Although the negative inotropic effects of both acute and chronic ethanol (EtOH) exposure are well known, little is known concerning the acute-to-chronic transition of such effects. In this study, our objective was to address this question by detailing the effects acute EtOH exposure induces on cellular excitation-contraction (E-C) coupling, and subsequently comparing if and how such changes translate to the early chronic EtOH condition in a rat model known to develop alcohol-induced cardiomyopathy. Acute EtOH exposure, as formerly reported, indeed induced dose-dependent negative inotropic changes in cellular E-C coupling manifest as reductions in cell-shortening, Ca²⁺ transient amplitude, Ca²⁺ decay-rate and sarcoplasmic reticulum (SR) Ca²⁺ content of isolated rat ventricular cardiac myocytes. Supplementary, we found Ca²⁺ spark character not to be significantly affected by acute EtOH exposure. In contrast, the results obtained from cardiac myocytes isolated from rats fed a diet containing ~9% v:v EtOH for 1 month revealed changes in these parameters reflecting positive inotropy; whereas at 3-months these parameters again reflected negative inotropy similar but not identical to that induced by acute EtOH exposure. No significant changes were evident at either 1 or 3 months chronic EtOH administration in echocardiographic parameters known to be perturbed in alcoholic cardiomyopathy, thus indicating that we were examining an asymptomatic stage in chronic EtOH administration consistent with an acute-to-chronic transition phase. Continued study of such transition-phase events should provide important insight into which molecular-cellular components of E-C coupling play pivotal roles in EtOH-induced disease processes such as ACM.