Creatine kinase MM TaqI and methylenetetrahydrofolate reductase C677T and A1298C gene polymorphisms influence exercise-induced C-reactive protein levels

Eur J Appl Physiol. 2012 Mar;112(3):941-50. doi: 10.1007/s00421-011-1961-9. Epub 2011 Jun 26.

Abstract

Physical training induces beneficial adaptations, but exhausting exercise increases reactive oxygen species, which can cause muscular injuries with consequent inflammatory processes, implying jeopardized performance and possibly overtraining. Acute strenuous exercise almost certainly exceeds the benefits of physical activity; it can compromise performance and may contribute to increased future risk of cardiovascular disease (CVD) in athletes. Polymorphisms in the muscle-type creatine kinase (CK-MM) gene may influence performance and adaptation to training, while many potentially significant genetic variants are reported as risk factors for CVD. Therefore, we investigated the influence of polymorphisms in CK-MM TaqI and NcoI, methylenetetrahydrofolate reductase (MTHFR C677T and A1298C) and C-reactive protein (CRP G1059C) genes on exercise-induced damage and inflammation markers. Blood samples were taken immediately after a race (of at least 4 km) that took place outdoors on flat tracks, and were submitted to genotyping and biochemical evaluation of aspartate aminotransferase (AST), CK, CRP and high-sensitivity CRP (hs-CRP). CK-MM TaqI polymorphism significantly influenced results of AST, CK and hs-CRP, and an association between MTHFR C677T and A1298C with CRP level was found, although these levels did not exceed reference values. The results indicate that these polymorphisms can indirectly influence performance, contribute to higher susceptibility to exercise-induced inflammation or protection against it, and perhaps affect future risks of CVD in athletes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Athletes
  • C-Reactive Protein / analysis
  • C-Reactive Protein / metabolism*
  • Cardiovascular Diseases / blood
  • Cardiovascular Diseases / etiology
  • Cardiovascular Diseases / genetics
  • Creatine Kinase, MM Form / genetics*
  • Deoxyribonucleases, Type II Site-Specific / metabolism*
  • Exercise / physiology*
  • Female
  • Gene Frequency
  • Genetic Predisposition to Disease
  • Humans
  • Male
  • Methylenetetrahydrofolate Reductase (NADPH2) / genetics*
  • Middle Aged
  • Polymorphism, Restriction Fragment Length / genetics
  • Polymorphism, Restriction Fragment Length / physiology*
  • Polymorphism, Single Nucleotide / physiology*
  • Risk Factors
  • Young Adult

Substances

  • C-Reactive Protein
  • Methylenetetrahydrofolate Reductase (NADPH2)
  • Creatine Kinase, MM Form
  • Deoxyribonucleases, Type II Site-Specific
  • TCGA-specific type II deoxyribonucleases