Angiotensin-converting Enzyme ID Genotypes Research Articles

Assessment of angiotensin converting enzyme gene polymorphism in patients with psoriasis

Psoriatic patients had diversity of clinical presentations and complications. Psoriasis can have significant interference with the patient's quality of life, recovery, and outcome. Some evidences suggest that the angiotensin converting enzyme (ACE) is present in the skin of psoriatic patients. This study intended to assess the patterns of ACE insertion/deletion (ACE ID) polymorphism and the levels of serum ACE among psoriatic patients in comparison to normal controls. The study included two groups: 20 patients with psoriasis and 20 apparently healthy adults with negative family history of psoriasis as a control group. Psoriasis area and severity index (PASI) was used to measure of severity of psoriasis. In both groups, ACE ID gene polymorphism was assessed by quantitative real-time polymerase reaction and serum ACE levels was evaluated using an enzyme-linked immunosorbent assay. ACE ID genotype was significantly higher among the psoriatic group in comparison to the control group (40.0% versus 15.0%, respectively, p=0.016). D allele was significantly higher among the psoriatic group than the control group (25.0% versus 7.5%, respectively, p=0.034). ACE ID genotype carried significantly higher risk in psoriatic group versus control group (OR=3.8). The D allele carried higher risk in psoriatic group versus control group (OR=4.1). ACE serum levels were significantly higher among the psoriatic group compared to the control group (87.4±7.03 versus 2.3±0.7, respectively; p < 0.001). We concluded that ACE ID gene polymorphism may be considered as a risk factor for developing psoriasis.

Association Between the Angiotensin-Converting Enzyme Gene Insertion/Deletion Polymorphism and Avascular Necrosis of the Femoral Head.

Objective: This study investigated the association between the angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism and avascular necrosis of the femoral head (ANFH). Materials and Methods: The ACE gene I/D polymorphism was determined in 279 nontraumatic, ANFH Han Chinese patients (divided into idiopathic and steroid- and alcohol-induced subgroups) and 276 age- and gender-matched healthy controls using the polymerase chain reaction. Results: The frequencies of the ACE DD genotype and D allele were significantly higher among the ANFH patients as a whole and also in the idiopathic and steroid- and alcohol-induced ANFH subgroups compared to healthy controls (p < 0.05 for all). Additionally, the DD genotype, compared with the ID+II, ID, and II genotypes, conferred a higher risk of developing ANFH across all clinical subgroups (p < 0.001, odds ratio [OR] = 2.508; p < 0.001, OR = 2.072; p < 0.001, OR = 3.684, respectively) as well in each of the subgroups examined individually, including the idiopathic subgroup (p < 0.001, OR = 2.579; p < 0.001, OR = 2.091; p < 0.001, OR = 3.994, respectively), the steroid-induced subgroup (p = 0.005, OR = 2.345; p = 0.031, OR = 2.050; p = 0.007, OR = 3.000, respectively), and the alcohol-induced subgroup (p < 0.001, OR = 2.488; p = 0.012, OR = 2.050; p = 0.011, OR = 2.659, respectively) of ANFH patients. The ID genotype, compared with the II genotype, conferred a higher risk across all subtypes analyzed together, and in the idiopathic subgroup (p = 0.013, OR = 1.778; p = 0.028, OR = 1.910) analyzed separately. Additionally, the D allele, in comparison with the I allele, conferred a relatively higher risk across all subgroups (p < 0.001, OR = 2.101) as well as in each of the three subgroups examined individually (idiopathic: p < 0.001, OR = 2.178; steroid-induced: p = 0.003, OR = 1.910; and alcohol-induced: p < 0.001, OR = 2.094). Conclusion: The ACE DD and ID genotypes and D allele may be risk factors for susceptibility to ANFH in the Chinese population.

Association of ACE I/D and AGTR1 A1166C Gene Polymorphisms and Risk of Uterine Leiomyoma: A Case-Control Study.

