Endurance training has long been known to improve the individual's resistance to exercise-induced hypoglycemia. Traditionally attributed to a reduction in glucose uptake subsequent to enhanced fat oxidation, this issue has only recently been directly addressed. This paper briefly reviews the evidence for reduced glucose uptake versus enhanced glucose production in the improved hypoglycemic resistance following training. While whole body glucose removal and production may be reduced following training, this has only been demonstrated under exercising conditions in which glycemia demonstrates little deviation from rest. Under exercise conditions where untrained animals demonstrate substantial reductions in blood glucose, training enhanced hypoglycemic resistance has been shown to result entirely from enhanced glucose production via gluconeogenesis. Using the in situ perfused liver preparation, the authors have provided direct evidence for a training enhanced hepatic gluconeogenic capacity. The site of adaptation within the gluconeogenic pathway has now been constrained to below the level of the triose phosphates. Lack of evidence for suppressed skeletal muscle glucose uptake following training, a uniform observation for humans and rats, is also discussed. It is concluded that the improved hepatic gluconeogenic capacity of endurance trained individuals, at least in rats, is critical to their demonstrated resistance to exercise-induced hypoglycemia.