Myotonic dystrophy type 1 (DM1) is a genetic disorder characterized by progressive muscle weakness and dysfunction, with disease severity often linked to the length of CTG repeat expansions in affected individuals. Effective in vitro modeling of DM1 is essential for advancing therapeutic strategies. To address this, we developed three distinct 3D engineered muscle tissue (EMT) models derived from induced pluripotent stem cell (iPSC) lines with differing DM1 genetic profiles. Two lines originated from DM1 patient iPSCs with medium and long CTG repeat expansions, while the third was engineered from the long-repeat line using CRISPR/Cas9 to eliminate all CTG repeats. Using the Mantarray platform, we observed distinct functional stratification among the three lines, with contractile output inversely correlating with CTG repeat length. Notably, these clinically relevant distinctions in muscle contractility did not correspond with myotube fusion efficiency, suggesting that alternative mechanisms may drive muscle dysfunction in DM1. This finding indicates that muscle contractility could serve as a more precise marker of disease severity than fusion rate or nuclear foci numbers, which are commonly used metrics in DM1 research. Our findings highlight the utility of this platform for assessing DM1 phenotypes in a functionally predictive and high-throughput manner, providing a valuable tool for disease modeling and longitudinal observations required for therapeutic development.