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      Effect of ACTN3 Gene on Strength and Endurance in Soccer Players

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          Abstract

          Sports efficiency in activities in which strength and speed are the determining factors has been associated to the ACTN3 gene, which is responsible for the expression of α-actinin-3. Soccer is a mainly aerobic sport because of its long duration, but the acute actions that define the game demand a lot of strength and speed. The purpose of the present study was to compare the performance capacity of soccer players with different genotype groups of ACTN3 (XX, RX, and RR) in strength, speed, and endurance tests. Two hundred professional players of Brazilian soccer first division teams participated in this study. Speed, jump, and endurance test results were compared with the polymorphisms of the ACTN3 gene. It was noticed that RR individuals spent less time to run a 10-m path, compared with XX individuals (p < 0.05). The RR individuals also presented lower time rates at the 20- and 30-m path, compared with RX and XX individuals (p < 0.05). In jump tests, RR individuals presented higher rates, compared with RX and XX individuals (p < 0.05). As for aerobic tests, the XX individuals presented higher rates of V[Combining Dot Above]O2 max, compared with the RR group (p < 0.05), and did not differ from the RX group. The main conclusion of this study is that soccer players of genotype ACTN3/RR are the fastest in short distances and present higher jump potential. ACTN3/XX individuals presented the highest aerobic capacity. These findings can be used in training load adjustment and can influence the development of tactical schemes in soccer matches.

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          Most cited references33

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          A simple salting out procedure for extracting DNA from human nucleated cells

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            The yo-yo intermittent recovery test: physiological response, reliability, and validity.

            To examine the physiological response and reproducibility of the Yo-Yo intermittent recovery test and its application to elite soccer. Heart rate was measured, and metabolites were determined in blood and muscle biopsies obtained before, during, and after the Yo-Yo test in 17 males. Physiological measurements were also performed during a Yo-Yo retest and an exhaustive incremental treadmill test (ITT). Additionally, 37 male elite soccer players performed two to four seasonal tests, and the results were related to physical performance in matches. The test-retest CV for the Yo-Yo test was 4.9%. Peak heart rate was similar in ITT and Yo-Yo test (189 +/- 2 vs 187 +/- 2 bpm), whereas peak blood lactate was higher (P < 0.05) in the Yo-Yo test. During the Yo-Yo test, muscle lactate increased eightfold (P < 0.05) and muscle creatine phosphate (CP) and glycogen decreased (P < 0.05) by 51% and 23%, respectively. No significant differences were observed in muscle CP, lactate, pH, or glycogen between 90 and 100% of exhaustion time. During the precompetition period, elite soccer players improved (P < 0.05) Yo-Yo test performance and maximum oxygen uptake ([OV0312]O(2max)) by 25 +/- 6 and 7 +/- 1%, respectively. High-intensity running covered by the players during games was correlated to Yo-Yo test performance (r = 0.71, P < 0.05) but not to [OV0312]O(2max) and ITT performance. The test had a high reproducibility and sensitivity, allowing for detailed analysis of the physical capacity of athletes in intermittent sports. Specifically, the Yo-Yo intermittent recovery test was a valid measure of fitness performance in soccer. During the test, the aerobic loading approached maximal values, and the anaerobic energy system was highly taxed. Additionally, the study suggests that fatigue during intense intermittent short-term exercise was unrelated to muscle CP, lactate, pH, and glycogen.
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              ACTN3 genotype is associated with human elite athletic performance.

              There is increasing evidence for strong genetic influences on athletic performance and for an evolutionary "trade-off" between performance traits for speed and endurance activities. We have recently demonstrated that the skeletal-muscle actin-binding protein alpha-actinin-3 is absent in 18% of healthy white individuals because of homozygosity for a common stop-codon polymorphism in the ACTN3 gene, R577X. alpha-Actinin-3 is specifically expressed in fast-twitch myofibers responsible for generating force at high velocity. The absence of a disease phenotype secondary to alpha-actinin-3 deficiency is likely due to compensation by the homologous protein, alpha-actinin-2. However, the high degree of evolutionary conservation of ACTN3 suggests function(s) independent of ACTN2. Here, we demonstrate highly significant associations between ACTN3 genotype and athletic performance. Both male and female elite sprint athletes have significantly higher frequencies of the 577R allele than do controls. This suggests that the presence of alpha-actinin-3 has a beneficial effect on the function of skeletal muscle in generating forceful contractions at high velocity, and provides an evolutionary advantage because of increased sprint performance. There is also a genotype effect in female sprint and endurance athletes, with higher than expected numbers of 577RX heterozygotes among sprint athletes and lower than expected numbers among endurance athletes. The lack of a similar effect in males suggests that the ACTN3 genotype affects athletic performance differently in males and females. The differential effects in sprint and endurance athletes suggests that the R577X polymorphism may have been maintained in the human population by balancing natural selection.
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                Author and article information

                Journal
                Journal of Strength and Conditioning Research
                Journal of Strength and Conditioning Research
                Ovid Technologies (Wolters Kluwer Health)
                1064-8011
                2013
                December 2013
                : 27
                : 12
                : 3286-3292
                Article
                10.1519/JSC.0b013e3182915e66
                23539075
                64075cd6-124a-469c-a1af-e721fbe2aa49
                © 2013
                History

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