Saturated sediments are hotspots of biogeochemical reactivity in river corridors. High reactivity is promoted by the exchange of surface water and groundwater within the hyporheic zone, as well as by the delivery of surface water to the riparian zone during flood events. Carbon, nutrients, and terminal electron acceptors are rapidly delivered to, and consumed by, microbial communities in shallow groundwater, promoting high aerobic metabolism. In turn, high metabolism causes oxygen to be consumed faster than it can be replenished, creating localized zones of anoxia. While prevailing models assume that anoxia only occurs in regions where bulk (i.e., volume averaged) oxygen concentrations are depleted, growing evidence suggests that anoxic metabolic reactions occur within local microzones embedded within bulk oxic regions. This proposal is motivated by the questions (1) what mechanisms control the abundance and lifetime of anoxic microzones, and (2) to what extent do anoxic microzones contribute to anoxic gas fluxes from bulk oxic sediments? We seek EMSL support to test the hypothesis that the spatio-temporal distribution of microzones and the production of anoxic metabolic products are controlled by the clogging of pore spaces by microbial biofilms. This work builds on a collaboration with EMSL researchers that involves the continued development of micromodels that allow us to simultaneously track the spatio-temporal distribution of microbial biomass and dissolved oxygen concentrations in a model porous medium. We now propose to relate these distributions to observations of integrated reactive transport at the pore network scale, by leveraging EMSL’s unique real-time mass spectrometry capabilities. The results from this research will link microscale observations and upscaled observations of anoxic metabolic reactivity, which is a critical step to developing predictive models of river corridor biogeochemistry that capture the dynamic interactions between flow and biota.