MOLECULAR MECHANISMS OF FATIGUE

The fatigue after exercise has been objective of continuous study, however Its causes and effects still not properly elucidated, although it is already known that their causes can be peripheral (muscular), neuromuscular (neuromuscular junction) and central (neurological). In this work we revised possible causes and molecular mechanisms of the fatigue, at central level, metabolic and muscular. There is evidence of the participation of tryptophan, hyperammonemia and cytocines concentration in the central fatigue, while focus will be given in the participation of ATPases from skeletal muscle in the peripheral fatigue, being involved the main three: Na+-K+-ATPase, Ca2+-ATPase and myosin II. Besides, several metabolic factors as the substract depletion and the accumulation of their by-products will be approached in this revision. The data here gathered will show indications of several paths related with the process of fatigue, and to point ways for the prevention of this process, although it is necessary caution in the observation and analyzing of data to postulate the biochemical map of the fatigue. We can conclude that, although we are able to identify the main effects of the fatigue in several isolated proteins, the entire process should be the result of an extensive biochemical cascade that acts in the main proteins related with the muscular contraction, as well as important components of the central nervous system.