Objective:Uterine leiomyoma (UL) can be considered as the most common benign gynecological tumors of the smooth muscle cells in the myometrium. They are likely to be associated with infertility and recurrent abortion as well as obstructed labor and post-partum hemorrhage. Moreover, altered vascular-related genes can be linked to developing leiomyoma. Polymorphisms of the angiotensin-converting enzyme (ACE) gene are associated with some vascular diseases. The present study was carried out to investigate the association of ACE I/D and AGTR1 A1166C gene polymorphisms and the risk of uterine leiomyoma in a sample of Iranian population. Methods:The study was carried out on a total of 413 women divided into 202 patients with diagnosed uterine leiomyomas and a control group of 211. Genotyping was performed using the PCR or PCR-RFLP methods. Results:The ID and DD genotypes of ACE I/D polymorphism were associated with 2 and 2.9 fold higher risk of UL compared to II genotype (OR, 2 [95% CI, 1.3 to 3.2]; P = 0.004 and OR, 2.9 [95% CI, 1.6 to 5]; P = 0.0002). The frequencies of ACE D alleles were 53.7% in women with UL and 40.3% in controls, which were observed to be statistically different (P < 0.0001). The alleles and genotypes of AGTR1 A1166C polymorphism were not different between UL and control women (P=0.9). Conclusion:The ACE ID and DD genotypes were associated with a higher risk of UL. No relationship was found between AGTR1 A1166C polymorphism and UL.

Childhood adiposity, adult adiposity, and the ACE gene insertion/deletion polymorphism: evidence of gene-environment interaction effects on adult blood pressure and hypertension status in adulthood.

Genetic variants may modify the associations of adiposity measures with blood pressure (BP) and hypertension. The insertion/deletion (I/D) polymorphism in the angiotensin-converting enzyme (ACE) gene is an attractive candidate. To examine interaction effects between I/D polymorphism and adiposity measures (BMI, waist circumference, waist-to-hip ratio, and skinfold thickness) during childhood and adulthood in relation to adult BP and hypertension. Data were available for 4835 participants from three prospective cohort studies. Multivariable linear regression models for adult SBP and DBP, and multivariable logistic regression models for hypertension were fit that included interaction effects between child or adult adiposity and I/D polymorphism. Evidence for interaction effects on BP/hypertension were found across the three studies. Compared with childhood measures, the effect modification appeared to be more consistent when using adult adiposity. In particular, the adverse effects of greater adult waist circumference on increasing adult SBP and DBP appeared to be larger among carriers of ACE DD (or GG) [adjusted linear regression coefficients 0.26, 95% CI (0.21-0.31) and 0.28 (0.24-0.32) for SBP and DBP, respectively] and ID (or AG) genotypes [0.25 (0.21-0.29) and 0.25 (0.21-0.28), respectively], whereas those with II (or AA) genotypes had smaller effects [0.15 (0.09-0.21) and 0.19 (0.13-0.23)]. ACE genetic variation may modify the effect of adult adiposity on increasing BP and risk of hypertension in adulthood. Individuals with ACE DD (or GG) and/or ID (or AG) genotypes, compared with those with II (or AA) genotype, appear more vulnerable to the impact of excess adiposity.

Prevalence of alpha actinin-3 gene (ACTN3) R577X and angiotensin converting enzyme (ACE) insertion / deletion gene polymorphisms in national and amateur Turkish athletes

Studies to date showed the importance of alpha- actinin-3 (ACTN3) R577X and angiotensin converting enzyme (ACE) ID polymorphisms on determining athletic performance. Therefore, in this study, we aimed to examine polymorphisms given to Turkish athletes and compare them with sedentary individuals. Genomic DNAs were extracted from peripheral blood by using commercially available DNA isolation kit (Macherey-Nagel, NucleoSpin®, Germany). For this study, a total of 84 volunteers (23 national athletes, 27 amateur athletes and 34 sedentary controls) was recruited. ACE ID genotypes were determined by conventional polymerase chain reaction, and ACTN3 R577X polymorphisms by polymerase chain reaction- restriction fragment length polymorphism methodology. In ACTN3 R577X polymorphism, RX was the dominating genotype, and we detected no RR genotype in national athletes. (no RR genotype was detected in national athletes) X allele is more frequent in national athletes and R allele was more frequent in both amateur athletes and control group. II genotype was more frequent in national athletes and in control group, whereas DD genotype was more frequent in amateur athletes for ACE ID polymorphism. When we consider alleles, D allele was found more frequently in amateur athletes and control group whereas I allele was more frequent in national athletes in ACE ID polymorphism. For ACTN3, X allele was superior to R allele. ACTN3 R577X and ACE ID polymorphisms were important biomarkers in determining athletic performance. However, our results in Turkish athletes suggest that ACE D allele and ACTN3 X alleles may be beneficial to athletes potentially, regardless of the distance they perform.

