Introduction: Exercise has been used as a model to study the metabolism of ammonia (NH 3 + NH 4 + ), which is highly toxic to the central nervous system. A ketogenic diet leads to several metabolic adaptations to maintain the ATP/ ADP ratio, including a lack of glycogen reservoirs, the use of amino acids as carbon skeleton donors and increased -oxidation of fatty acids. The formation of ammonia during high-intensity exercise is well studied, but its role in moderate-intensity exercise remains unclear. Here we investigate ammonia metabolism during moderate-intensity exercise associated with a ketogenic diet as a model system. Materials and Methods: Athletes (n=7) were physically evaluated and had their maximum oxygen consumption (VO 2max ) and heart rate (HR max ) determined. The subjects remained on a ketogenic diet 72h prior to exercise. They then exercised for 60min at a power output of 60% of that at VO 2max , and at 70%-75% of HR max . Results: Basal ammonemia increased by 35% due to dietetic modifi cations, while exercise caused a 250% increase in ammonemia in parallel with this effect. Uremia was increased by 60% due to the ketogenic diet without response to exercise. We measured a 10% increase in serum urate that did not change during the exercise protocol. No changes were found in glycemia or lactatemia. Discussion: Our data suggest that moderate-intensity exercise associated with a ketogenic diet can be used to study the increase in ammonemia and as a model to understand ammonia metabolism during metabolic stress.
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Bachini et al. (2009) studied this question.
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