Submitted on August 12, 2007
Accepted on September 19, 2007
ACE ID genotype affects blood Creatine Kinase response to eccentric exercise
Chen Yamin1, Offer Amir2, Moran Sagiv3, Eric Attias1, Yoav Meckel4, Nir Eynon1, Michael Sagiv1, and Ruthie E. Amir1*
1 Genetics and Molecular Biology, Zinman College of Physical Education and Sport Sciences at the Wingate Institute, Netanya, Israel
2 Cardiology, Lady Davis Carmel Medical Center, Haifa, Israel
3 Netanya, Israel; Genetics and Molecular Biology, Zinman College of Physical Education and Sport Sciences at the Wingate Institute, Netanya, Israel
4 Genetics and Molecular Biology, Zinman College of Physicl Eductin and Sport Scinces at the Wingate Institute, Netanya, Israel; Genetics and Molecular Biology, Zinman College of Physical Education and Sport Sciences at the Wingate Institute, Netanya, Israel
* To whom correspondence should be addressed. E-mail: ruthieam{at}012.net.il.
Unaccustomed exercise may cause muscle breakdown with marked increase in serum creatine kinase (CK) activity. Skeletal muscle renin-angiotensin system (RAS) plays an important role in exercise metabolism and tissue injury. A functional insertion (I) / deletion (D) polymorphism in the angiotensin-I converting enzyme (ACE) gene (rs4646994) has been associated with ACE activity. We hypothesized that ACE ID genotype may contribute to the wide variability in individuals' CK response to a given exercise. Young individuals performed maximal eccentric contractions of the elbow flexor muscles. Pre- and post-exercise CK activity was determined. ACE genotype was significantly associated with post-exercise CK increase and peak CK activity. Individuals harboring one or more of the I allele had a greater increase and higher peak CK values than individuals with the DD genotype. This response was dose-dependent (mean ± S.E.M. U/L: II, 8882 ± 2362; ID, 4454 ± 1105; DD, 2937 ± 753, ANOVA, P = 0.02; P = 0.009 for linear trend). Multivariate stepwise regression analysis, which included age, sex, BMI, and genotype subtypes revealed that ACE genotype was the most powerful independent determinant of peak CK activity (adjusted odds ratio 1.3, 95% confidence interval 1.03 - 1.64, P = 0.02). In conclusion, we indicate a positive association of the ACE ID genotype with CK response to strenuous exercise. We suggest that the II genotype imposes increased risk for developing muscle damage, while the DD genotype may have protective effects. These findings support the role of local RAS in the regulation of exertional muscle injury.
