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Kritchevsky SB, Nicklas BJ, Visser M, et al. Angiotensin-Converting Enzyme Insertion/Deletion Genotype, Exercise,
and Physical Decline. JAMA. 2005;294(6):691–698. doi:10.1001/jama.294.6.691
Author Affiliations: The Sticht Center on Aging
and Center for Human Genomics, Department of Internal Medicine (Drs Kritchevsky,
Nicklas, Penninx, and Pahor) and Department of Public Health Sciences (Dr
Lange), Wake Forest University School of Medicine, Winston-Salem, NC; Institute
of Health Sciences (Dr Visser) and Department of Psychiatry (Dr Penninx),
Vrije Universiteit, the Netherlands; Gerontology Research Center, National
Institute on Aging, Baltimore, Md (Dr Simonsick); Departments of Epidemiology
(Dr Newman) and Medicine (Dr Goodpaster), University of Pittsburgh, Pittsburgh,
Pa; Laboratory of Epidemiology, Demography, and Biometry, National Institute
on Aging, Bethesda, Md (Dr Harris); Department of Preventive Medicine, University
of Tennessee, Memphis (Dr Satterfield); Department of Kinesiology, University
of Wisconsin, Madison (Dr Colbert); Prevention Sciences Group, University
of California, San Francisco (Ms Rubin); Department of Aging and Geriatric
Research, University of Florida, Gainesville (Dr Pahor).
Context 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.
Objective To determine whether the ACE genotype interacts with significant physical
activity to affect the incidence of mobility limitation in well-functioning
Design, Setting, and Participants 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.
Main Outcome Measure 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).
Results Physically active participants (those reporting expending ≥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.
Conclusions 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.
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