Association of GSTM1, GSTT1, GSTP1-ILE105VAL and ACE I/D polymorphisms with ankylosing spondylitis.

Ankylosing spondylitis (AS) is a chronic inflammatory disease of unknown origin. The aim of this study is to clarify the relationships between susceptibility and severity of AS and GST-mu1 (GSTM1), GST-theta1 (GSTT1), GST-pi1 (GSTP1)-Ile105Val and angiotensin-converting enzyme (ACE) I/D polymorphisms in AS patients. One hundred thirty-eight AS patients and seventy-one healthy controls were enrolled in this study. Erythrocyte sedimentation rate and C-reactive protein (CRP) levels of the AS patients were recorded. The scores of the numeric rating scale (NRS) pain, the Bath Ankylosing Spondylitis Activity Index, the Bath Ankylosing Spondylitis Metrology Index and the Bath Ankylosing Spondylitis Functional Index were calculated. The genotypes distributions and allele frequencies of GSTM1, GSTT1, GSTP1-Ile105Val and ACE I/D polymorphisms were compared between patients and healthy controls. The Multiplex polymerase chain reaction (PCR) and the PCR-restriction fragment length polymorphism methods were used to detect the polymorphisms of ACE I/D, the GSTT1 and GSTM1 genes and the GSTP1-Ile105Val polymorphism, respectively. There were significantly higher levels of the GSTT1 null and the ACE II genotypes in AS patients compared to those in healthy controls (p = 0.002 and 0.005, respectively). We found significantly higher levels of CRP and the NRS pain scores in the patients with ACE ID or DD genotypes compared to those in the patients with ACE II genotypes (p = 0.005 and 0.035, respectively). The present results showed that genes involved in protection from oxidative stress and ACE gene may influence disease development and course in AS.

Associations of ACE Gene Insertion/Deletion Polymorphism, ACE Activity, and ACE mRNA Expression with Hypertension in a Chinese Population

BackgroundThe present study was designed to explore the association of angiotensin converting enzyme (ACE) gene insertion/deletion (I/D, rs4646994) polymorphism, plasma ACE activity, and circulating ACE mRNA expression with essential hypertension (EH) in a Chinese population. In addition, a new detection method for circulating ACE mRNA expression was explored.MethodsThe research was approved by the ethics committee of Zhejiang Provincial Center for Disease Prevention and Control. Written informed consent was obtained prior to the investigation. 221 hypertensives (cases) and 221 normotensives (controls) were interviewed, subjected to a physical examination, and provided blood for biochemical and genetic tests. The ACE mRNA expression was analyzed by real time fluorescent quantitative Reverse Transcription PCR (FQ-RT-PCR). We performed logistic regression to assess associations of ACE I/D genotypes, ACE activity, and ACE mRNA expression levels with hypertension.ResultsThe results of the multivariate logistic regression analysis showed that the additive model (ID, DD versus II) of the ACE genotype revealed an association with hypertension with adjusted OR of 1.43(95% CI: 1.04-1.97), and ACE ID genotype with adjusted OR of 1.72(95% CI: 1.01-2.92), DD genotype with adjusted OR of 1.94(95% CI: 1.01-3.73), respectively. In addition, our data also indicate that plasma ACE activity (adjusted OR was 1.13(95% CI: 1.08-1.18)) was significantly related to hypertension. However, the plasma ACE mRNA expressions were not different between the cases and controls.ConclusionACE I/D polymorphism and ACE activity revealed significant influence on hypertension, while circulating ACE mRNA expression was not important factors associated with hypertension in this Chinese population. The detection of circulating ACE mRNA expression by FQ-RT-PCR might be a useful method for early screening and monitoring of EH.

