O exercício como modelo para estudo do metabolismo de aminoácidos e amônia

Abstract

Intracelular increase of AMP during sub maximal exercise leads to an activation of AMP deaminase following production of inosine monophosphate and ammonia. In the same direction amino acids (AAs) are used as a carbon donors for the tricarboxylic acid cycle to maintain the ATP concentration in the cell. Both metabolic pathways lead to an increase in intracellular and blood ammonia concentration. In these events, the blood ammonia concentration can raise up to 400% the resting levels. Hyperammonemia is linked with lack in neurotransmitter regulation and can be associated with neuronal excitotoxicity and/or death. Raise in ammonia synthesis during exercise is related to decrease in neuro-physical capacity in health athletes and can affect the performance. The temporary disturbances in the central nerve system caused by exercise are similar to the observed in hepatic disease and neurodegenerative disorders. Here we evaluate different exercises intensities associated with metabolic modifications induced by diet and/or supplementation to understand ammonia metabolism. We showed the blood appearance kinetics of muscle injury markers and some metabolites. We suggested that the increase in these enzymes came primarily from muscle damage instead of liver and that white blood cells are selectively mobilized independently of hemoconcentration. We also had shown the early appearance of muscle injury markers in different kinds of exercise. Our results suggest that we are able to use exercise as a general model to study ammonia metabolism in humans without requiring external ammonia exposure.