Long-term exposure to pressure/volume overload of the heart due to hypertension or aortic stenosis induces pathological hypertrophy and remodeling, and eventually causes heart failure. This process accompanies pathological phenomena such as inflammation, apoptosis, and arrhythmia. On the other hand, physical exercise promotes physiological hypertrophy and remodeling of the heart, thereby enhancing cardiac performance. Interestingly, recent research has suggested that enhancement of heart function is a result not only of physiological hypertrophy of pre-existing cardiomyocytes, but also of cardiac stem cell activation and myocyte formation. Furthermore, exercise improves exacerbated cardiac function in heart diseases, including dilated cardiomyopathy (DCM) and myocardial infarction (MI). The suggested mechanisms of action of exercise remedies for these diseases include angiogenesis, cardiac resynchronization, and inhibition of inflammatory cytokines. However, excessive exercise can cause arrhythmogenic remodeling and sudden death. In this chapter, we elaborate the mechanisms of hypertrophy and remodeling under physiological and pathological conditions and discuss future directions for coping with pathological hypertrophy and remodeling.