Resistance training (RT) is accompanied by cardiac hypertrophy but the role of Renin-Angiotensin-System (RAS) in this response is elusive. We evaluated this question in 36 male Wistar rats in 6 groups: Control (n=6); Trained (n=6); Control+Losartan (10mg/kg/day, n=6); Trained+Losartan (n=6); Control+High Salt diet (1%, n=6); Trained+High Salt diet (1%, n=6), high salt was used to inhibit the systemic RAS and Losartan to block AT1 receptor. The exercise consisted of: 4 x 12 bouts, 5x/week/8 weeks, with 65-75% of 1 Repetition Maximum(1RM). Left ventricle weight to body weight ratio increased only in Trained and Trained + High Salt diet groups (8.5% and 10.6%, p<0.05) compared with control. None of the pathological cardiac hypertrophy markers, ANP and MHC/MHC ratio, were changed. ACE activity was analyzed by fluorometric assay (systemic and cardiac) and plasma renin activity (PRA) by RIA and remained unchanged upon RT, whereas PRA decreased significantly with high salt diet. Interestingly, using Western blotting analysis and RT-PRC, no changes were observed in cardiac AT2 receptor levels, whereas the AT1 receptor gene (56%, p<0.05) and protein (31%, p<0.05) expressions were upregulated in Trained group. Also, cardiac Ang II concentration evaluated by imunoreactive assay remains unchanged (23.27±2.4 vs 22.01±0.8 pg/mg). Administration of subhypotensive dose of Losartan prevented left ventricle hypertrophy in response to the resistance training. Altogether, we provide evidence that resistance training-induced cardiac hypertrophy is accompanied by induction of AT1 receptor expression with no changes in cardiac Ang II which suggests a local activation of the RAS consistent with the hypertrophic response.