title: Habitual physical activity in children: the role of genes and the environment.
abstract: 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.
  
  
  METHODS
  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.
authors.affiliation: National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Phoenix, AZ 85014, USA. pfranks@niddk.nih.gov
authors.forename: Paul W
authors.initials: PW
authors.lastname: Franks
authors.forename: Eric
authors.initials: E
authors.lastname: Ravussin
authors.forename: Robert L
authors.initials: RL
authors.lastname: Hanson
authors.forename: Inge T
authors.initials: IT
authors.lastname: Harper
authors.forename: David B
authors.initials: DB
authors.lastname: Allison
authors.forename: William C
authors.initials: WC
authors.lastname: Knowler
authors.forename: P Antonio
authors.initials: PA
authors.lastname: Tataranni
authors.forename: Arline D
authors.initials: AD
authors.lastname: Salbe
mesh_terms: D015502:Absorptiometry, Photon; D001481:Basal Metabolism / Q000235:genetics* / Q000502:physiology; D001823:Body Composition / Q000502:physiology*; D001835:Body Weight / Q000235:genetics / Q000502:physiology; D002648:Child; D002675:Child, Preschool; D003903:Deuterium; D004734:Energy Metabolism / Q000235:genetics* / Q000502:physiology; D004777:Environment; D015444:Exercise / Q000502:physiology*; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D008019:Life Style; D008297:Male; D010101:Oxygen Consumption; D010641:Phenotype; D014429:Twins, Dizygotic; D014430:Twins, Monozygotic
chemical_list: D003903:Deuterium