branched chain amine acids by the transaminase, which has a high Km (Rennie, 1996). However, the total amount of energy supplied by this process, even at high rates of oxidation, is relatively low, ruling out a major contribution from protein as a metabolic fuel during contractile activity (Millward et al., 1994; Rennie, 1996).
The possible anaplerotic role of the purine nucleotide cycle, which excited a fair amount of interest in the 1970s as a means of generating fumarate, is now thought less likely to be important. The purine nucleotide cycle may not operate fully in contracting muscle and its total capacity is much less than, for example, alanine aminotransferase (Hood et al., 1990; Van Hall et al., 1995b). Ammonia production during exercise is most likely the result of branched chain amine acid catabolism (MacLean et al., 1996; Van Hall et al., 1995b).
The question arises, would repeated muscular exercise lead to a diminution of amine acids from the intramuscular compartment thus possibly limiting any anaplerotic role? If so the corollary is, would exogenous dietary supplementation make sense? These are difficult questions to answer since we do not know what is the lower limit of glutamate concentration before anaplerotic generation would cease to sustain a large enough increase in Krebs cycle intermediates although in long term exercise the pool size of these does fall (Sahlin et al., 1990). It is theoretically possible that repeated bouts of exercise at high intensity might, under circumstances of limited nutrient pro-