Diabetes mellitus (DM) is a metabolic disorder that affects an estimated 171 million people world wide. DM and its related complications are among the leading cause of adult blindness and renal failure in the developed nations. Equally alarming, greater than half of all patients with long-standing diabetes develop polyneuropathy, a debilitating progressive deterioration of peripheral and autonomic nerves. Currently, diabetic polyneuropathy (DPN) is untreatable. Maintenance of euglycemia as an indirect means of delaying the development of diabetic complications is the recommended therapeutic approach. Innovative treatment strategies designed to prevent or delay peripheral nerve injury in the diabetic patient are critically needed. Moderate exercise is a safe and integral approach to the management of patients with diabetes. Recent clinical studies suggest that exercise may help in the treatment of DPN. However, the mechanism by which exercise protects against diabetes-induced nerve dysfunction is unknown. In this dissertation we hypothesized that forced-exercise protects against experimental DPN by preventing glucose-associated alterations of voltage-gated calcium currents (VGCC) in small diameter dorsal root ganglion (DRG) neurons. Using behavioral, nerve-electrophysiology and patch-clamp methodology we examined the functional consequences of forced-exercise (treadmill, 5.4 km/week) on VGCC in dissociated small diameter DRG neurons from rats conferred diabetic by streptozotocin (STZ) treatment. Vehicle treated rats were used as controls. Exercised-STZ, rats in comparison to sedentary-STZ, rats demonstrated a 4 week delay in the onset of tactile hyperalgesia that was independent of changes in blood glucose levels. Interestingly, forced-exercise induced protection against diabetes-induced tactile hyperalgesia was reversed in a dose dependent manner by the opioid antagonist, naloxone. Forced-Exercise also prevented peripheral nerve conduction deficits in STZ–treated rats. Small diameter DRG neurons harvested from hyperglycemic sedentary-STZ rats with demonstrated hyperalgesia exhibited 2-fold increase in peak high-voltage activated (HVA) Ca²⁺ current density and low-voltage activated (LVA) Ca ²⁺ current component. The steady-state inactivation (SSI) (measure of channel availability) of LVA currents demonstrated a rightward shift in the sedentary-STZ rats (+7.5 mV shift; V₅₀ = -50.9 ± 0.6 mV; vehicle treated rats V₅₀ = -58.4 ± 0.9 mV). Forced-exercise prevented the increase in both, peak HVA Ca²⁺ current density and LVA SSI shift (V₅₀ = -58.2 ± 1.4 mV), but did not alter LVA current component. We conclude that forced-exercise delayed the onset of diabetic tactile hyperalgesia by preventing the alteration of VGCCs in small diameter DRG neurons, possibly by decreasing total calcium influx and dampening neuronal over-excitability.