title: ACE ID genotype affects blood creatine kinase response to eccentric exercise.
abstract: Unaccustomed exercise may cause muscle breakdown with marked increase in serum creatine kinase (CK) activity. The 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 postexercise CK activity was determined. ACE genotype was significantly associated with postexercise 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 +/- SE U/L: II, 8,882 +/- 2,362; ID, 4,454 +/- 1,105; DD, 2,937 +/- 753, ANOVA, P = 0.02; P = 0.009 for linear trend). Multivariate stepwise regression analysis, which included age, sex, body mass index, 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, whereas the DD genotype may have protective effects. These findings support the role of local RAS in the regulation of exertional muscle injury.
authors: Department of Genetics and Molecular Biology, The Zinman College of Physical Education and Sport Sciences at the Wingate Institute, Netanya, Israel.
authors: Chen
authors: C
authors: Yamin
authors: Offer
authors: O
authors: Amir
authors: Moran
authors: M
authors: Sagiv
authors: Eric
authors: E
authors: Attias
authors: Yoav
authors: Y
authors: Meckel
authors: Nir
authors: N
authors: Eynon
authors: Michael
authors: M
authors: Sagiv
authors: Ruthie E
authors: RE
authors: Amir
mesh_terms: D000328:Adult; D052283:Creatine Kinase, MM Form / Q000097:blood*; D015444:Exercise; D005260:Female; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D016014:Linear Models; D008297:Male; D009119:Muscle Contraction / Q000235:genetics*; D018482:Muscle, Skeletal / Q000201:enzymology*; D016017:Odds Ratio; D007703:Peptidyl-Dipeptidase A / Q000235:genetics* / Q000378:metabolism; D010641:Phenotype; D011110:Polymorphism, Genetic; D012206:Rhabdomyolysis / Q000201:enzymology / Q000235:genetics* / Q000503:physiopathology; D018570:Risk Assessment; D012307:Risk Factors; D013997:Time Factors
chemical_list: D052283:Creatine Kinase, MM Form; D007703:Peptidyl-Dipeptidase A