Single repeated exposures to social stressors induce robust shifts of cardiac sympathovagal balance towards sympathetic dominance, both during and after each agonistic interaction. However, little evidence is available regarding possible persistent pathophysiological changes due to chronic social challenge. In this study, male CD-1 mice (n=14) were implanted with a radiotelemetry system for electrocardiographic recordings. We assessed the effects of chronic psychosocial stress (15-days' sensory contact with a dominant animal and daily 5-min defeat episodes) on: (i) sympathovagal responsiveness to each defeat episode, as measured via timedomain indexes of heart rate variability (R-R interval, SD_RR and r-MSSD); (ii) circadian rhythmicity of heart rate across the chronic challenge (night phase, day phase and rhythm amplitude values); (iii) amount of myocardial structural damage (volume fraction, density and extension of fibrosis). This study indicated that there was habituation of acute cardiac autonomic responsiveness, i.e. the shift of sympathovagal balance towards sympathetic dominance was significantly reduced across repeated defeat episodes. Moreover, animals exhibited significant changes in heart rate rhythmicity, i.e. increments in day and night values and reductions in the rhythm amplitude, but limited to the first five days of chronic psychosocial stress. The volume fraction of fibrosis was 6-fold larger than in control animals, due to the appearance of many microscopic scarrings. In summary, although mice appeared to adapt to chronic psychosocial stress in terms of acute cardiovascular responsiveness and heart rate rhythmicity, structural alterations occurred at myocardial level.