Please use this identifier to cite or link to this item: https://hdl.handle.net/10316/106703
Title: Neuronal adenosine A2A receptors signal ergogenic effects of caffeine
Authors: Aguiar, Aderbal S. 
Speck, Ana Elisa 
Canas, Paula M. 
Cunha, Rodrigo A. 
Issue Date: 7-Aug-2020
Publisher: Springer Nature
Project: Prémio Maratona da Saúde, CAPES-FCT (039/2014), CNPq (302234/2016-0) 
POCI-01-0145-FEDER-03127 
CENTRO-01-0145-FEDER- 000008:BrainHealth 2020 
CENTRO-01-0246-FEDER-000010 
Serial title, monograph or event: Scientific Reports
Volume: 10
Issue: 1
Abstract: 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.
URI: https://hdl.handle.net/10316/106703
ISSN: 2045-2322
DOI: 10.1038/s41598-020-69660-1
Rights: openAccess
Appears in Collections:I&D CNC - Artigos em Revistas Internacionais
FMUC Medicina - Artigos em Revistas Internacionais

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