More than 50 years ago it was proposed that …’the importance of calorie expenditure and its relation to intake has begun to reassert itself…(through) a desire to find out more about the mechanisms which relate intake to expenditure – what regulates appetite in fact…(p286)…the differences between the intakes of food must originate in the differences in energy expenditure’ (p297) [1]. This view has been overlooked for decades, but recent research on appetite control within an energy balance framework has provided evidence for an impact of Energy Expenditure (EE) on Energy Intake (EI).. The body’s energy requirements reflected in Fat Free Mass (FFM) [2] and Resting Metabolic Rate (RMR) [3] are closely associated with homeostatic indices such as meal size and Total Daily Energy Intake. This has prompted interest in the impact of behavioural EE, and especially the role of sedentariness, on appetite control. Alongside the question: ‘can you outrun a bad diet?’, we can ask: ‘can you out eat an active lifestyle?’ These questions demand a study of appetite control within an energy balance framework. The schema of Mayer [4] proposed that physical activity (or total EE) is related to EI by a U-shaped function. At average to high levels of EE the appetite system appears well controlled (Zone of Regulation), but below a normal activity level (sedentary zone or Zone of Dysregulation) appetite is weakly controlled. Sedentariness is dangerous not only because it lowers EE but also because it can promote overeating. It has been hypothesised that ‘Body signals go awry in sedentary lifestyles; .. Sedentary persons may lose the innate ability to compensate for inactivity by reducing their eating’ [5]. This passive overconsumption can be expected to lead to fat gain. Using a 24-hour monitoring system it can be demonstrated that sedentary behaviour is positively associated with percent body fat and with traits of appetite dysregulation. In contrast the amount of moderate to vigorous activity is negatively related to body adipose tissue [6]. Prescribed mandatory medium term interventions that increase physical activity bring about a significant reduction in Fat Mass (FM) with a preservation (or increase) in FFM This objective evidence is a strong refutation of claims about the ‘myth of physical inactivity and obesity’ [7].However there is large individual variability probably reflecting allelic and biological diversity leading to the identification of responder and non-responder phenotypes. Individuals behave differently due (in part) to the operation of a dual action of exercise on appetite mechanisms; this can take the form of an increase in hunger coupled with an increase in the strength of post-prandial satiety signalling. This satiety effect is associated with changes in Gastro-Intestinal peptide levels (ghrelin, GLP-1, PYY and CCK), and also with an increase in insulin and leptin sensitivity. These findings indicate a complex (bi-directional) relationship between EE and EI that cannot be described by one simple formula. Sedentariness is a risk factor for fat gain and for weakened satiety control. However, it should be remembered that a high Energy Density diet can raise EI above the EE from a PAL of 1.7/1.8. These findings endorse the importance of studying appetite control within an energy balance framework and point to the need to control both diet and activity