Swim training applied at early age is critical to adrenal medulla catecholamine content and to attenuate monosodium L-glutamate-obesity onset in mice D.X. Scomparin, S. Grassiolli, A.C. Marçal, C. Gravena, A.E. Andreazzi, P.C.F. Mathias ⁎ Laboratory of Secretion Cell Biology, Department of Cell Biology and Genetics, State University of Maringá, Av. Colombo 5790, Bloco H-67, S/019, 87020-900 Maringá PR Brazil Received 29 January 2006; accepted 11 July 2006 Abstract Exercise has been recommended as a remedy against a worldwide obesity epidemic; however, the onset of excessive weight gain is not fully understood, nor are the effects of exercise on body weight control. Activity deficits of the sympathetic nervous system, including the sympathoadrenal axis, have been suggested to contribute to high fat accumulation in obesity. In the present work, swim training was used to observe fat accumulation and adrenal catecholamine stocks in hypothalamic-obese mice produced by neonatal treatment with monosodium L-glutamate (MSG). MSG-treated and normal mice swam for 15 min/day, 3 days a week, from weaning up to 90 days old (EXE 21–90); from weaning up to 50 days old (EXE 21–50) and from 60 up to 90 days old (EXE 60–90). Sedentary MSG and normal mice (SED groups) did not exercise at all. Animals were sacrificed at 90 days of age. MSG treatment induced obesity, demonstrated by a 43.08% increase in epididymal fat pad weight; these adult obese mice presented 27.7% less catecholamine stocks in their adrenal glands than untreated mice (p b 0.001). Exercise reduced fat accumulation and increased adrenal catecholamine content in EXE 21–90 groups. These effects were more pronounced in MSG-mice than in normal ones. Halting the exercise (EXE 21–50 groups) still changed fat accretion and catecholamine stocks; however, no effects were recorded in the EXE 60–90 groups. We conclude that metabolic changes imposed by early exercise, leading to an attenuation of MSG-hypothalamic obesity onset, are at least in part due to sympathoadrenal activity modulation. © 2006 Elsevier Inc. All rights reserved. Keywords: Catecholamines; Adrenal gland; MSG-obesity; Swim training; Mice Introduction Overweight and obesity occur worldwide. In spite of better economic access to food in Europe and USA, developing countries are showing a high prevalence of obesity. Recently, a significant increase in obesity was also found among children (de Vasconcelos and da Silva, 2003; Filozof et al., 2001). Therefore, public health strategies are being implemented to halt the rise in obesity. These are mainly focused on reduction in food intake and changes in sedentary lifestyle through exercise programs (Jakicic, 2003). Beyond the strategies created to reduce overweight by public health policies, some concepts on obesity etiologies, such as overfeeding and lack of exercise, are accepted. However, the pathophysiologic mechanisms that lead to malfunction of energy intake and expenditure are still unclear. The autonomic nervous system (ANS) is one of the key factors in the regulation of energy balance and body fat storage. In human and in several animal experimental models of obesity, such as rodents with lesions on specific brain areas, e.g. hypothalamus, and genetically obese rodents, high parasympathetic and low sympathetic activity has been found (Atef et al., 1992; Leigh et al., 1992; Weyer et al., 2001). Exercise is able to stimulate sympathetic nervous system (SNS) activity that leads to energy mobilization and therefore reduces fat tissue deposits (Scheurink et al., 1992). Catechola- mines, epinephrine and norepinephrine stored in the adrenal medulla are also released by exercise stimulus (Scheurink et al., Life Sciences 79 (2006) 2151 – 2156 www.elsevier.com/locate/lifescie ⁎ Corresponding author. Tel./fax: +55 44 3261 4892. E-mail address: pmathias@uem.br (P.C.F. Mathias). 0024-3205/$ - see front matter © 2006 Elsevier Inc. All rights reserved. doi:10.1016/j.lfs.2006.07.012