Endurance training increases brain lactate uptake during hypoglycemia by up regulation of brain lactate transporters

• We examined the effects of exercise and diabetes on brain lactate uptake during hypoglycemia.
• Diabetes and exercise increased MCT1 and MCT2 expressions in cortex and hippocampus.
• Training increased blood–brain barrier permeability to lactate during hypoglycemia.
• Counterregulatory responses to hypoglycemia were blunted in diabetic trained animals.
• Diabetic patients should monitor glycemic targets both during and following exercise.

The capacity of the brain to metabolize non-glucose substrates under hypoglycemic state maintains its energy requirements. We hypothesized that exercise-induced increase in capacity for brain utilization of lactate by up regulation of the monocarboxylate transporters (MCTs) may contribute metabolic substrates during hypoglycemia in diabetic rats induced by streptozotocin. The induced diabetes increased MCT1 and MCT2 expression in the cortex and the hippocampus in the sedentary diabetic animals. There were exercise-induced increases in MCT1 in the cortex and the hippocampus and MCT2 expression in the cortex in trained diabetic animals; whereas, no changes were found in the healthy trained animals. Both diabetic and healthy trained animals showed higher values for brain lactate uptake during insulin-induced hypoglycemia when animals were intraperitoneally injected by L(+)-lactic acid. However, the response of counterregulatory hormones during hypoglycemia were blunted in the diabetic trained animals which indicates to carefully monitoring of glycemic targets both during and following prolonged exercise.