Heart

 The goal of cardiac metabolism is to produce chemical energy (ATP) to fuel the heart function. By doing so, the heart is able to continuously pump oxygenated blood to the rest of the body. In normal, healthy cardiac metabolism an efficient rate of ATP fuels heart muscle function. In the context of heart failure, cardiac metabolism becomes weaken(damage). The consequences of this metabolic remodeling include ATP inefficiency, impaired heart function, and progression to a more severe heart failure. Many researchers hypothesize that the treatment of cardiac metabolism has a high potential for therapeutic approaches in the treatment of heart failure patients.

Here’s how normal cardiac metabolism works: adenosine triphosphate (ATP) is the primary energy source for the heart and is used to fuel the heart’s activities – 60-70% of ATP is used to fuel the contraction of the heart muscle, and the remaining 30-40% is used in ion pumps. ATP is a highly energetic molecule because it contains high-energy phosphate bonds. The ATP pool in the heart is small and can be exhausted in a few seconds. As a result, cardiac function is highly dependent on ATP continuous synthesis, and impaired cardiac metabolism may be a precursor or direct cause of heart failure. Most (70-90%) of cardiac ATP comes from fatty acids, and the remaining ATP is derived from glucose, lactate, ketone bodies, and other amino acids.

. An average person hydrolyzes about 50 kg of ATP per day but makes exactly the same amount from ADP and inorganic phosphate

Unlike bacteria, most eukaryotic cells do not have an H+ electrochemical gradient across their plasma membranes. Rather, it is sodium ions that are more concentrated outside the cell than inside (Fig. 12.3). Typically, the sodium concentration in the cytosol is about 10 mmol liter−1 while the concentration in the extracellular medium is about 150 mmol liter−1.

In general, most research has shown that there is a reduction in the hearts preferred fuel source (i.e. fatty acids) in heart failure patients. As 70-90% of cardiac ATP (energy) comes from fatty acid oxidation, typically the failing heart will attempt to compensate by increasing glucose oxidation. However, this is less efficient and does not produce as much ATP.

Whole-body insulin resistance can affect(change) cardiac energy metabolism, even in structurally normal hearts.

The failing heart faces an energy deficit, primarily because of a decrease in mitochondrial oxidative capacity. This is partly compensated for by an increase in ATP production from glycolysis.