Myocardial hypertrophy secondary to hypertension is associated with a parallel addition of sarcomeres that characteristically increases cardiomyocyte cell size and width. From a cellular perspective, concentric hypertrophy differs from eccentric hypertrophy in that with eccentric hypertrophy, cardiomyocytes adapt by increasing sarcomeres in series thereby inducing an increase in cell length. Recently, specific signaling cascades have been associated with concentric and eccentric hypertrophic phenotypes, i.e. calcineurin and IGF, respectively. Even though compensatory concentric hypertrophy is often regarded as an adaptation to normalize wall stress in hypertension, it is frequently manifest with abnormal cardiac function. While recent reports have questioned the necessity of wall stress normalization, the mechanisms associated with the dichotomous adaptive and maladaptive aspects of myocardial hypertrophy are important to understand. Few data exist with respect to how exercise training superimposed on hypertension impacts LV remodeling. Several recent studies in animals have shown that exercise superimposed on hypertension can induce cardiomyocyte proliferation and reduce apoptosis while potentiating cardiomyocyte hypertrophy. Interestingly, neither Akt nor calcineurin abundance seems to underlie exercise-induced hypertrophy in hypertension. In fact, calcineurin abundance is blunted in exercise trained hypertensive hearts. In humans, exercise training in hypertensive patients has been shown to either regress or not change the extent of cardiac hypertrophy. Overall there are only a few studies examining cardiac morphometry and function in subjects with hypertension. The purpose of this review will be to cover the major human and animal findings on this topic, address relevant hypertrophic signaling pathways with exercise superimposed on hypertesnion, and broaden the discussion of exercise and hypertension towards how exercise impacts the cardiomyocyte cell cycle.