HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Franks, P. W Articles by Salbe, A. D Search for Related Content PubMed PubMed Citation Articles by Franks, P. W Articles by Salbe, A. D Agricola Articles by Franks, P. W Articles by Salbe, A. D

Habitual physical activity in children: the role of genes and the environment^1,2,3

¹ From the National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Phoenix, AZ (PWF, RLH, ITH, WCK, PAT, and ADS); the Pennington Biomedical Research Center, Baton Rouge, LA (ER); the Section on Statistical Genetics, Department of Biostatistics & Clinical Nutrition Research Center, The University of Alabama at Birmingham, Birmingham, AL (DBA)

Background:Understanding the factors that contribute to physical inactivity in children is important because sedentary behavior strongly relates to metabolic disorders such as obesity and diabetes.

Objective:We aimed to quantify the genetic and environmental influences on physical activity energy expenditure (PAEE) in 100 sex-concordant dizygotic (n = 38) and monozygotic (n = 62) twin pairs aged 4-10 y.

Design:Resting metabolic rate (RMR) was assessed by using respiratory gas exchange, total energy expenditure (TEE) by using doubly labeled water, and body composition by using dual-energy X-ray absorptiometry. Structural equation modeling was used to partition the phenotypic variance into additive genetic (a²) and common (c²) and unshared (e²) environmental components.

Results:Because PAEE [TEE – (RMR + 0.1 x TEE)] depends on body weight, which is highly heritable, we tested several models: 1) after adjustment for age, sex, ethnicity, study date, season, and weight, a² explained none of the phenotypic variance in PAEE (95% CI: 0%, 38%), whereas c² and e² accounted for 69% (33%, 77%; P = 0.001) and 31% (23%, 39%; P < 0.001) of the variance, respectively; 2) after adjustment for the cofactors in model 1, a² explained 19% of the phenotypic variance in TEE (0%, 60%; P = 0.13), whereas c² and e² accounted for 59% (16%, 79%; P = 0.007) and 23% (17%, 31%; P < 0.0001) of the variance, respectively; 3) in models adjusted as above (excluding weight), a² explained no variance in physical activity level (TEE/RMR) (0%, 32%; P = 0.50), whereas c² and e² explained 65% (34%, 60%; P = 0.001) and 35% (28%, 45%; P < 0.0001) of the variance, respectively.

Conclusions:Our data suggest that the familial resemblance in physical activity in these children is explained predominantly by shared environmental factors and not by genetic variability.

Key Words: Physical activity energy expenditure • physical activity level • genetics • children • twins • doubly labeled water

This article has been cited by other articles:

				M. Teran-Garcia, T. Rankinen, and C. Bouchard Genes, exercise, growth, and the sedentary, obese child J Appl Physiol, September 1, 2008; 105(3): 988 - 1001. [Abstract] [Full Text] [PDF]

				P. W. Franks Muscling in on the genetics of quantitative disease traits J Appl Physiol, October 1, 2007; 103(4): 1111 - 1112. [Full Text] [PDF]

				J O'Loughlin, E Dugas, K Maximova, and N Kishchuk Reporting of ethnicity in research on chronic disease: update Postgrad. Med. J., November 1, 2006; 82(973): 737 - 742. [Abstract] [Full Text] [PDF]

				N. F Butte, G. Cai, S. A Cole, and A. G Comuzzie Viva la Familia Study: genetic and environmental contributions to childhood obesity and its comorbidities in the Hispanic population. Am. J. Clinical Nutrition, September 1, 2006; 84(3): 646 - 654. [Abstract] [Full Text] [PDF]