Habitual physical activity in children, the role of genes and the environment

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 re-spiratory 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 com-mon (c2) and unshared (e2) environmental components. Results: Because PAEE [TEE (RMR 0.1 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, respec-tively; 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 vari-ance 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. A