In response to changes in hemodynamic stresses and other environmental alterations the heart alters its size, shape, and cell biology. These changes generally enable the heart to adapt functionally to its new environment and to maintain performance measures within normal limits, at least for a limited time. The function of the heart is to pump blood by actively generating contractile force. Therefore, remodeling of the cardiomyocyte, the cell specifically containing the contractile elements, is of central interest. Indeed, in patients subjected to the isolated, pure volume loading of aortic regurgitation, loss of contractility is the best predictor of outcome in unoperated patients as well as in those who undergo aortic valve replacement. The prototypical and most dramatic example of physiological remodeling is the response to intensive athletic training. Undoubtedly, more modest cardiac remodeling, perhaps imperceptible with measuring tools, occurs in response to less intense variations in human activity.