Declines in auditory nerve (AN) function contribute to suprathreshold auditory processing and communication deficits in individuals with normal hearing, hearing loss, hyperacusis, and tinnitus. Procedures to characterize AN loss or dysfunction in humans are limited. We report several novel complementary metrics to characterize AN function noninvasively in humans using the compound action potential (CAP), a direct measure of summated AN activity. We examined how these metrics change with stimulus intensity, and interpreted these changes within a framework of known physiological properties of the basilar membrane and AN. Our results reveal how neural synchrony and the recruitment of AN fibers with later first-spike latencies likely contribute to the CAP, affect auditory processing, and differ with noise exposure history in younger adults despite normal pure-tone thresholds. Moving forward, these new metrics, when applied to patient populations, can provide a means to characterize cochlear synaptopathy and other deficits in AN function in humans.New and noteworthyLoss or inactivity of auditory nerve (AN) fibers is thought to contribute to suprathreshold auditory processing deficits, but evidence-based methods to assess these effects are not available. We describe several novel metrics that may be used to quantify neural synchrony and characterize AN function.