Central nervous system effects of caffeine and adenosine on fatigue

American Journal of Physiology - Regulatory Integrative and Comparative Physiology - Tập 284 Số 2 - Trang R399-R404 - 2003
J. Mark Davis1, Zuowei Zhao1, Howard S. Stock2, Kristen A. Mehl1, James Buggy2, Gregory A. Hand1,2
1Departments of Exercise Science and
2Pharmacology and Physiology, Schools of Public Health and Medicine, University of South Carolina, Columbia, South Carolina 29208

Tóm tắt

Caffeine ingestion can delay fatigue during exercise, but the mechanisms remain elusive. This study was designed to test the hypothesis that blockade of central nervous system (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 5′- N-ethylcarboxamidoadenosine (NECA) on spontaneous locomotor activity. Thirty minutes before measurement of spontaneous activity or treadmill running, male rats received caffeine, NECA, caffeine plus NECA, or vehicle during four sessions separated by ∼1 wk. CNS caffeine and NECA (intracerebroventricular) 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% vs. 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 after peripheral (intraperitoneal) drug administration. Results suggest that caffeine can delay fatigue through CNS mechanisms, at least in part by blocking adenosine receptors.

Từ khóa


Tài liệu tham khảo

Arogyasami J, 1989, Med Sci Sports Exerc, 21, 167

Arogyasami J, 1989, Med Sci Sports Exerc, 21, 173

10.1016/0006-8993(83)90591-7

10.1016/0301-0082(90)90027-E

10.1152/ajpregu.1998.275.2.R596

10.1152/ajpendo.1995.268.1.E127

10.1123/ijsn.6.1.14

Costill DL, 1978, Med Sci Sports, 10, 155

10.1097/00005768-199701000-00008

Dunwiddie TV, 1991, J Pharmacol Exp Ther, 249, 31

10.1055/s-2008-1034637

10.1007/BF02386182

10.1016/0014-2999(85)90063-9

Fredholm BB, 1999, Pharmacol Rev, 51, 83

10.1016/S0091-3057(96)00435-2

10.1016/0014-2999(94)90029-9

10.1016/0091-3057(94)90115-5

10.1152/ajpregu.2001.280.3.R639

10.2165/00007256-200131110-00002

10.1111/j.1469-7793.2000.00837.x

10.1152/jappl.1998.85.3.883

10.1152/jappl.1991.71.6.2292

10.1152/jappl.1995.78.3.867

10.1016/0014-2999(78)90107-3

10.1016/S0014-2999(97)00040-X

10.1016/0306-4522(96)00021-8

10.1152/jappl.1996.81.4.1658

10.1152/jappl.1998.85.2.709

10.1046/j.1471-4159.2001.00607.x

Laurent D, 2000, J Clin Endocrinol Metab, 85, 2170

10.1016/S0304-3940(01)01980-2

10.1016/0024-3205(82)90715-9

10.1016/0006-8993(86)90975-3

10.1016/S0014-2999(96)00938-7

10.3109/07853899908998788

10.3177/jnsv.47.139

10.1055/s-2008-1025666

10.1152/jappl.1998.85.4.1493

10.1249/00005768-198604000-00008

Thông tin
Thông tin xuất bản

American Journal of Physiology - Regulatory Integrative and Comparative Physiology

Tập 284 Số 2

R399-R404

Thông tin tác giả