*4.8. Problematic Use of Physical Activity and Compulsivity*

Continuing normal to high activity levels despite weight loss and a negative energy balance is recognized as an exclusive specificity of AN patients compared to individuals in a situation of starvation due to other causes such as those implicating an increase in circulating inflammatory cytokines [103] in humans as well in animal models [104,105].

In animal models mimicking several symptoms of AN in an attempt to give a rather biological approach, a reduction in food intake and body weight was paradoxically accompanied by a progressive increased activity level. The most described animal model combining food restriction and voluntary physical activity is the "Activity-Based Anorexia" model (ABA model) developed in the rat by Routtenberg and Kuznesof [106], then in the mouse. This model is also called "starvation-induced hyperactivity" [107] or "semi-starvation induced hyperactivity" [108]. In fact, the rodents have free access to a running wheel and showed hyperactivity occurring in response to a limited food supply due to limited access time to food (1–2 h per day). Such behavior, occurring at 2–3 days after the

beginning of the protocol, led to feedback inhibition of food intake or self-starvation and death in 5–6 days [109]. Thus, the negative energy balance state that becomes life threatening, eventually leads to death [2,110]. A lot of research has been done on animal models to try understanding and determining the biological phenomenon underneath this particular hyperactivity, which occurred several hours before food distribution and is called food anticipatory activity. Similar activity has been also described in AN patients [111]. The animal models will not be detailed as it is beyond the scope of this systematic review.
