Many bacteria kill competitors using short-range weapons, such as the Type VI secretion system and contact dependent inhibition (CDI). Although these weapons can deliver powerful toxins, they rely on direct contact between attacker and target cells. We hypothesized that movement enables attackers to contact more targets and thus greatly empower their weapons. To explore this, we developed individual-based and continuum models of contact-dependent combat which show that motility greatly improves toxin delivery through two underlying processes. First, genotypic mixing increases the inter-strain contact probability of attacker and sensitive cells. Second, target switching ensures attackers constantly attack new cells, instead of repeatedly hitting the same cell. We test our predictions with the pathogen Pseudomonas aeruginosa, using genetically engineered strains to study the interaction between CDI and twitching motility. As predicted, we find that motility works synergistically with CDI, in some cases increasing weapon efficacy up to 10,000-fold compared with non-motile scenarios. Moreover, we demonstrate that both mixing processes occur using timelapse single-cell microscopy and quantify their relative importance by combining experimental data with our model. Our work shows how bacteria can combine cell movement with contact-based weapons to launch powerful attacks on their competitors.