J Strength Cond Res 33(10): 2655-2664, 2019-The purpose of this study was to evaluate indicators of muscle damage and hormonal responses after soccer matches and its relation to alpha-actinin-3 (ACTN3) gene expression (XX vs. RR/RX), considering that the R allele produces alpha-actinin-3 and provides greater muscle strength and power.
Israeli runners of Ethiopian origin had a greater frequency of the PPARD CC + PARGC1A Gly/Gly polymorphism, associated with improved endurance performance, compared with Israeli runners of non-Ethiopian origins (24 vs. 3%, respectively, p < 0.01); a lower frequency of the ACSL AA polymorphism, favoring endurance trainability (8 vs. 20%, respectively, p < 0.05); a greater frequency of the ACTN3 RR polymorphism, associated with sprint performance (35 vs. 20%, respectively, p < 0.05); a greater frequency of the MCT1 AA genotype, associated with improved lactate transport (65 vs. 45%, respectively, p < 0.05); and a lower frequency of IL-6 174C carriers, associated with reduced postexercise muscle damage (27 vs. 40%, respectively, p < 0.01).
The ACTN3R577X gene variant results in the absence of the α-actinin-3 protein in ∼18% of humans worldwide and has been associated with athletic performance and increased susceptibility to eccentric muscle damage.
X-allele triathletes in the ACTN3R577X polymorphism presented greater signs of exercise-induced muscle damage during a half-ironman race than RR homozygotes.
The ACTN3rs1815739" genes_norm="89">R577X (rs1815739) polymorphism determines the presence or absence of functional ACTN3, which may influence the extent of exercise-induced muscle damage.
The aim of this study was to compare acute inflammatory responses, muscle damage and hormonal variations according to the eccentric training in soccer professional athletes with different genetic profiles of ACTN3 (XX, RX and RR).
This study suggests a protective role of alpha-actinin-3 protein in muscle damage after eccentric training and an improved stress-sensor signaling, although effects are small.