High-intensity ultraendurance promotes early release of muscle injury markers.

OBJECTIVE: To evaluate the impact of high-intensity ultraendurance (HIU) cycling, using it as a possible way to understand muscle injury kinetics and blood immune cells' release during high-intensity prolonged exercise DESIGN: Male amateur triathletes enrolled during a cycling race of the International Bike Championship 800 km cycling relay (approximately 23 h). Each athlete alternately cycled 20-25 minutes until exhaustion and performed a total of approximately 200 km. RESULTS: Creatine kinase levels in blood reached a 300% rise in a sigmoidal pattern, while lactate dehydrogenase levels increased by 30-40% following a hyperbolic pattern. Aspartate aminotransferase and alanine aminotransferase levels increased by up to 250% and 140%, respectively. Liver injury markers such as alkaline phosphatase and gamma-glutamyltransferase remained stable. Platelets increased by 20-30% from pre-exercise, and there was no change in haematocrit during the race. White blood cells rose by nearly 200%. Leucocytes rose 210% during the race, with a major component coming from neutrophils, which increased more than 300%. Triacylglycerol levels were decreased at the finish and total cholesterol levels remained unchanged. Urate increased (by up to 35%) during the first half of the race, and urea levels increased with a different pattern, increasing by 45% in the second half. CONCLUSIONS: This study showed the blood appearance kinetics of muscle injury markers and some metabolites. It is suggested that the increase in these enzymes came primarily from muscle damage, rather than liver damage, and that white blood cells are selectively mobilised independently of haemoconcentration. The early appearance of muscle injury markers in this kind of exercise was also shown.

Glutamine protects against increases in blood ammonia in football players in an exercise intensity-dependent way.

OBJECTIVE: High-intensity and prolonged exercise significantly enhances the levels of plasma ammonia, a metabolite with toxic effects on the central nervous system. The main purpose of the present study was to evaluate the metabolic response of athletes to glutamine (Gln) and alanine (Ala) supplementation, since these amino acids have a significant influence on both anaplerosis and gluconeogenesis. METHODS: Professional football players were assigned to groups receiving either Gln or Ala supplementation (100 mg kg(-1) body weight); this supplementation was either short-term or long-term and was given immediately before exercise. The players were evaluated using two exercise protocols, one with intervals (n = 18) and the other with continuous intensity (n = 12). RESULTS: Both types of exercises increased ammonia, urate, urea and creatinine in blood. Chronic Gln supplementation partially protected against hyperammonemia after a football match (intermittent exercise: Gln -140 (SEM 13)% vs Ala -240 (SEM 37)%) and after continuous exercise at 80% of the maximum heart rate (Gln -481 (SEM 44)% vs placebo -778 (SEM 99)%). Urate increased by 10-20% in all groups, independently of supplementation. Glutamine once a day supplementation induced a greater elevation in urate as compared to alanine at the end of the game; however, long-term supplementation provoked a lesser increment in urate. Exercise induced similar increases in creatinine as compared to their respective controls in either acute or chronic glutamine administration. CONCLUSIONS: Taken together, the results suggest that chronically supplemented Gln protects against exercise-induced hyperammonemia depending on exercise intensity and supplementation duration.