It has been proposed that the increase produced by insulin in electrical potential differences across membranes of target cells may be a mechanism by which the cell surface insulin-receptor complex causes at least some of the metabolic effects of insulin. If insulin-induced hyperpolarization is a transducer of common effector responses it must precede those responses. The problem has not been addressed previously, so that rapid responses to insulin have not been sought. Two methods were used. In one method, the bathing solution was changed rapidly so as to include insulin in supramaximal concentrations, and a series of measurements of membrane potentials. Er, were made. Insulin hyperpolarized by 9.4 mV within 1 min. In the other method, nanoliter amounts of highly concentrated insulin solution were ejected from a micropipette onto the surface of an impaled muscle fiber. In 21 out of 32 insulin injections, hyperpolarization occurred with 1 s; in 11 control injections there was no change. This is the most rapid response to insulin yet reported, and is consistent with the hypothesis that insulin-induced hyperpolarization may transduce effector responses.