This review provides a discussion of the pathophysiologic significance of animal models of the activity-stress paradigm and the role of plasma glucose level in the appearance of physical stress responses of those models. Many research reports have demonstrated that animal models exposed to activity-stress are useful as a "symptomatic model" of anorexia nervosa and obsessive-compulsive disorder as well as peptic ulcer. Our findings show that a decrease in plasma glucose concentration is an important factor in determining the activity-stress-induced physical responses. Further investigation of the pathophysiology of activity-stressed animal models may contribute to the development of new therapeutics for diseases such as anorexia nervosa and obsessive-compulsive disorder.