Our data suggest that caffeine might decrease systemic urea by decreasing the glutamine serum concentration, which decreases the transportation of ammonia to the liver and thus urea synthesis.

During exercise, ammonia levels are related to the appearance of both central and peripheral fatigue. Therefore, controlling the increase in ammonia levels is an important strategy in ameliorating the metabolic response to exercise and in improving athletic performance. Free amino acids can be used as substrates for ATP synthesis that produces ammonia as a side product. Keto analogues act in an opposite way, being used to synthesise amino acids whilst decreasing free ammonia in the blood. Adult male rats were divided into four groups based on receiving either keto analogues associated with amino acids (KAAA) or a placebo and resistance exercise or no exercise. There was an approximately 40 % increase in ammonaemia due to KAAA supplementation in resting animals. Exercise increased ammonia levels twofold with respect to the control, with a smaller increase (about 20 %) in ammonia levels due to exercise. Exercise itself causes a significant increase in blood urea levels (17 %). However, KAAA reduced blood urea levels to 75 % of the pre-exercise values. Blood urate levels increased 28 % in the KAAA group, independent of exercise. Supplementation increased glucose levels by 10 % compared with control animals. Exercise did not change glucose levels in either the control or supplemented groups. Exercise promoted a 57 % increase in lactate levels in the control group. Supplementation promoted a twofold exercise-induced increase in blood lactate levels. The present results suggest that an acute supplementation of KAAA can decrease hyperammonaemia induced by exercise.