Abstract
AbstractAdenosine 2A receptors (A2ARs) are abundant in the striatum, and they are found co-localized with dopamine D2 receptors (D2R) and in the heterodimer form A2AR-D2R. Previous we demonstrated that caffeine delays central fatigue through adenosine 2A receptors (A2ARs) antagonism, striatal neuroplasticity and mitochondrial metabolism enhancement. In this study we demonstrate the participation of striatal A2AR-D2R in the ergogenic outcomes. Two-hundred swiss adult mice were treated systemically (i.p.) and centrally (striatum-st.) with caffeine, SCH58261 (A2AR antagonist), DPCPX (A1R antagonist) and haloperidol (D2R antagonist), and performed the open field test, treadmill incremental exercise and grip strength meter test We observed that A2AR-D2R antagonic effects are linked to motor control (p< 0.05) and enhancement of power (p< 0.05). However, the role of A2AR-D2R in the mechanism of strength generation seems to differ from motor control.
Publisher
Cold Spring Harbor Laboratory