Promoting metabolic and functional recovery with metabolic support represents a novel concept in the treatment of heart failure after acute ischemia. Animal experiments suggest that glutamate increases myocardial tolerance to ischemia and that glutamate promotes post-ischemic recovery. Intravenous glutamate improved metabolic and hemodynamic recovery in humans early after CABG. Early clinical experience with intravenous metabolic support showed that the need for inotropes could be substantially reduced while clinical outcomes with regard to postoperative mortality, postoperative renal dysfunction and long-term survival compared favourably with the literature. This encouraging experience contributed to the initiation of the first GLUTAMICS-trial.