TRIM63 (MuRF-1) gene polymorphism is associated with biomarkers of exercise-induced muscle damage
| Autor: | Claire E. Stewart, Barry Drust, Philipp Baumert, Mark Lake, Robert M. Erskine |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
Male
0301 basic medicine medicine.medical_specialty Physiology Ubiquitin-Protein Ligases PG SNPs Muscle Proteins Single-nucleotide polymorphism Inflammation Isometric exercise Biology Muscle damage Polymorphism Single Nucleotide Tripartite Motif Proteins RC1200 Young Adult 03 medical and health sciences E3 ubiquitin-protein ligase 0302 clinical medicine single nucleotide polymorphism (SNP) exercise-induced muscle damage (EIMD) Internal medicine Delayed onset muscle soreness Genetics medicine Humans Eccentric Muscle Skeletal Exercise Genetic Association Studies tripartite motif containing 63 (TRIM63) 030104 developmental biology Endocrinology biology.protein MURF1 gene Female Titin Gene polymorphism medicine.symptom delayed-onset muscle soreness (DOMS) phenotype Biomarkers 030217 neurology & neurosurgery |
| Zdroj: | Physiological Genomics |
| ISSN: | 1531-2267 1094-8341 |
| DOI: | 10.1152/physiolgenomics.00103.2017 |
| Popis: | Unaccustomed strenuous exercise can lead to muscle strength loss, inflammation and delayed-onset muscle soreness, which may be influenced by genetic variation. We investigated if a missense single nucleotide polymorphism (A>G, rs2275950 ) within the TRIM63 gene (encoding MuRF-1 and potentially affecting titin mechanical properties) was associated with the variable response to unaccustomed eccentric exercise. Sixty-five untrained, healthy participants (genotyped for rs2275950 : AA, AG, and GG) performed 120 maximal eccentric knee extensions (ECC) to induce muscle damage. Isometric and isokinetic maximal voluntary knee extension contractions (MVCs) and muscle soreness were assessed before, immediately after, and 48 h after ECC. AA homozygotes were consistently stronger [baseline isometric MVC: 3.23 ± 0.92 Nm/kg (AA) vs. 2.09 ± 0.67 Nm/kg (GG); P = 0.006] and demonstrated less muscle soreness over time ( P = 0.022) compared with GG homozygotes. This may be explained by greater titin stiffness in AA homozygotes, leading to intrinsically stronger muscle fibers that are more resistant to eccentric damaging contractions. |
| Databáze: | OpenAIRE |
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