The heart’s developed pressure (DP) in Langendorff heart experiments increases with preload via the Frank-Starling mechanism up to a critical transition point at which DP starts to decrease with preload. A similar behavior is found at the cellular level, where the tension developed by skinned cardiac fibers or myocytes in isometric tension test increases with sarcomere length up to a transition point beyond which, the tension decreases. This cellular-level behavior is termed myofilament length dependent activation. While these two behaviors are similar, they occur at vastly different scales. Specifically, the DP – preload and sarcomere length – tension relationships occur, respectively, at the organ and cellular scales. Correspondingly, it remains unclear how much these behaviors are related. To address this issue, we use computer modeling that connects cellular to organ mechanics found in the ex-vivo beating rat heart experiments to determine whether the DP – preload relationship at the organ level can be explained solely by the sarcomere length – tension relationship at the cellular level. We found that the non-monotonic behavior of the DP with preload is consistent with a model predicted feature of myocardial contractility. The LV sarcomere length at the transition where DP and myocardial contractility start to reduce is 2.12 ± 0.03 μm. This transition sarcomere length is outside the range of 2.2 – 2.4 μm that is associated with the peak tension found in skinned rat cardiac fibers or myocytes with isometric tension test. This disparity suggests the presence of other factors affecting the DP – preload relationship found in Langendorff heart experiments such as the prescribed initial length of sarcomere that vary between different rat species.