**1. Introduction**

The myocardium is one of the most energy-dependent structures. It demands about 6 kilograms of ATP per day [115]. In order to sustain an efficient energy supply, it has an advanced system producing enough ATP. In the organism, there are two ways to support this demand: production and accumulation. Accumulation is not suitable for the heart due to specific anatomy—most of the cytoplasms consist of myofibrils. According to this fact, in the adult heart, we observe low concentrations of ATP and many ATP-hydrolases. Total resynthesis of all ATP volume takes only 10 seconds in a normal myocardium [32, 55]. Most of the energy resources (~70%) are used for contraction and the rest—for ion pump function (K, Na, Ca pumps ATPases). This system is well coordinated, which helps to maintain the normal flux of energy substrates and ions.

In average, the heart consumes about 20 g of carbohydrates, 30 g of free fatty acids (FFA), and triglycerides (TG). These substrates are oxidized in 35 L of oxygen to produce ATP from ADP [171].

Oxidative phosphorylation of FFA gives about 60% of all produced ATP, while glucose, lactate, and other carbohydrates oxidation produce about 30% of all macroergic compounds. In addition, for energy supplement ketone bodies and amino acids can be utilized. Glucose utilization can be the main energy source in specific conditions (high-carbohydrate diet). Therefore, in understanding myocardial metabolic features, changes during heart failure could provide vital information for early diagnostics and therapy of myocardial diseases [99, 112].

Heart failure syndrome is a consequence of the main heart disease and associated with compensatory mechanism dysfunction, formation, and activation of pathological interactions between components of neurohumoral regulation systems [203]. Decompensation is a condition, which is always connected with reduced energy production and suppressed myocardial metabolism. For example, systolic dysfunction leads to sympathoadrenal system hyperactivation, which is associated with increased heart rate. Catecholamines activate beta-adrenergic receptors, which increase myocardial oxygen consumption due to raised FFA utilization to produce enough energy. This situation leads to increased ADP volume and negative inotropic effect, which is badly tolerated during heart failure and geometrically progress during chronic sympathetic tonus [36, 96, 115, 122, 164].
