exchange with the protein pool through protein turnover. The MD includes both net protein synthesis (i.e., the repletion of postabsorptive losses and any growth) and irreversible amine acid metabolism and oxidative metabolism. The latter component is shown divided into three parts: (l) the metabolic demands for nonprotein products that eventually give rise to an obligatory N loss, (2) adaptive oxidative amino acid catabolism, which is also part of the MD, and (3) any additional oxidative amine acid catabolism due to an inefficiency of protein utilization. Within this metabolic framework the determination of protein requirements is a problem of assessing both intrinsic, fixed MDs and the adaptive oxidative catabolism, which together define the MD. Assessment of this latter component accounts for the major practical and conceptual difficulties in applying N balance techniques to the study of protein requirements.
There is an important but complex implication of diurnal feeding and fasting for the IAA pattern of the MD. Clearly, from the above discussion, with increasing dietary protein intake, there will be an increasing MD generated by the adaptive oxidative losses. With both adaptive and obligatory MD occurring continuously, overall daily balance is achieved within a complex diurnal cycle of postprandial repletion of tissue proteins mobilized to provide for the postabsorptive demand. Furthermore, the amplitude of this cycle increases with increasing habitual level of protein intake (Price et al., 1994). The key question is: To what extent does this diurnal cycle of body protein influence the IAA composition of the adaptive MD? Does it mean that regardless of the amine acid composition of the intake that induces the adaptive MD, the adaptive MD will have a tissue protein pattern of amine acids to enable postprandial protein deposition? Young and El-Khoury (1995) have assumed this to be the case and a partial justification for their assertion that the maintenance requirement pattern is like that of tissue protein.
In fact, the actual amount of amine acids needed in the diet to provide for this adaptive requirement cannot be predicted for three reasons. First, the amount of actual postabsorptive tissue protein loss depends on the extent of the true postabsorptive state. Price et al. (1994) utilized 12 + 12-hour diurnal cycles in their studies, but the actual amount will vary with the pattern of meal feeding, and individuals consuming both an early breakfast and late supper may spend less than 12 hours in a true postabsorptive state and mobilize less tissue protein. In subjects in the postprandial state, the diet will directly provide for the losses without inducing tissue protein loss.
Second, when true postabsorptive losses of tissue protein do occur it does not follow that all IAAs liberated from the net tissue proteolysis are oxidized. Although increases in the concentrations of the BC, aromatic, and sulfur amine acids liberated from tissue protein are minimized by increasing their oxidation,