Neuronal adenosine A2A receptors signal ergogenic effects of caffeine
Autor(a) principal: | |
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Data de Publicação: | 2020 |
Outros Autores: | , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
Texto Completo: | http://hdl.handle.net/10316/106703 https://doi.org/10.1038/s41598-020-69660-1 |
Resumo: | Caffeine is one of the most used ergogenic aid for physical exercise and sports. However, its mechanism of action is still controversial. The adenosinergic hypothesis is promising due to the pharmacology of caffeine, a nonselective antagonist of adenosine A1 and A2A receptors. We now investigated A2AR as a possible ergogenic mechanism through pharmacological and genetic inactivation. Forty-two adult females (20.0 ± 0.2 g) and 40 male mice (23.9 ± 0.4 g) from a global and forebrain A2AR knockout (KO) colony ran an incremental exercise test with indirect calorimetry (V̇O2 and RER). We administered caffeine (15 mg/kg, i.p., nonselective) and SCH 58261 (1 mg/kg, i.p., selective A2AR antagonist) 15 min before the open field and exercise tests. We also evaluated the estrous cycle and infrared temperature immediately at the end of the exercise test. Caffeine and SCH 58621 were psychostimulant. Moreover, Caffeine and SCH 58621 were ergogenic, that is, they increased V̇O2max, running power, and critical power, showing that A2AR antagonism is ergogenic. Furthermore, the ergogenic effects of caffeine were abrogated in global and forebrain A2AR KO mice, showing that the antagonism of A2AR in forebrain neurons is responsible for the ergogenic action of caffeine. Furthermore, caffeine modified the exercising metabolism in an A2AR-dependent manner, and A2AR was paramount for exercise thermoregulation. |
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Neuronal adenosine A2A receptors signal ergogenic effects of caffeineAnimalsBody Temperature RegulationCaffeineEstrous CycleFemaleMaleMiceMice, KnockoutNeuronsPhysical Conditioning, AnimalProsencephalonPyrimidinesReceptor, Adenosine A2ASignal TransductionTriazolesAdenosine A2 Receptor AntagonistsCentral Nervous System StimulantsPerformance-Enhancing SubstancesCaffeine is one of the most used ergogenic aid for physical exercise and sports. However, its mechanism of action is still controversial. The adenosinergic hypothesis is promising due to the pharmacology of caffeine, a nonselective antagonist of adenosine A1 and A2A receptors. We now investigated A2AR as a possible ergogenic mechanism through pharmacological and genetic inactivation. Forty-two adult females (20.0 ± 0.2 g) and 40 male mice (23.9 ± 0.4 g) from a global and forebrain A2AR knockout (KO) colony ran an incremental exercise test with indirect calorimetry (V̇O2 and RER). We administered caffeine (15 mg/kg, i.p., nonselective) and SCH 58261 (1 mg/kg, i.p., selective A2AR antagonist) 15 min before the open field and exercise tests. We also evaluated the estrous cycle and infrared temperature immediately at the end of the exercise test. Caffeine and SCH 58621 were psychostimulant. Moreover, Caffeine and SCH 58621 were ergogenic, that is, they increased V̇O2max, running power, and critical power, showing that A2AR antagonism is ergogenic. Furthermore, the ergogenic effects of caffeine were abrogated in global and forebrain A2AR KO mice, showing that the antagonism of A2AR in forebrain neurons is responsible for the ergogenic action of caffeine. Furthermore, caffeine modified the exercising metabolism in an A2AR-dependent manner, and A2AR was paramount for exercise thermoregulation.Springer Nature2020-08-07info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articlehttp://hdl.handle.net/10316/106703http://hdl.handle.net/10316/106703https://doi.org/10.1038/s41598-020-69660-1eng2045-2322Aguiar, Aderbal S.Speck, Ana ElisaCanas, Paula M.Cunha, Rodrigo A.info:eu-repo/semantics/openAccessreponame:Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)instname:Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãoinstacron:RCAAP2023-04-18T08:34:08Zoai:estudogeral.uc.pt:10316/106703Portal AgregadorONGhttps://www.rcaap.pt/oai/openaireopendoar:71602024-03-19T21:23:07.197588Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãofalse |
dc.title.none.fl_str_mv |
Neuronal adenosine A2A receptors signal ergogenic effects of caffeine |
title |
Neuronal adenosine A2A receptors signal ergogenic effects of caffeine |
