Search

The aim of this study was to investigate the influence of Angiotensin-I 3 Converting Enzyme (ACE) genotype and the influence of circulating ACE activity 4 on the extent of muscle growth and strength development achieved during 5 strength training. It was hypothesized that ACE Deletion (D) allele carriers would 6 have higher force output values before and after the 12 week strength training 7 programme. Forty male Caucasian recreationally active volunteers were 8 genotyped for ACE Insertion/Deletion (I/D) polymorphism, but only eighteen 9 subjects identified with the DD or the II genotype were qualified to participate. 10 Eleven II and seven DD subjects underwent a 12 week strength training program 11 for the quadriceps muscle group of the trained leg, with both legs assessed 12 weekly by isokinetic dynamometry at joint angles of 30°, 60° and 90°(isometric 13 knee extension) and 60°/sec and 180°/sec (isokinetic maximal torque). Biopsy 14 samples were obtained from the vastus lateralis of the trained leg pre- and post-15 training, and they were analyzed using light microscopy and computer-based 16 planimetry to identify the cross-sectional area of each major fiber type as an 17 index of hypertrophy. A number of histochemical staining methods (H&E, SDH, 18 GPDH, IHC, mATPases) were used for delineation of the fiber types. Circulating 19 ACE activity was determined in blood samples and DNA samples were extracted 20 from saliva for genotyping. ACE genotype was not associated with circulating 21 ACE activity, with DD individuals presenting similar plasma ACE activity levels 22 with II individuals (39.7 ± 40 and 40.5 ± 3.30 respectively, P = 0.89 pre-training, 23 41.9 ± 3.7 and 35.5 ± 4.30 respectively, P = 0.30 post-training). ACE activity did 24 not change significantly with training (40.2 ± 2.5 nmol His-Leu/min/mL pre-25 training, 38.1 ± 3 nmol His-Leu/min/mL post training, P = 0.41) and correlated 26 significantly with baseline isometric force of the untrained leg at 5° (r = 0.46, P 27 = 0.05) and isokinetic strength at 180°/sec (r = 0.52, P = 0.03). When strength 28 was presented as force production per kilogram of body mass, the above 29 correlations became non-significant. Isometric force at 60º post-training 30 revealed a significant effect of the genotype, in favour of the DD individuals, on 31 the trained leg F (1, 64) = 4.242, P = 0.04, observed power = 0.53, partial eta 32 squared = 0.062). The effect persisted after adjustment for weight, but when it 33 was adjusted for body mass index and physical activity (assessed by 34 questionnaires), the effect became non-significant (F (1, 63) = 3.13391, P = 0.08, 35 5 partial eta squared = 0.047, observed power = 0.41); and F (1, 63) = 3.1628, P = 1 0.08, partial eta squared = 0.048, observed power = 0.42, respectively).The 2 average cross-sectional area (AVECSA) of Type IIA fibres for the DD individuals 3 increased significantly post-training (4070 ± 506 μm² pre-training, 4674 ± 399 4 μm² post-training, t (6) = -2.999, P = 0.02) and so did the AVECSA of the Type I 5 fibers of II individuals (3345 ± 207 μm² pre-training, 3988 ± 239 μm² post-6 training, t (10) = -3.063, P = 0.01). The finding shows that the strength training 7 programme applied resulted in muscle hypertrophy, but the changes in AVECSA 8 were not genotype-related. In conclusion, our findings suggest a possible role for 9 ACE gene polymorphism in the regulation of human skeletal muscle strength, but 10 limited statistical power and confounding factors prevented us from drawing 11 clear conclusions.