Background/Aims: The high prevalence of childhood obesity, and its associated metabolic disorders (e.g. insulin resistance, IR), is often attributed to the lack of physical activity (PA) undertaken by contemporary children. However, there is little convincing evidence that physical inactivity causes obesity or indeed that the promotion of PA will impact on it The aims of this thesis will help determine i) whether inactivity is a risk factor for obesity (Aim 1) or metabolic disturbance (Aim 2) ii) what proportion of children/adolescents are deemed inactive (Aim 3) and iii), whether we can get children to be more active (Aim 4) and if not, why not (Aim 5). Methods: Aims 1, 2 and 3 used data from the EarlyBird Diabetes Study, a longitudinal study with annual measures of body fat percentage (BF%), metabolic disturbance and accelerometer-based PA from 5-16y in -300 children. Aim 1 examined both directions of causality between PA and BF% from 7-10y. Aim 2 examined the relationship between PA and metabolic disturbance (JR, lipids, BP etc.) in childhood (5-By) and in adolescence (9-16y). Aim 3 established the proportion of children that were deemed inactive (i.e. undertook less than 60mins/day of moderate-and-vigorous PA, MVPA) every year from 5-15y. Aim 4 involved a systematic review of childhood PA intervention studies that had measured PA with accelerometers. Aim 5 used data from the EarlyBird Three Schools Study (accelerometer-based PA in -200 children, aged 9y) to compare the school time and non-school time PA across three schools with varying amounts of timetabled P.E. (-2 to -9hrs/wk). Results: Aim 1: Inactivity does not appear to be a risk factor for obesity given that changes in BF% from 7-10y were not associated with PA at 7y (p=0.8), but changes in PA from 7-10y were associated with BF% at 7y (p=0.02). Aim 2: Inactivity may be a slight risk factor for metabolic disturbance given the small or temporary associations found with some metabolic markers (e.g. the mid-adolescent peak in IR was 17% lower in the more active children, but this difference had disappeared by late-adolescence). Aim 3: The proportion deemed inactive was high during childhood (-70%) and even higher during adolescence (-80%). Aim 4: It may be difficult to make children more active given that PA interventions have only led to small increases in MVPA (-4mins/day). Aim 5: Such small intervention effects could be due to the compensation of PA given that children receiving -9hrs/wk of P.E., compared to -2hrs/wk, off-set almost all of the 15mins/day difference in school time MVPA by undertaking 14mins/day less MVPA in non-school time. Conclusions: Despite most children being deemed inactive, we conclude that the promotion of PA should not be used as the tool for tackling the childhood obesity epidemic due to the limited risk that inactivity poses to obesity-related health, and the inability of interventions to increase activity levels by a meaningful amount.