This report examines the hypothesis that electrocardiographic T-wave amplitude is sensitive to graded increases in beta-sympathetic stimulation of the heart. Beta-adrenergic activity was manipulated pharmacologically in 9 healthy men by bolus infusion of isoproterenol in each of six doses: 0.1, 0.25, 0.5, 1.0, 2.0, and 4.0 micrograms. Results indicated that elevations in heart rate above placebo values increased as a linear function of isoproterenol dose. In contrast, the dose-response curve for T-wave amplitude was best described by a quadratic function: an initial reduction in T-wave amplitude at low levels of isoproterenol infusion was followed by a significant reversal of this effect at higher doses. Comparison of the heart rate and T-wave amplitude data points to limitations in the use of the latter as an index of beta-adrenergic activity. One of several possible explanations for the T-wave results would entail a mechanism that preserves ventricular function at high levels of beta-sympathetic stimulation.