Glutamate could influence outcome after myocardial ischemia by two different biochemical mechanisms. First, glutamate improves myocardial tolerance to ischemia by facilitated anaerobic metabolism and substrate level phosphorylation during ischemia. The second mechanism is related to the anaplerotic role of glutamate. Glutamate plays a key role for replenishment of Krebs cycle intermediates lost during ischemia, which enhances post-ischemic recovery of myocardial oxidative metabolism and function.