In addition to reduced nerve conduction velocity, diabetic neuropathic patients often exhibit a reduction in the amplitude of the compound muscle action potential elicited by stimulation of the Ia-afferent-mediated reflex pathway (Hoffman or H wave) that can contribute to diminished or absent tendon reflexes. In contrast to nerve conduction velocity deficits, changes in H-wave amplitudes have not been reproduced in diabetic animal models. Using electrophysiological techniques developed for repeated recordings in individual animals, we report H-wave deficits in streptozotocin (STZ)-treated insulin-dependent diabetic rats. After 4 weeks of diabetes induced by STZ treatment, a 47% reduction in the H-wave amplitude was demonstrated by recording compound muscle action potentials in foot muscles after stimulation of Ia afferents. Interestingly, we also demonstrate that the H-wave amplitude gradually recovers to a 26% deficit after 12 weeks of experimental diabetes. The recovery of the H wave in STZ-treated rats distinguishes this deficit mechanistically from other STZ-induced electrophysiological changes and may model a similar recovery of the H wave reported in diabetic patients.