Physical activity is likely determined by a complex mixture of biological, social, cultural and environmental factors. Most studies so far have focused on sociodemographic factors, features of the built environment and social support . Studies of physical activity in the DOHaD context are still rare [10–12, 18, 19]. In a prospective birth cohort study in Brazil, we evaluated the association between early growth, both in terms of weight and length/height, and objectively-measured physical activity. In summary, we found similar patterns of weight gain between those classified as active or inactive at 13.3 years of age, thus suggesting that prenatal, infancy and childhood weight gains are not major determinants of physical activity levels in adolescence in our cohort; however we also observed subtle differences in early length gain patterns between active and sedentary adolescents, and this observation offer a preliminary insight into a topic meriting further research.
Results on the association between birth-weight and physical activity are still inconclusive. Some studies reported lower motor skills and reduced aerobic fitness among those born with very low birthweight , but studies in population-based samples have, in general, failed to detect associations between birthweight and physical activity . Studies from low and middle-income countries have consistently reported that adequate birthweight and rapid weight and length gains in the first two years of life are associated with increased human capital, and does not increase – or even reduces - the risk of most precursors for chronic diseases . Rapid weight gain after the age of two years, however, is consistently associated with the later appearance of risk factors for chronic diseases [21–23]. The null findings we report here suggest that reduced physical activity levels in adolescence are not part of the pathway leading from early growth patterns to later health.
Analyses comparing the early growth trajectories of subjects experiencing chronic diseases as adults  are useful but differences between groups may appear small in part because other subsequent exposures have diluted the magnitude of the effect. Nevertheless, our results suggest that there is a likely link between length gain in infancy and subsequent physical activity practice, and these findings were confirmed by the conditional growth analyses.
Some limitation of the present study should be mentioned. We do not have data at the age of two years, a well-known threshold in terms of length gain . Puberty status was not taken into account, but it is known that it can influence adolescent health and development. Although our subsample is comparable to the full cohort in terms of some key variable, the possibility of some degree of selection bias cannot be ruled out.
If our results on the association between length gain in infancy and later physical activity are confirmed by others, one possible explanation is that adolescent physical activity is affected by early hormonal programming. Early growth in height is associated with IGF-1 levels. Faster growth in infancy implies higher IGF-1, which might have effects on later metabolism. An alternative explanation is that there may be subtle genetic differences, in terms of genes which affect both early growth and later physical activity. For example, Elks and colleagues found that a proportion of the genes associated with adult obesity were also associated with early growth patterns .