Branched-chainα-amino acid chronic treatment: responses of plasmaα-keto-related compounds and ammonia when used in physical exercise performance.

To examine the effects of acute branched-chainα-amino acids (BCAA) oral administration following chronic BCAA intake, a group of well trained young swimmers (n = 12) was submitted to a one month chronic BCAA treatment (0.2g/Kg body weight per die; Leu: Val: Ileu = 2:1:1) and a physical exercise test before and after this period of treatment was carried out. The exercise tests (60min swim) were performed in a high circulating BCAA level state which was obtained through oral BCAA administration (or placebo) just before the beginning of the exercise. The groups will be referred to as BCAA/before, BCAA/after, placebo/before, placebo/after. Blood and plasma (antecubital vein) samples were collected from the different groups at different times: on the morning of the day before the test (basal time, rest 0), the following day 30min after an acute administration (oral dose placebo or BCAA acute treatment: Leu 4.8g, Val 2.4g, Ileu 2.4g), just before the beginning of the exercise performance (time 0min, rest 1), at the end of the exercise (time 60min, EE) and during recovery (time 120min, Re). Plasma ammonia levels increased significantly from rest 1 to the end of the exercise in all subjects, but it was significantly higher in BCAA treated than in placebo subjects in both the before and after chronic treatment groups (BCAA/before: from 38 ± 7 to 204 ± 65mmol/l; placebo/before: from 36 ± 10 to 93 ± 29mmol/l; BCAA/after: from 36 ± 9 to 171 ± 43mmol/l; placebo/after: from 30 ± 6 to 65 ± 16mmol/l). Plasma ammonia level increments observed before a chronic one month BCAA treatment were significantly higher than after this treatment (p < 0.05). Plasma alanine was at all times of the test higher before the BCAA chronic treatment than after; this difference resulted significant at rest 0, rest 1 and recovery times (p < 0.05). After acute BCAA administration, plasma BCAA levels increased from 618 ± 52mmol/l to 1893 ± 284mmol/l (p < 0.05) from the onset of exercise and remained elevated throughout the test. Placebo and basal (rest 0) levels both before and after the chronic treatment did not demonstrate any significant differences. Plasma BCAA and BCKA levels, in the BCAA/before demonstrated significantly higher levels than placebo/before at rest 1 time (BCAA/before vs placebo/before: Leu 86 ± 27 vs 620 ± 97mmol/l; KIC 60 ± 3 vs 87 ± 5mmol/l, Ileu 51 ± 19 vs 359 ± 56mmol/l, KMV 26 ± 1 vs 43 ± 2mmol/l, Val 290 ± 79 vs 915 ± 133mmol/l, KIV 14 ± 1 vs 24 ± 2mmol/l). The levels after the chronic treatment maintained circa these differences in the two groups BCAA/after and placebo/after. The plasma BCAA as well as the BCKA levels of acutely treated athletes, in physical exercise, showed a different profile before and after the chronic treatment. The chronic treated BCAA/after group in fact depicted a decreasing BCKA level profile at the end of the exercise and during recovery; on the contrary, before the chronic treatments, acutely treated athletes demonstrated a tendency to increase these levels during recovery. These data seem to confirm that increased BCAA availability, before exercise, result in significantly greater plasma ammonia responses during exercise than does placebo administration; furthermore this increment is lower after chronic treatment. The interpretation of the ammonia data is difficult since the exercise type could have an influence on this phenomenon. The differences in the profile patterns of alanine, BCAA and BCKA levels seem to indicate that the chronic treatment brings about a state in which there is a better use of BCAA compounds as energy supply.