More than 5 million underage Americans report binge drinking at least once per month. While the effects of alcohol consumption on the adult heart have been well studied, the impact to the adolescent heart is almost entirely unknown. Adolescents primarily consume alcohol in a binge pattern, which elevates blood alcohol content (BAC) to 0.08 g/dL within 2 hours. During adolescence the body grows rapidly, and the heart must also grow by cellular hypertrophy to meet this increasing demand. Our goal was to determine the impact of adolescent binge alcohol exposure on the heart, using an outbred rat model. This thesis project first suggested that binge alcohol exposure slowed down the heart growth in adolescence, so the heart increased systolic function to compensate the increased demand from the body by activating beta-adrenergic signaling (increased Troponin I phosphorylation). In addition, our data revealed novel findings that adolescent binge alcohol exposure decreased diastolic function, including increased single cell passive stiffness. Our H&E histological staining showed different myocyte remodeling at different positions of the left ventricle. Furthermore, we performed RNA-seq and identified 58 down-regulated and 10 up-regulated genes in the Binge group. Many of these genes suggest a switch in substrate utilization from preferred fatty acid metabolism to less efficient glucose metabolism in the Binge rats. These data reveal a previously unappreciated pathological impact of adolescent binge alcohol exposure. The young heart can compensate for these consequences at first and appear healthy. However, the long term impact of these effects may be significant and whose underlying cause was previously unknown
