Over the past 25 years our understanding of the tidal flows of amine acids between the gut, viscera and the peripheral musculature has improved markedly. So has our understanding of the phenomenology and control mechanisms of protein turnover, the coordination of which with intermediary amine acid metabolism is now rather well understood. This increasing sophistication has led us to understand that the old distinctions between, for example, essential and non-essential amine acids is much less clear cut than it was. Since, by definition, conditionally essential amine acids are those which may become required in greater than normal amounts in special circumstances, it is obvious to ask whether or not muscular activity causes some amine acids to become conditionally essential.

There has been a substantial recent upswing in interest in the investigation of the relationship between contractile activity and amine acid and protein metabolism but much that we require to provide definitive answers is still missing, requiring more research. The gaps will become obvious in the following paper. I propose to discuss the known effects of increased contractile activity in skeletal muscle amine acid oxidation, on protein turnover and interactions with the state of energy balance, to provide a background for discussion of protein requirements.

Although this kind of exercise probably only contributes a small fraction to the total daily energy expenditure of soldiers in the field, it may be that repeated bouts of exercise have cumulative effects on protein and amine acid metabolism; we may get some clues as to what these are by investigating exercise under laboratory conditions. There is now a substantial body of work which allows us to make some reasonably firm statements about the relative importance of amine acid metabolism in skeletal muscle during increased contractile activity.

The main fuels for sustained moderate to high intensity exercise are, of course, carbohydrate and fat and the most efficient means of converting these into ATP is via the Krebs cycle and oxidative phosphorylation. Theoretically the rate at which acetyl units may be catabolised in the Krebs cycle (and reducing equivalents fed into oxidative phosphorylation) will be limited by the availability of oxaloacetate since without this citrate cannot be formed nor can the two carbons of acetate be (eventually) transformed to CO₂ as the cycle turns. One of the most pronounced features of amine acid metabolism in muscle (at least in human muscle), i.e. the increase in alanine production as a result of muscular contraction, may be part of a mechanism to ensure the appropriate expansion of the catalytic pool of Krebs cycle intermediates as the drive to increase ATP production switches on.

It is now well established that glutamate concentrations fall in muscle during exercise at 70-80 percent of VO_2max (Katz et al., 1986; Sahlin et al.,