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The purpose of the present study was to examine genetic and environmental contributions to individual differences in maximal isometric, concentric and eccentric muscle strength and muscle cross-sectional area (MCSA) of the elbow flexors. A generality versus specificity hypothesis was explored to test whether the 4 strength variables share a genetic component or common factors in the environment or whether the genetic/environmental factors are specific for each strength variable. The 4 variables under study were measured in 25 monozygotic and 16 dizygotic male Caucasian twin pairs (22.4 +/- 3.7 years). The multivariate genetic analyses showed that all 4 variables shared a genetic and environmental component, which accounted for 43% and 6% in MCSA (h2 = 81%), 47% and 20% in eccentric (h2 = 65%), 58% and 4% in isometric (h2 = 70%) and 32% and 1% in concentric strength (h2 = 32%) respectively. The remaining variation was accounted for by contraction type specific and muscle cross-sectional area specific genetic and environmental effects, which accounted for 38% and 14% in MCSA, 18% and 15% in eccentric, 12% and 26% in isometric and 0% and 67% in concentric strength respectively. This exploratory multivariate study suggests shared pleiotropic gene action for MCSA, eccentric, isometric and concentric strength, with a moderate to high genetic contribution to the variability of these characteristics. [ABSTRACT FROM AUTHOR]

This study explores the associations between polymorphisms in two candidate genes-myostatin gene (MSTN or GDF8) and angiotensin-converting enzyme (ACE) gene-with interindividual differences in human muscle mass and strength responses to strength training. The MSTN AluI A55T (exon 1), BanII K153R, TaqI E164 K and BstNI P198A (all in exon 2) markers and the ACE insertion (I)/deletion (D) polymorphism were typed in 57 males [22.4 (3.7) years] who participated in a 10-week, high-resistance training program for the elbow flexors. Maximal strength, and maximal isometric and concentric elbow flexor torques were measured at baseline and after training. Information on muscle cross-sectional area of the upper arm was obtained by computer tomography scans. Only one individual was heterozygous for the MSTN BanII K153R variant. No allelic variant was detected at the other MSTN sites in this population. For the ACE I/D polymorphism, no evidence was found for an association of the D or I allele with baseline strength, isometric and concentric torque or arm muscle cross-sectional area [analysis of covariance (ANCOVA) 0.25< P<0.97]. Responses to the strength-training program were not associated with the ACE I/D genotype (ANCOVA 0.057< P<0.70). Borderline significance was found for larger strength gains in dynamic flexion torques for I/I genotypes. This study therefore does not support the hypothesis that an increased muscle fiber hypertrophic effect of strength training is present in D-allele carriers. [ABSTRACT FROM AUTHOR]