Neither recurrent hypoglycemia nor chronic aerobic training alter the content of MCTs in the ventromedial hypothalamus

Many individuals with diabetes use medications or exercise to control blood glucose concentrations, which can lead to episodes of hypoglycemia. Although chronic hyperglycemia leads to many diabetic complications, hypoglycemia is an acute threat to the health of individuals, and can lead to myocardial ischemia and arrhythmias, as well as increasing inflammation, oxidative stress, and thrombotic and fibrinolytic processes. Either antecedent exercise or antecedent hypoglycemia lead to a blunted counter-regulatory response to a subsequent hypoglycemia episode. Acute exercise has been shown to increase monocarboxylate transport proteins (MCTs) in the ventromedial hypothalamus (VMH) of the brain, which is involved in regulating the counter-regulatory response to restore euglycemia. The MCTs shuttle lactate in and out of cells, however when is lactate infused into the VMH has been shown to interfere with the counter-regulatory response. Additionally, antecedent recurrent hypoglycemia has been shown to increase lactate transport in the brain. Therefore, the current studies investigated what effect exercise training or recurrent antecedent hypoglycemia had on MCT proteins in the VMH. Adult male Sprague-Dawley rats were used for both studies, randomized to receive either 6-7 weeks of aerobic training, sedentary behavior, 3 days of insulin induced hypoglycemia, or 3 days of saline injection. The increases in cytochrome c oxidase activity among the aerobically trained group showed that training adaptations occurred, however, there were no significant differences in MCT proteins within the VMH between the trained versus sedentary rats. While each of the 3 days of hypoglycemia or saline injection showed differences in 30 minute post-injection glucose concentrations, no significant differences in MCTs were observed in the VMH between the 2 groups on day 4