DEAMINATION OF AMINO-ACIDS AS A SOURCE FOR AMMONIA PRODUCTION IN HUMAN SKELETAL-MUSCLE DURING PROLONGED EXERCISE

1. The influence of pre-exercise muscle glycogen content on ammonia pr oduction, adenine nucleotide breakdown and amino acid metabolism was i nvestigated during prolonged exercise in six subjects having one leg w ith a normal and one leg: with a low muscle glycogen content. One-leg knee-extensor exercise was performed for 90 min, at a workload of 60-6 5% of the maximal power output, first with one leg and then with the o ther. 2. During exercise ammonia was released in gradually increasing amounts and plateaued after 1 h exercise at a rate of approximately 80 mu mol min(-1). The total ammonia production was 9.1 +/- 0.4 and 9.5 +/- 1.4 mmol (kg dry muscle)(-1) in the normal and low glycogen conten t leg, respectively. 3. Levels of muscle phosphocreatine (PC), total a denine nucleotides and inosine monophosphate (IMP) were similar at res t and after 90 min of exercise. 4. Only minor differences were observe d between rest and exercise and between legs for the muscle concentrat ions of glutamine, alanine and the branched-chain amino acids. Muscle glutamate concentration decreased by 60-70% within the first 10 min of exercise. Glutamate consumption over 90 min quantitatively equalled a mmonia production. Most of the glutamate was consumed within the first 10 min of exercise, while ammonia production gradually increased duri ng exercise. Therefore deamination of glutamate cannot be the main sou rce of ammonia production during the later stage of exercise. 5. It is concluded that during prolonged one-leg exercise at moderate intensit y: (a) ammonia production is not affected by pre-exercise muscle glyco gen content, (b) ammonia production exceeds by far the breakdown of ad enine nucleotides to IMP and therefore has to be derived from alternat ive sources, and (c) deamination of amino acids is a likely source of ammonia production during prolonged exercise.