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Angiotensin-I Converting Enzyme Genotype-Dependent Benefit from Hormone Replacement Therapy in Isometric Muscle Strength and Bone Mineral Density¹

Department of Cardiovascular Genetics (D.W., S.E.H., H.M.), Rayne Institute, University College London, London WC1E 6JJ, United Kingdom; Institute of Human Performance (G.O., R.W., S.B.), University College London, Royal National Orthapaedic Hospital, Stanmore HA7 4LP, United Kingdom; and Department of Cellular and Integrate Biology (D.S.), Division of Biomedical Sciences, Imperial College School of Medicine at St. Mary’s, London W2 1PG, United Kingdom

Address all correspondence and requests for reprints to: Major David Woods, M.D., Department of Diabetes and Endocrinology, Freeman Hospital, Newcastle Upon Tyne NE7 709, United Kingdom.

Low bone mineral density (BMD) and muscle weakness are major risk factors for postmenopausal osteoporotic fracture. Hormone replacement therapy (HRT) reverses the menopausal decline in maximum voluntary force of the adductor pollicis and reduces serum angiotensin-I converting enzyme (ACE) levels. The insertion (I) allele of the ACE gene polymorphism is associated with lower ACE activity and improved muscle efficiency in response to physical training. Therefore, we examined whether the presence of the I allele in postmenopausal women would affect the muscle response to HRT. Those taking HRT showed a significant gain in normalized muscle maximum voluntary force slope, the rate of which was strongly influenced by ACE genotype (16.0 ± 1.53%, 14.3 ± 2.67%, and 7.76 ± 4.13%, mean ± SEM for II, ID, and DD genotype, respectively; P = 0.017 for gene effect, P = 0.004 for I allele effect). There was also a significant ACE gene effect in the response of BMD to HRT in Ward’s triangle (P = 0.03) and a significant I allele effect in the spine (P = 0.03), but not in the neck of femur or total hip. These data suggests that low ACE activity associated with the I allele confers an improved muscle and BMD response in postmenopausal women treated with HRT.

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