Ace Insertion/Deletion Polymorphism and Submaximal Exercise Cardiovascular Hemodynamics in Postmenopausal Women

A common insertion (I)/deletion (D) polymorphism at the angiotensin converting enzyme (ACE) locus has been shown to be related to a number of physiological and pathological phenotypes within the central and peripheral cardiovascular system. We sought to determine if the ACE I/D polymorphism was associated with 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 submaximal exercise in postmenopausal women. We also sought to determine if an ACE gene-exercise interaction was associated with these hemodynamic variables by studying postmenopausal women with different habitual physical activity (PA) levels (sedentary, physically-active, athlete). Sixty-two postmenopausal women participated in a maximal exercise test (VO2max) and on a separate day, treadmill exercise at 40, 60 and 80% of VO2max. ACE genotype was significantly associated with systolic and diastolic BP (p ≈ 0.01), HR (p ≈ 0.002), and a-vO2 difference (p ≈ 0.04) during submaximal exercise. ACE II genotype women had a significantly higher systolic BP (10 mmHg) and a greater a-vO2 difference (0.9 ml/100 ml) than ID and DD genotype women during submaximal exercise. Diastolic BP in the ACE II and ID genotype women was significantly higher (6 and 4 mmHg respectively) than the DD genotype women and HR of the II and DD genotype women was significantly greater (7 and 4 bpm respectively) than the ID genotype women during submaximal exercise. CO, SV and TPR were not significantly associated with ACE genotype; however, there was a significant interaction (p ≤ 0.02) between ACE genotype and PA for all the submaximal exercise hemodynamic variables. We conclude that the ACE I/D polymorphism is associated with submaximal cardiovascular hemodynamics in postmenopausal women and that there are significant gene-environment interactions associated with cardiovascular hemodynamics and different levels of habitual PA. Supported by AARP-Andrus Foundation and Pennsylvania AHA; NIH grants HL-39107, HL-45778, and DK-46204.