AI Article Synopsis

  • The study investigated how the ACTN3 R577X gene variant influences muscle damage and inflammation after exercise by measuring levels of creatine kinase and interleukin-6 in participants.
  • Ninety-five active Japanese individuals performed eccentric elbow flexion exercises, and their muscle function and serum levels were evaluated at multiple time points post-exercise.
  • Results showed that those without ACTN3 (XX genotype) had significantly higher changes in creatine kinase levels, indicating a link between the gene variant and muscle damage response, while other measures remained unaffected.

Article Abstract

Objective: This study explored the interaction among ACTN3 R577X polymorphism, muscle damage, and post-exercise inflammatory response by assessing changes over time in serum creatine kinase and interleukin-6 levels.

Design: Ninety-five active Japanese participants (50 men and 45 women: 22.2 ± 2.3 years) who did not perform daily upper limb strength exercises were enrolled. Participants executed five sets of six maximal eccentric elbow flexion exercises. The exercise duration was 9 min, including rest between sets (90 s). Maximum voluntary isometric contraction, range of motion, muscle soreness, and serum creatine kinase and interleukin-6 levels were assessed pre and post and 1, 2, 3, and 5 d after exercise. Genotype groups were classified as RR + RX and XX based on the absence of ACTN3 expression.

Results: A significant time and group interaction (p = 0.045) on creatine kinase levels was observed between the groups, indicating that the absence of ACTN3 significantly affects creatine kinase changes. Conversely, no significant interaction on change in interleukin-6, maximum voluntary isometric contraction, range of motion, and muscle soreness was observed between groups.

Conclusion: The results highlight an interaction on creatine kinase activity post-exercise by ACTN3 R577X polymorphism, with elevated activity in the XX genotype.

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Source
http://dx.doi.org/10.1097/PHM.0000000000002623DOI Listing

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