Author(s): MARTIN, D., STEBBINGS, G., ANTROBUS, M., BRAZIER, J., JACKSON, A., CALLUS, P., HEFFERNAN, S., ERSKINE, R., WILLIAMS, A., Institution: MANCHESTER METROPOLITAN UNIVERSITY INSTITUTE OF SPORT, Country: UNITED KINGDOM, Abstract-ID: 1116

INTRODUCTION:
The heritability of strength- and power-based phenotypes has been investigated extensively, particularly in team sport athletes. However, few attempts have been made to investigate how these traits influence in-game performance, especially in rugby union (RU). RU is an intermittent, contact-intensive sport, made up of distinct playing positions, each with a diverse set of physiological demands. Adenosine monophosphate (AMP) deaminase is a key regulator of skeletal muscle energy metabolism. The C34T (rs17602729) polymorphism brings about a reduction in AMP deaminase activity in skeletal muscle via a C-to-T transition in the AMPD1 gene, converting a glutamine codon into a premature stop codon. It is plausible that reduced AMP deaminase activity would be inhibitory to elite RU performance via premature fatigue. As such, we aimed to identify whether AMPD1 C34T (rs17602729) genotype was associated with elite RU athlete status, playing position, and in-game performance.
METHODS:
The study included 621 male RU athletes and 1029 male and female non-athletes, all European ancestry. Athletes were organised into groups (forwards and backs) and subgroups relating to playing position. All athletes had competed in ≥5 matches in the highest league in a major rugby-playing nation and were thus classified as elite. Real-time PCR using TaqMan reagents determined genotype. Performance data for 347 athletes were obtained via Stats Perform OPTA (2012/13 to 2019/20 seasons), with metrics relating to both attack and defence. Due to low N of TT genotypes, CT and TT genotypes were grouped in some analyses. P values for multiple comparisons were subject to Benjamini-Hochberg correction to control for false discovery rate (5%).
RESULTS:
No differences in genotype or allele frequencies between athletes and non-athletes were observed. RU athletes of CC genotype played 13% longer per game than CT genotypes, and CC forwards played 13% longer per game than T allele carriers. In front 5 forwards, CC genotypes played 26% longer per game than T allele carriers. CC centres played 12% longer per game than T allele carriers. Interestingly, front 5 T allele carriers made 75% more clean breaks than CC genotypes.
CONCLUSION:
More minutes per appearance observed in CC genotypes suggests impaired fatigue resistance in T allele carriers. The improved performance of T allele carriers in front 5 forwards is surprising, suggesting a compensatory mechanism that allows those athletes to perform despite AMP deaminase deficiency. In conclusion, ascension to the elite level of RU is possible regardless of AMPD1 C34T polymorphism and performance is mostly unaffected, but RU players of CC genotype play more minutes per game.