No abstract

Aim-There is little information on the plasma free amino acid patterns of elite athletes against which fatigue and nutrition can be considered. Therefore the aim was to include analysis of this pattern in the medical screening of elite athletes during both especially intense and light training periods. Methods-Plasma amino acid analysis was undertaken in three situations. (1) A medical screening service was oVered to elite athletes during an intense training period before the 1992 Olympics. Screening included a blood haematological/ biochemical profile and a microbial screen in athletes who presented with infection. The athletes were divided into three groups who diVered in training fatigue and were considered separately. Group A (21 track and field athletes) had no lasting fatigue; group B (12 judo competitors) reported heavy fatigue at night but recovered overnight to continue training; group C (18 track and field athletes, one rower) had chronic fatigue and had been unable to train normally for at least several weeks. (2) Athletes from each group were further screened during a post-Olympic light training period. (3) Athletes who still had low amino acid levels during the light training period were reanalysed after three weeks of additional protein intake. Results-(1) The pre-Olympics amino acid patterns were as follows. Group A had a normal amino acid pattern (glutamine 554 (25.2) µmol/l, histidine 79 (6.1) µmol/l, total amino acids 2839 (92.1) µmol/l); all results are means (SEM). By comparison, both groups B and C had decreased plasma glutamine (average 33%; p<0.001) with, especially in group B, decreased histidine, glucogenic, ketogenic, and branched chain amino acids (p<0.05 to p<0.001). None in group A, one in group B, but ten athletes in group C presented with infection: all 11 athletes had plasma glutamine levels of less than 450 µmol/l. No intergroup diVerences in haematological or other blood biochemical parameters, apart from a lower plasma creatine kinase activity in group C than in group B (p<0.05) and a low neutrophil to lymphocyte ratio in the athletes with viral infections (1.2 (0.17)), were found.(2) During post-Olympic light training, group A showed no significant amino acid changes. In contrast, group B recovered normal amino acid levels (glutamine 528 (41.4) µmol/l, histidine 76 (5.3) µmol/l, and total amino acids 2772 (165) µmol/l) (p<0.05 to p<0.001) to give a pattern comparable with that of group A, whereas, in group C, valine and threonine had increased (p<0.05), but glutamine (441 (24.5) µmol/l) and histidine (58 (5.3) µmol/l) remained low. Thus none in group A, two in group B, but ten (53%) in group C still had plasma glutamine levels below 450 µmol/l, including eight of the 11 athletes who had presented with infection.(3) With the additional protein intake, virtually all persisting low glutamine levels increased to above 500 µmol/l. Plasma glutamine rose to 592 (35.1) µmol/l and histidine to 86 (6.0) µmol/l. Total amino acids increased to 2761 (128) µmol/l (p<0.05 to p<0.001)...

The results are of interest in connection with the recent paper of Grafe, Reinwein and Singer,2 who found that the rates of respkation of surviving tissues of animals varying in size from the mouse to the ox, are of substantially the same magnitude, whereas the oxygen absorption per kilogram of the whole living animal is some 20 times greater for the mouse than for the ox, thus demonstrating that the constant relation between metabolism and surface area is a function of the intact animal, and not a result of inherent characteristics of the protoplasm. These authors seek an explanation in considerations of oxygen supply to the tissues and the relative number of patent capillaries. In the case of' our thyroidless rats the metabolism of the living animal is 23 to 30 per cent below the average normal, as is also the respiration of its isolated tissues under conditions of maximum oxygen supply.My thanks are due to Professor P. E. Smith, who gave me the thyroidectomized animals. Further work is in progress.