Performance enhancing genetic variants, oxygen uptake, heart rate, blood pressure and body mass index of elite high altitude mountaineers

To analyse and compare the ACE (angiotensin-converting enzyme), ACTN3 (actinin-3) and AMPD1 (adenosine monophosphate deaminase 1) genetic variants, oxygen uptake (VO2max), heart rate (HR), blood pressure (BP) and body mass index (BMI) of elite high altitude mountaineers and average athletes. Elite Bulgarian alpinists (n = 5) and control group of athletes (n = 72) were recruited. VO2max was measured using a treadmill graded protocol. HR, BP and BMI were recorded. Genotyping was done by polymerase chain reaction (PCR) amplification followed by agarose gel electrophoresis. Chi2-test and Fisher's exact test were used for statistical analysis. Alpinists showed significantly higher frequencies of 60% ACE I allele (p = 0.002), 50% ACTN3 X allele (p = 0.032) and 30% AMPD1 T allele (p = 0.003) compared to controls - 39%, 36%, 13%, respectively. ACE ID genotype prevalence and null DD genotype were observed in mountaineers. Higher absolute VO2max, but no differences in VO2max ml kg-1 min-1, HR, oxygen pulse, blood pressure and BMI were found. The ID genotype and higher frequencies of ACE I allele could contribute to successful high altitude ascents in mountaineers. The genetic make-up of the two mountaineers who made the summit of Mt Everest was distinctive, revealing ACE ID genotype, mutant ACTN3 XX and AMPD1 TT genotypes.

Role of the ACE ID and PPARG P12A Polymorphisms in Genetic Susceptibility of Diabetic Nephropathy in a South Indian Population

BackgroundDiabetic nephropathy (DN) is one of the life-threatening disorders characterized by persistent albuminuria, raised arterial blood pressure, a lowered glomerular filtration rate, and high risk of cardiovascular morbidity and mortality. The vascular genes ACE (Angiotensin-converting enzyme), and PPARG (peroxisome proliferator activated receptor gamma) are involved in alterations in vascular endothelium, and are suggested to play a role in the susceptibility of diabetic nephropathy.ObjectivesThe aim of our study was to find out the role of ACE ID and PPARG P12A polymorphisms in genetic susceptibility of diabetic nephropathy in south Indian population.Patients and MethodsA total of 54 cases with diabetic nephropathy and 67 control subjects with diabetes were enrolled for our study. DNA was isolated from peripheral blood leucocytes, and genotyped using PCR-electrophoresis (ACE ID) or PCR-RFLP (PPARG P12A) methods.ResultsACE ID genotypes followed Hardy-Weinberg equilibrium in both cases and controls. But P12A genotypes deviated from Hardy-Weinberg equilibrium in diabetic controls. Chi2 test was applied for the analysis of genotypic distributions in genotypic and dominant models. Odds ratios were also calculated. No significant differences in genotype frequencies of ACE ID and PPARG P12A polymorphisms were found on comparing patients with diabetic nephropathy with diabetic controls. The synergistic role of ACE ID* PPARG P12A interaction, did not show any association in patients with diabetic nephropathy when compared to diabetic controls.ConclusionsIn conclusion, the ACE and PPARG genes do not have a key role in conferring risk for diabetic nephropathy.