spellingShingle |
Neuronal adenosine A2A receptors signal ergogenic effects of caffeine Aguiar, Aderbal S. Animals Body Temperature Regulation Caffeine Estrous Cycle Female Male Mice Mice, Knockout Neurons Physical Conditioning, Animal Prosencephalon Pyrimidines Receptor, Adenosine A2A Signal Transduction Triazoles Adenosine A2 Receptor Antagonists Central Nervous System Stimulants Performance-Enhancing Substances |
title_short |
Neuronal adenosine A2A receptors signal ergogenic effects of caffeine |
title_full |
Neuronal adenosine A2A receptors signal ergogenic effects of caffeine |
title_fullStr |
Neuronal adenosine A2A receptors signal ergogenic effects of caffeine |
title_full_unstemmed |
Neuronal adenosine A2A receptors signal ergogenic effects of caffeine |
title_sort |
Neuronal adenosine A2A receptors signal ergogenic effects of caffeine |
author |
Aguiar, Aderbal S. |
author_facet |
Aguiar, Aderbal S. Speck, Ana Elisa Canas, Paula M. Cunha, Rodrigo A. |
author_role |
author |
author2 |
Speck, Ana Elisa Canas, Paula M. Cunha, Rodrigo A. |
author2_role |
author author author |
dc.contributor.author.fl_str_mv |
Aguiar, Aderbal S. Speck, Ana Elisa Canas, Paula M. Cunha, Rodrigo A. |
dc.subject.por.fl_str_mv |
Animals Body Temperature Regulation Caffeine Estrous Cycle Female Male Mice Mice, Knockout Neurons Physical Conditioning, Animal Prosencephalon Pyrimidines Receptor, Adenosine A2A Signal Transduction Triazoles Adenosine A2 Receptor Antagonists Central Nervous System Stimulants Performance-Enhancing Substances |
topic |
Animals Body Temperature Regulation Caffeine Estrous Cycle Female Male Mice Mice, Knockout Neurons Physical Conditioning, Animal Prosencephalon Pyrimidines Receptor, Adenosine A2A Signal Transduction Triazoles Adenosine A2 Receptor Antagonists Central Nervous System Stimulants Performance-Enhancing Substances |
description |
Caffeine is one of the most used ergogenic aid for physical exercise and sports. However, its mechanism of action is still controversial. The adenosinergic hypothesis is promising due to the pharmacology of caffeine, a nonselective antagonist of adenosine A1 and A2A receptors. We now investigated A2AR as a possible ergogenic mechanism through pharmacological and genetic inactivation. Forty-two adult females (20.0 ± 0.2 g) and 40 male mice (23.9 ± 0.4 g) from a global and forebrain A2AR knockout (KO) colony ran an incremental exercise test with indirect calorimetry (V̇O2 and RER). We administered caffeine (15 mg/kg, i.p., nonselective) and SCH 58261 (1 mg/kg, i.p., selective A2AR antagonist) 15 min before the open field and exercise tests. We also evaluated the estrous cycle and infrared temperature immediately at the end of the exercise test. Caffeine and SCH 58621 were psychostimulant. Moreover, Caffeine and SCH 58621 were ergogenic, that is, they increased V̇O2max, running power, and critical power, showing that A2AR antagonism is ergogenic. Furthermore, the ergogenic effects of caffeine were abrogated in global and forebrain A2AR KO mice, showing that the antagonism of A2AR in forebrain neurons is responsible for the ergogenic action of caffeine. Furthermore, caffeine modified the exercising metabolism in an A2AR-dependent manner, and A2AR was paramount for exercise thermoregulation. |
publishDate |
2020 |
dc.date.none.fl_str_mv |
2020-08-07 |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://hdl.handle.net/10316/106703 http://hdl.handle.net/10316/106703 https://doi.org/10.1038/s41598-020-69660-1 |
url |
http://hdl.handle.net/10316/106703 https://doi.org/10.1038/s41598-020-69660-1 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
2045-2322 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.publisher.none.fl_str_mv |
Springer Nature |
publisher.none.fl_str_mv |
Springer Nature |
dc.source.none.fl_str_mv |
reponame:Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) instname:Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação instacron:RCAAP |
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Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação |
instacron_str |
RCAAP |
institution |
RCAAP |
reponame_str |
Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
collection |
Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
repository.name.fl_str_mv |
Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação |
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