Bermudagrass and goosegrass are problematic weeds with limited herbicides available for POST control in creeping bentgrass. Metamifop effectively controls these weeds with greater selectivity in cool-season grasses than other ACCase inhibitors. The objectives of this research were to determine the physiological basis for metamifop selectivity in turfgrasses. In greenhouse experiments, metamifop rate required to reduce shoot biomass 50% from the nontreated (GR50) at 4 wk after treatment was > 6,400, 2,166, and 53 g ai ha−1 for creeping bentgrass, Kentucky bluegrass, and goosegrass, respectively. The GR50 for bermudagrass treated with diclofop-methyl or metamifop was 2,850 and 60 g ha−1, respectively. In laboratory experiments, peak absorption of 14C-metamifop was reached at 48, 72, and 96 h after treatment (HAT) for goosegrass, creeping bentgrass and Kentucky bluegrass, respectively. Grasses translocated < 10% of the absorbed radioactivity out of the treated leaf at 96 HAT, but creeping bentgrass translocated three times more radioactivity than goosegrass and Kentucky bluegrass. Creeping bentgrass, Kentucky bluegrass, and goosegrass metabolized 16, 14, and 25% of 14C-metamifop after 96 h, respectively. Goosegrass had around two times greater levels of a metabolite at retention factor 0.45 than creeping bentgrass and Kentucky bluegrass. The concentration of metamifop required to inhibit isolated ACCase enzymes 50% from the nontreated (I50) measured > 100, > 100, and 38 μM for creeping bentgrass, Kentucky bluegrass, and goosegrass, respectively. In other experiments, foliar absorption of 14C-metamifop in bermudagrass was similar to 14C-diclofop-methyl. Bermudagrass metabolized 23 and 60% of the absorbed 14C-diclofop-methyl to diclofop acid and a polar conjugate after 96 h, respectively, but only 14% of 14C-metamifop was metabolized. Isolated ACCase was equally susceptible to inhibition by diclofop acid and metamifop (I50 = 0.7 μM), suggesting degradation rate is associated with bermudagrass tolerance levels to these herbicides. Overall, the physiological basis for metamifop selectivity in turfgrass is differential levels of target site inhibition.