Recent experimental evidence has demonstrated that somatic outer hair cell (OHC) motility is important for amplification in the mammalian cochlea [1,2]. However, under the ‘somatic electromotility’ theory, the transmembrane potential that is responsible for driving the somatic OHC force is subject to low-pass filtering by the electrical RC time constant of the OHC membrane . Numerous mechanisms have been proposed to compensate for the attenuation of the membrane potential by the low membrane time constant at high frequencies [3,4-10]. We present a micromechanical model derived from an engineering-based analysis of cochlear mechanics and experimental data. Our model does not require novel compensatory mechanisms and demonstrates that adequate OHC gain with negative feedback significantly extends closed-loop system bandwidth and increases resonant gain. The OHC gain-bandwidth product, not just bandwidth, determines if high-frequency amplification is possible. Thus, fast cochlear amplification is possible with slow OHCs simply due to in situ feedback dynamics, though our model does not preclude other compensatory mechanisms.