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Am J Physiol Regul Integr Comp Physiol (October 24, 2002). doi:10.1152/ajpregu.00386.2002
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Articles in PresS, published online ahead of print October 24, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00386.2002
Submitted on June 26, 2002
Accepted on October 21, 2002

Central Nervous System Effects of Caffeine and Adenosine on Fatigue

J. Mark Davis1*, Zuowei Zhao1, Howard S Stock2, Kristen A Mehl1, James Buggy2, and Gregory A Hand3

1 Exercise Science, University of South Carolina, Columbia, SC, USA
2 Pharmacology and Physiology, University of South Carolina, Columbia, SC, USA
3 Exercise Science, University of South Carolina, Columbia, SC, USA; Pharmacology and Physiology, University of South Carolina, Columbia, SC, USA

* To whom correspondence should be addressed. E-mail: jmdavis{at}sc.edu.

Caffeine ingestion can delay fatigue during exercise, but the mechanisms remain elusive. This study was designed to test the hypothesis that blockade of CNS adenosine receptors may explain the beneficial effect of caffeine on fatigue. Initial experiments were done to confirm an effect of CNS caffeine and/or the adenosine A1/A2 receptor agonist, NECA, on spontaneous locomotor activity. Thirty min prior to measurement of spontaneous activity or treadmill running, male rats received Caffeine, NECA, Caffeine-plus-NECA, or Vehicle during 4 sessions separated by approximately 1 week. CNS Caffeine and NECA (i.c.v.) were associated with increased and decreased spontaneous activity, respectively, but Caffeine-plus-NECA did not block the reduction induced by NECA. CNS Caffeine also increased run time to fatigue by 60% and NECA reduced it by 68% versus Vehicle. However, unlike the effects on spontaneous activity, pretreatment with Caffeine was effective in blocking the decrease in run time by NECA. No differences were found following peripheral (i.p.) drug administration. Results suggest that caffeine can delay fatigue through CNS mechanisms, at least in part by blocking adenosine receptors.




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