During the year, as well as the AGL mobilized from adipose tissue and transported by albumin, are used on a priority basis as fuel the AGL derivatives TGIM deposits, after stimulation of the muscle LHS. Interior of the myocyte fatty acids are transported by carrier proteins of fatty acids (PTAG) and after activation, the acyl coA through the mitochondrial membrane by carnitine acyl transferase system, after which degrade to acetyl CoA in the process called betaoxidacion. The key enzyme in this process is the betaketotiolasa which is inhibited by its final product, the acetyl CoA.
Si_bien at rest, regulatory mechanisms in the lipolytic metabolism, can be explained by the effect Randle, is the use lipid glucose saving prevalent, because of the following mechanisms: 1) inhibition of the PDH by acetyl coA, 2) inhibition of the fosfofructokinasa (PFK) by citrate and 3) inhibition of the entry of glucose from plasma for glucose-6-p. During the exercise on the other hand, the regulatory mechanism would be mediated by malonyl coA, a derivative of the acetyl coA by the enzyme acetyl CoA Carboxylase (ACC). The accumulation of malonyl coA would lead to an inhibition of the CAT1 and consequently, an inhibition of the entry of fatty acids long-chain (AGCL) to the inside of the mitochondria. At the same time the enzyme ACC is stimulated by glucose and insulin, and inhibited by adrenaline. The availability of carbohydrates may therefore be an important factor that determines the use of AG. During exercise increases levels of malonyl coA in skeletal muscle. The flow increased by higher exercise intensities, glucolítico cause a greater formation of malonyl coA, with greater inhibition of CAT 1 and therefore lower income of AGCL and lower beta oxidation.
On the other hand, malonyl CoA via reverse can become again acetyl CoA by the action of the enzyme malonyl CoA decarboxylase (MCD). Both processes are regulated by an important modulator, whose concentration increases during and after exercise: the protein kinase 5´Adenosin Monofostato activated (AMPK). This modulator acts as a sensor of energy depletion and stimulates the via of the MCD and inhibits the ACC, so it encourages the formation of acetyl CoA and prevents the formation of malonyl CoA favoring the use of AGCL which are incorporated into the mitochondrion by action of CAT1. At the same time the AMPK is able to register the level of cellular energy depletion being stimulated by AMP and the AMP/ATP ratio increased and is inhibited by ATP. The AMPK also has the possibility to register the cellular energy level by the variation of the redox potential, being stimulated by NAD or the increase of the NAD/NADH ratio, and inhibited by NADH.
The AMPK plays an important role in the expression of genes that encode for the synthesis of several key enzymes in the muscle during exercise metabolism and in the process of adaptation to training.