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Exercise-induced muscle damage has been identified as one of the main causes of the progressive decrease in running and muscular performance in marathoners. The aim of this investigation was to determine the influence of the ACTN3 genotype on exercise-induced muscle damage produced during a marathon. Seventy-one experienced runners competed in a marathon race. Before and after the race, a sample of venous blood was obtained and maximal voluntary leg muscle power was measured during a countermovement jump. In the blood samples, the ACTN3 genotype (R577X) and the changes in serum creatine kinase and myoglobin concentrations were measured. Data from RX heterozygotes and XX mutant homozygotes were grouped as X allele carriers and compared to RR homozygotes. At the end of the race, X allele carriers presented higher serum myoglobin (774 ± 852 vs 487 ± 367 U L−1; P = 0.02) and creatine kinase concentrations (508 ± 346 vs 359 ± 170 ng mL−1; P = 0.04) than RR homozygotes. Pre-to-post-race maximal voluntary leg muscle power reduction was more pronounced in X allele carriers than RR homozygotes (−34.4 ± 16.1 vs −27.3 ± 15.4%; P = 0.05). X allele carriers self-reported higher levels of lower limb muscle pain (7 ± 2 vs 6 ± 2 cm; P = 0.02) than RR homozygotes at the end of the race. In comparison to RR homozygotes, X allele carriers for the R577X polymorphism of the ACTN3 gene presented higher values for typical markers of exercise-induced muscle damage during a competitive marathon. Thus, the absence of a functional α-actinin-3 produced by the X allele might induce higher levels of muscle breakdown during prolonged running events. Universidad Camilo José Cela (Proyecto DAMUS) 2.401 JCR (2017) Q2, 27/81 Sport sciences; Q3, 45/83 Physiology 1.186 SJR (2017) Q1, 435/2878 Medicine (miscellaneous), 37/285 Orthopedics and Sports Medicine, 80/554 Public Health, Environmental and Occupational Health, 29/127 Sports Science; Q2, 36/107 Physiology (medical) No data IDR 2017 UEM

Alpha-actinin-3, encoded by the ACTN3 gene, is an actin-binding protein with an important role in myofibril contraction and muscle force output. In humans, there is a relatively common deficiency of the α-actinin-3 due to homozygosity in a polymorphism of the ACTN3 gene (R577X, rs1815739), that has been related to decreased resistance to strain during voluntary muscle contractions. The purpose of this study was to investigate the influence of the ACTN3 genotype on the level of exercise-induced muscle damage attained by 23 experienced triathletes during an official half-ironman competition. Before and after the race, a sample of venous blood was obtained and jump height was measured during a countermovement jump. The changes in serum creatine kinase (CK-MM isoform) were measured in the blood samples and muscle pain was measured with a visual analogue scale (0–10 cm). Data from RX heterozygotes and XX mutant homozygotes were grouped as X-allele carriers (n = 13) and compared to RR homozygotes (n = 10). Race time was very similar between groups (313 ± 31 vs. 313 ± 25 min; P = 0.45); however, pre-to-post-competition reduction in jump height was greater in X-allele carriers than RR homozygotes (−18.4 ± 11.4 vs. −8.2 ± 6.9%; P = 0.04). At the end of the race, X-allele carriers presented higher serum CK-MM concentrations (682 ± 144 vs. 472 ± 269 U/L; P = 0.03), and there was also a tendency for higher self-reported values of lower limb muscle pain (7.7 ± 1.1 vs. 6.3 ± 2.3 cm; P = 0.06). X-allele triathletes in the ACTN3 R577X polymorphism presented greater signs of exercise-induced muscle damage during a half-ironman race than RR homozygotes.