Angiotensin-Converting Enzyme Gene Insertion/Deletion Polymorphism in Patients with Chronic Pancreatitis and Pancreatic Cancer

The purpose of this study was to determine the frequency of angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism and to investigate its role as a potential risk factor in patients with chronic pancreatitis and pancreatic cancer. Deletion polymorphism of the 287-bp fragment of intron 16 of the ACE gene results in higher levels of circulating enzyme and therefore may represent a risk factor for disease development. The study included 55 patients with chronic pancreatitis, 45 patients with pancreatic cancer and 128 healthy subjects. The presence of I and D variants in the ACE gene was analyzed by a polymerase chain reaction (PCR) method. Distribution of ACE ID genotypes was analyzed by means of logistic regression. When chronic pancreatitis and pancreatic cancer groups were compared in the univariate analysis, the following factors were identified as statistically significant predictors of pancreatic disease: age, gender, smoking, fat intake, ACE II genotype and ACE DD genotype. However, in the multivariate analysis, only age, gender and smoking were singled out as predictors for the occurrence of pancreatic disease. Our findings indicate that the ACE I/D polymorphism could play a role in the development of chronic pancreatitis and pancreatic cancer through interaction with other genetic and environmental factors.

The angiotensin converting enzyme D allele is an independent risk factor for early onset coronary artery disease

Objective The role of angiotensin converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism in early onset coronary artery disease age < 55 years (ECAD) is controversial. The aim of this study was to further evaluate the role of this ACE(I/D) gene polymorphism on the risk of premature CAD in patients from western Iran. Methods The ACE(I/D) genotypes were detected by PCR-RFLP in 323 individuals undergoing their first coronary angiography. Patients were placed into two groups: ECAD and late onset CAD age ≥ 55 years (LCAD). Results We found a statistically significant association of the ACE D allele, as homozygous or ACE ID plus DD genotypes (ID + DD), only in the ECAD subjects OR = 1.35, p = 0.015, OR = 3.27, p = 0.014, and OR = 2.8, p = 0.013, respectively. In addition, there was a significant association after adjustment for the absence of history of diabetes, presence of normolipidemia and absence of history of blood pressure [OR 1.38, p = 0.017 and 2.35, p = 0.02]. Our results indicated that the ACE D allele is a risk factor for early onset of CAD even after correcting for conventional risk factors. The incidence of triple vessel disease was significantly higher in individuals carrying ACE(D/D) genotype in ECAD patients compared to those who carried ACE(I/I) genotype (OR 3.38; p = 0.019; 57.5% vs. 42.5%; p = 0.013). Conclusion The presence of D allele of ACE can be important independent risk factor in the onset of CAD patients less than 55 years old in a west population of Iran. Larger collaborative studies are needed to confirm these results.

Effects of green tea, black tea and Rooibos tea on angiotensin-converting enzyme and nitric oxide in healthy volunteers

Tea has been reported to reduce cardiovascular mortality, but the underlying mechanisms are largely unknown. The aim of the current project was to investigate the effect of green tea (Japanese Sencha), black tea (Indian Assam B.O.P.) and Rooibos tea (South Africa) on angiotensin-converting enzyme (ACE) and nitric oxide (NO). Seventeen healthy volunteers received a single oral dose of 400 ml green tea, black tea or Rooibos tea in a randomized, three-phase, crossover study. ACE activity and NO concentration were measured (at 0, 30, 60 and 180 min) in all phases. ACE activity was analysed by means of a commercial radioenzymatic assay. Nitrite was analysed as a marker of NO concentration. In addition, ACE genotype was determined using a PCR method. Oral intake of a single dose of Rooibos tea significantly inhibited ACE activity after 30 min (P < 0.01) and after 60 min (P < 0.05). A significant inhibition of ACE activity was seen with green tea for the ACE II genotype 30 min after intake of the tea (P < 0.05) and for the ACE ID genotype 60 min after intake (P < 0.05). A significant inhibition of ACE activity was also seen with Rooibos tea for the ACE II genotype 60 min after intake (P < 0.05). No significant effect on NO concentration was seen. These results suggest that green tea and Rooibos tea may have cardiovascular effects through inhibition of ACE activity.

