Exercise-training and hypertension induced cardiac hypertrophy but modulate differently left ventricle (LV) function. Objective: To evaluate cardiac adaptations induced by moderate exercise-training in normotensive- and untreated severe-hypertensive rats. Methods: Four groups of animals were studied; normotensive (Ctl) and severe-hypertensive (HT) Wistar rats were assigned to sedentary (-Sed) or performed a moderate exercise-training (-Ex) over a 10-week period. Severe hypertension was induced in rat by a two-kidney-one-clip model. At the end of training period, haemodynamic parameters and LV morphology and function were assessed using catheterism and conventional pulsed-Doppler echocardiography. LV histology was performed to study fibrosis infiltrations. Results: Severe-hypertension increased systolic blood pressure to 202±9 mmHg, induced pathological hypertrophy (LV hypertrophy index was 0.34±0.02 vs. 0.44±0.02 in Ctl-Sed and HT-Sed groups respectively) with LV relaxation alteration (E/A ratio = 2.02±0.11 vs. 1.63±0.12). Blood pressure was not altered by exercise-training but arterial stiffness was reduced in trained-hypertensive rats (pulse pressure was 75±7 mmHg vs. 62±3 mmHg in HT-Sed and HT-Ex groups respectively). Exercise-training induced eccentric hypertrophy in both -Ex and -Ex groups by increasing LV cavity without alteration of LV systolic function. However, LV hypertrophy index was significantly decreased in normotensive rats only (0.34±0.02 vs. 0.30±0.02 in Ctl-Sed and Ctl-Ex groups respectively). Moreover, exercise-training improved LV passive filling in Ctl-Ex rats but not in Ht-Ex rats. Conclusion: In this study, exercise-training did not reduce blood pressure and induced an additional physiologic hypertrophy in untreated severe-hypertensive rats which was slightly blunted when compared to normotensive. However, cardiac function was not worsening by exercise-training.