuity pathway analysis identified 10 miRNAs known to regulate 15 genes associated with human neurological pathologies. Two studies found significant changes in global methylation in concussed participants and one study found a decrease in H3K27Me3 in the context of DNA damage and concussion. Conclusions: The review findings suggest that epigenetic mechanisms may play an important role in the pathophysiological mechanisms that could influence outcome, recovery, and potential long-term consequences of concussion for individuals.

Isometric resistance training (IRT) can reduce resting and ambulatory blood pressure (AmBP) yet established exercise methods lack versatility and may present with participation barriers. An isometric training band (ITB) has been identified as an alternative modality; however, its long‐term effects on resting and ambulatory blood pressure (BP) remains unknown. This study assessed the effects of the ITB on resting BP and AmBP following 4 weeks of IRT. Forty‐two normotensive adults (22 male, 20 female; mean ± SD, age 31 ± 14 years, systolic [sBP], 120 ± 5 mmHg, diastolic [dBP], 72 ± 7 mmHg), were randomised to a control (CON), isometric handgrip (IHG) or ITB group. Resting (systolic, diastolic, mean arterial BP and heart rate [HR]) and AmBP (24‐h, daytime and night‐time) were measured pre‐ and post‐4 weeks of supervised IRT (4 x 2‐min contractions at 30% MVC [IHG] or 4 x 2‐min contractions at CR‐10 values equivalent to 30% MVC [ITB]). Resting sBP was reduced for IHG (−4.6 mmHg, p < 0.05) and ITB (−4.5 mmHg, p < 0.05) following 4 weeks of IRT, alongside significant within‐group differences in night‐time sBP for both training groups (ITB −4 mmHg, IHG, −4.7 mmHg). No differences were seen within or between groups for resting dBP, mBP, HR and 24‐h and daytime AmBP ( p > 0.05 across all measures). These findings suggest 4 weeks of IRT using the ITB can elicit reductions in resting BP and night‐time AmBP in normotensives comparable to IHG, indicating the ITB may offer a practical and cost‐effective alternative to established interventions.