ACE Gene Polymorphism in Peripheral Vascular Disease

Peripheral vascular disease is an atherosclerotic process. It has been suggested that angiotensin converting enzyme insertion/deletion polymorphism is associated with atherosclerosis. The aim of this study was to investigate the role of the insertion/deletion polymorphism of the angiotensin-converting enzyme in Turkish patients with peripheral vascular disease in Western part of Turkey. We also investigated the relationship between serum angiotensin converting enzyme activity and distribution of genotypes in both patients and control group. The study group consisted of 78 patients with peripheral vascular disease. The control group consisted of 73 healthy adults. Serum angiotensin converting enzyme activities in patients were higher than those of the control group (p<0.05). Angiotensin converting enzyme genotype frequencies in patients were observed as 28.2%, 18% and 53.8% for DD, II and ID polymorphism, respectively. These frequencies in controls were 42.5%, 20.5% and 37% for DD, II and ID, respectively. Serum angiotensin converting enzyme activities in both groups with II genotype were significantly lower than those with ID and DD genotype (p<0.05). Although conflicting results have been reported about this polymorphism in patients with peripheral vascular disease, we suggest that the angiotensin converting enzyme ID genotype may be a risk factor for peripheral vascular disease.

The angiotensin-converting enzyme insertion/deletion polymorphism and serum levels of angiotensin-converting enzyme in venous thromboembolism

The angiotensin-converting enzyme (ACE) has been suggested to affect blood coagulation and fibrinolysis. Results from literature on the role of the frequent insertion/deletion (I/D) polymorphism in the ACE gene in venous thromboembolism (VTE) are controversial. Only limited data on ACE serum levels inVTE exist. We determined the ACE I/D polymorphism by genotyping and ACE serum levels by an enzymatic assay in 100 high-risk patients with objectively confirmed recurrentVTE and at least one event of an unprovoked deep venous thrombosis or pulmonary embolism. One hundred twenty-five age- and sex-matched healthy individuals served as controls. ACE genotype frequencies were not significantly different between patients (DD: 26.0%, ID: 52.0%, II: 22.0%) and controls (DD: 29.6%, ID: 44.8%, II: 25.6%; p = 0.56). Neither individuals with ACE DD genotype nor those with ACE ID genotype had a higher risk for VTE in comparison to those with ACE II genotype (odds ratio and [95% confidence interval]: 1.0 [0.5-2.1] and 1.4 [0.7-2.6], respectively). Serum ACE levels (U/l) did not differ between patients (median = 25.25, 25th -75th percentile: 20.20-33.70) and controls (24.20, 17.85-34.50, p = 0.49). In the total population involved in the study the ACE DD genotype (n = 63: 36.00 [26.40-43.00]) was associated with higher ACE levels than the ACE ID genotype (n = 108: 24.10 [19.80-31.48], p < 0.001) and the ACE II genotype (n = 54: 19.35 [15.00-22.95], p < 0.001). In conclusion, we found a significant association of the ACE I/D polymorphism with ACE serum levels. However, neither the serum levels nor the I/D genotype were associated with VTE.

Angiotensin-Converting Enzyme Insertion/Deletion Genotype, Exercise, and Physical Decline

Physical performance in response to exercise appears to be influenced by the angiotensin-converting enzyme (ACE) insertion (I)/deletion (D) genotype in young adults, but whether this relationship could help explain variation in older individuals' response to exercise has not been well studied. To determine whether the ACE genotype interacts with significant physical activity to affect the incidence of mobility limitation in well-functioning older adults. The Health Aging and Body Composition (Health ABC) Cohort Study, conducted in the metropolitan areas of Memphis, Tenn, and Pittsburgh, Pa. A total of 3075 well-functioning community-dwelling adults aged 70 through 79 years were enrolled from 1997 to 1998 and had a mean of 4.1 years of follow-up. Incident mobility limitation defined as the report of difficulty walking a quarter of a mile (0.4 km) or walking up 10 steps on 2 consecutive semiannual interviews (n = 1204). Physically active participants (those reporting expending > or =1000 kcal/wk in exercise, walking, and stair climbing) were less likely to develop mobility limitation regardless of genotype. However, activity level interacted significantly with the ACE genotype (P = .002). In the inactive group, the ACE genotype was not associated with limitation (P = .46). In the active group, those with the II genotype were more likely to develop mobility limitation after adjusting for potential confounders compared with those with ID/DD genotypes (adjusted rate ratio, 1.45, 95% confidence interval, 1.08-1.94). The gene association was especially strong among participants reporting weightlifting. Exploration of possible physiological correlates revealed that among active participants, those with the II genotype had higher percentage of body fat (P = .02) and more intermuscular thigh fat (P = .02) but had similar quadriceps strength as those with ID/DD. Among older individuals who exercised, those with the ACE DD or ID genotypes were less likely to develop mobility limitation than those with the II genotype. Regardless of genotype, individuals who exercised were less likely to develop mobility limitation than those who did not exercise.

