Low temperature directly alters turtle cardiovascular physiology, causing bradycardia, arterial hypotension and a reduction in systemic blood pressure. Additionally, blood viscosity, systemic resistance and sensitivity to cardiac preload increase. However, the long-term effects of these seasonal responses are unclear. We acclimated red-eared sliders to a control temperature (25 °C) or chronic cold (5 °C). To differentiate the direct effects of temperature from a cold-induced remodeling response, all measurements were conducted at the control temperature. In anesthetized turtles, cold acclimation reduced systemic resistance by 1.8-fold and increased systemic blood flow by 1.4-fold, resulting in a 2.3-fold higher right to left (R-L) cardiac shunt flow. Following a volume load by bolus injection of saline (calculated to increase stroke volume by 5-fold, ~2.2 % of total blood volume), systemic resistance was reduced while pulmonary blood flow and systemic pressure increased. An increased systemic blood flow meant the R-L cardiac shunt was further pronounced. In the isolated ventricle, passive stiffness increased following cold acclimation with 4.2-fold greater collagen deposition in the myocardium. Histological sections of the major outflow arteries revealed a 1.4-fold higher elastin content in cold-acclimated animals. These results suggest that cold acclimation alters cardiac shunting patterns with an increased R-L shunt flow, achieved through reducing systemic resistance and increasing systemic blood flow. Furthermore, our data suggests the that cold-induced cardiac remodeling may reduce the stress of high cardiac preload by increasing compliance of the vasculature and decreasing ventricular compliance. Together, these responses could compensate for reduced systolic function at low temperatures.