The influence of food consumption and running activity on the activity-stress ulcer in the rat

Abstract

Rats housed in activity cages and fed 1 hour daily died before the end of the 21-day experimental period and revealed extensive ulcers in the glandular stomach, whereas food-yoked control rats, not housed in activity cages, did not die and were ulcer-free. Rats demonstrating high running-activity levels under ad lib feeding conditions subsequently revealed a higher incidence of lesions as compared to low-activity rats. Attempts to attenuate activity and lesion incidence by reversing the light-dark cycle failed, but the higher mortality level in rats under the reversed light-dark condition was related to higher activity levels in these rats. Young rats with high activity levels died sooner and had ulcers when compared to older rats with low activity levels. These results suggested that running activity, and not reduced food intake, was critically involved in the development of the activity-stress ulcer.

Organ weights in rats with activity-stress ulcers

“…Rumenal lesions were not observed. These results are consistent with previous studies on the activity-stress ulcer (Pare, 1974(Pare, , 1975Vincent & pare, 1976).…”

“…The spleen, liver, and kidney data do resemble typical changes brought about by starvation, and it would be unreasonable to conclude that reduced feeding has no input in the development of the activity-stress ulcer. However, on th~ basis of previous studies (Pare, 1974(Pare, , 1975Vincent & Pare, 1976;Pare & Houser, 1973) and the present study, it is reasonable to suggest that the activity-stress ulcer is not a starva tion ulcer.…”

“…Glandular lesions occur in rats which are housed in running wheel activity cages and fed only 1 h each day (Pare, 1974(Pare, , 1975Vincent & Pare, 1976). Rats which are exposed to this regimen will die within 3 to 10 days and reveal lesions in the glandular stomach when autopsied.…”

Relevance of animal models to human eating disorders and obesity

“…Initially, animals compensate by increasing the amount of food eaten during the period of restricted access; however, with increased activity, animals no longer increase the amount consumed. "Activity/stress" model animals develop starvation-induced immunodeficiency and atrophy of the spleen and thymus (Watanabe et al 1992), as well as stress ulcers (Paré 1975), complications not observed in individuals with AN. In this model, administration of L-tryptophan and serotonin agonists and antagonists reduced physical activity (Pirke et al 1993) and tyrosine supplementation improved appetite and cognitive function and delayed the onset of fatigue in mice .…”

Activity-based anorexia: Ambient temperature has been a neglected factor

“…The rate of weight loss is much reduced and food intake greater with longer feeding periods (e.g., Paré 1980;Paré & Valdsaar, 1985;Paré, Vincent, & Natelson, 1985;Routtenberg, 1968;Routtenberg & Kuznesof, 1967;Watanabe, Hara, & Ogawa, 1992), with multiple rather than with single daily feeding periods (e.g., Lambert & Peacock, 1989;Tsuda, Tanaka, Jimori, Ida, & Nagasaki, 1981), with feeding during the dark cycle (e.g., Hara, Manabe, & Ogawa, 1981;Paré, 1975;, and with prior adaptation to the restricted feeding schedule (e.g., Paré, Vincent, Isom, & Reeves, 1978;Routtenberg, 1968). Further procedural factors include prior exposure to the running wheel (Routtenberg,1968), type of feeding site (Paré, 1974;Routtenberg, 1968), amount of access to the wheel Epling & Pierce, 1984;Paré, 1980), and dietary composition (Beneke & Vander Tuig, 1996).…”