ACE Genotype May Have an Effect on Single versus Multiple Set Preferences in Strength Training

A polymorphic variant of the human angiotensin converting enzyme (ACE) gene was identified. The 'D' (rather than 'I') variant was associated with improvements in strength related to physical training. We set out to determine whether the response to different patterns of strength training might also differ. Ninty-nine Caucasian male non-elite athletes were randomly allocated into one of three groups: 31 non-training/control (CG: 31), single-set (SSG: 35) and multiple-set (MSG: 33). SSG and MSG trained three times a week for 6 weeks. Both training groups were underwent a strength-training program with two mesocycles (12-15 repetition maximum (RM) and 8-12 RM mesocycles). One RM loads in half squat and bench press were assessed before training and after the first and second mesocycles. ACE polymorphisms analysed by polymerase chain reaction (PCR) methods. Subjects with ACE II genotype in the MST group had improved strength development in 12-15 RM, while SST and MST groups had similar gains in 8-12 RM. Subjects with ACE DD genotype in both the SSG and the MSG had similar benefits from both 12-15 RM and 8-12 RM. Strength gains for subjects with ACE ID genotype in the SSG were similar to MSG gains in response to 8-12 RM loads but not with 12-15 RM loads. Additionally, subjects with DD genotype had superior strength gains in both strength training groups. Tailoring strength training programmes (single-set vs. multiple set) according to the athlete's ACE genotype may be advantageous.

NO ASSOCIATION BETWEEN ACE INSERTION/DELETION POLYMORPHISM AND MAXIMAL EXERCISE CARDIOVASCULAR HEMODYNAMICS IN YOUNG WOMEN

A common insertion (I)/deletion (D) polymorphism at the angiotensin converting enzyme (ACE) locus has been shown to be associated with endurance performance and maximal oxygen uptake. Previously, we found that postmenopausal women with the ACE II geno-type had a significantly higher VO2max than those with the ACE ID or DD genotypes, regardless of their habitual level of physical activity. However, it is not known whether ACE genotype is associated with maximal CV hemodynamics in younger women. PURPOSE: To determine if the ACE I/D polymorphism was associated with VO2max, cardiac output (Q), stroke volume (SV), heart rate (HR), systolic and diastolic blood pressure (BP), total peripheral resistance (TPR) and a-vO2 difference responses during maximal exercise in young women. We also sought to determine if an ACE genotype-exercise interaction was associated with these maximal hemodynamic variables by studying young women with different habitual physical activity (PA) levels (sedentary and endurance-trained). METHODS: Seventy-seven young women (age 18–35 yrs) participated in a maximal ex-ercise test (VO2max) and a maximal cardiac output test on a treadmill using the acetylene rebreathing technique. RESULTS: ACE genotype was not significantly associated with VO2max (II 40.7 ± 3, ID 42.1 ± 1, DD 40.1 ± 1 ml/kg/min) or maximal HR (II 191.4 ± 2, ID 191.3 ± 1, DD 192.5 ± 2 bpm). Systolic or diastolic BP, a-VO2 difference, TPR, SV, and Q during maximal exercise also were not significantly associated with ACE genotype. In addition, there were no statistically significant interactions between ACE genotype and habitual PA levels for any of the maximal exercise hemodynamic variables. CONCLUSSION: The ACE I/D polymorphism is not associated with maximal cardiovascular hemodynamics in young women and there were no significant ACE genotype-habitual PA level interactions associated with maximal cardiovascular hemodynamics in these young women.