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glutamine observed in athletes in training who suffer the so-called overtraining syndrome is the result of the progressive exhaustion by repeated exercise of the homeostatic system for preserving glutamine (Rowbottom et al., 1995, 1996). This diminishes the supply of glutamine available to white cells and could diminish their capacity for fighting infection. There is some evidence in favour of this proposition (Rohde et al., 1996) but it appears to me that, for the purposes of the present discussion, we need to ask ourselves: are the levels of physical activity which are engaged in by top athletes during training and which lead to the overtraining syndrome similar to those experienced by military personnel on active duty? Personally I doubt this, although it is certainly possible during specific training early after recruitment. There has been a single report of a beneficial effect of glutamine in reducing infection rate of amateur athletes after long distance runs (Castell et al., 1996). We now need to repeat such studies and we need know what the dose-response relationship is between exogenous glutamine and adequate immune function. We also need to understand whether or not small doses of glutamine given at regular intervals would be as efficacious as irregular large doses. The whole area is one which requires further research.

THE CRUCIAL QUESTIONS

Does what we know about physical activity and metabolism suggest to us that protein requirements are increased as a result of exercise? My answer to this would be that in fact there is no evidence that there are increased requirements for protein per se. Most foods contain 10-15 percent of protein on an energy basis and the likelihood is that an adequate supply of energy from mixed rations will inevitably supply sufficient protein.

Is there an optimum of protein to carbohydrate + fat ratio and should the composition of rations be altered to this? So far as I can tell, most of the evidence suggests that exercise actually increases the efficiency of protein utilisation and therefore, if anything, the amount of protein in the diet could be reduced without deleterious effects. I do not think we know the lower limit at the present time, and more work is needed to answer the question.

We do know that increasing the protein content of the diet simply increases the activity of amine acid catabolizing enzymes and the capacity for branched chain amine acid oxidation during exercise is substantially increased by increasing total dietary protein (Figure 11-1). In studies we carried out on subjects habituated to a high protein diet, amine acid oxidation was higher than normal during exercise suggesting no net benefit would accrue. In any case it can be calculated that even with an increase of muscle mass of 15 kg over 3 years a 70 kg man would need less than 5 percent of the protein recommended nutritional intake (RNI) to supply the growth. Thus, it is likely that increasing dietary protein over the current US military ration of 100 g/day would simply lead to increased oxidation without any particular benefit. The classic results of



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