Hypertrophy of cardiac muscle occurs both as the normal mode of ventricular growth after birth and, as a pathophysiological response, in adaptation to mechanical overload [1–3]. Classically, cardiac myocytes lose their proliferative capacity shortly after birth, and subsequent enlargement is due to an increase in cell size, mediated in turn by an increase in total cellular protein. During “adaptive” hypertrophy, the resulting increase in protein synthesis and protein content is not merely a generalized effect, but is instead a highly regulated event marked by preferential modulation of specific subsets of genes [1–3]. For example, in rodent models, which have been the most thoroughly investigated for evidence of this plasticity, a switch occurs in the expression of myosin heavy chain (MHC) isoforms: selective reactivation of the “fetal” βMHC gene, whereas αMHC ordinarily predominates [4,5]. Expression of α-skeletal actin — a second contractile protein gene that is preferentially transcribed in the embryonic ventricle — is likewise specifically enhanced in hypertrophied hearts [5,6]. Altered expression of these contractile protein genes has been linked to altered mechanical performance of ventricular myocardium, as increased fractional content of PMHC is held to improve the economy of contraction, at the expense of the maximum velocity of unloaded shortening [7].