F. Bachini, J. P. S. W. Castro, Leonardo Cristiano Moretzsohn, A. Cameron, L. Cameron
{"title":"与生酮饮食相关的中等强度运动。氨代谢研究的模型?","authors":"F. Bachini, J. P. S. W. Castro, Leonardo Cristiano Moretzsohn, A. Cameron, L. Cameron","doi":"10.3900/FPJ.8.3.226.E","DOIUrl":null,"url":null,"abstract":"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.","PeriodicalId":164994,"journal":{"name":"Fitness & Performance Journal","volume":"35 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2009-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"MODERATE-INTENSITY EXERCISE ASSOCIATED WITH KETOGENIC DIET. A MODEL FOR THE STUDY OF AMMONIA METABOLISM?\",\"authors\":\"F. Bachini, J. P. S. W. Castro, Leonardo Cristiano Moretzsohn, A. Cameron, L. Cameron\",\"doi\":\"10.3900/FPJ.8.3.226.E\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"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.\",\"PeriodicalId\":164994,\"journal\":{\"name\":\"Fitness & Performance Journal\",\"volume\":\"35 1\",\"pages\":\"0\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2009-05-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Fitness & Performance Journal\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.3900/FPJ.8.3.226.E\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Fitness & Performance Journal","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3900/FPJ.8.3.226.E","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
MODERATE-INTENSITY EXERCISE ASSOCIATED WITH KETOGENIC DIET. A MODEL FOR THE STUDY OF AMMONIA METABOLISM?
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.