A New Study
No previous research effort has examined the possible direct central nervous system (CNS) effects of caffeine on fatigue during prolonged exercise. Now, a team of researchers from the University of South Carolina has hypothesized that the blockade of adenosine receptors by caffeine may be the most likely mechanism of CNS stimulation and delayed fatigue.
Their theory is based on the fact that adenosine is produced within the body and inhibits neuronal excitability and synapse transmission. Adenosine also inhibits the release of most brain excitatory neurotransmitters, particularly dopamine (DA), and may reduce DA synthesis. Decreases in dopamine (DA), along with increases in 5-HT (serotonin, which is generally associated with behavioral suppression), have been linked to central fatigue during exercise. In addition, adenosine has been shown to reduce arousal, induce sleep, and suppress spontaneous activity, which are all behaviors associated with increases in 5-HT.
The researchers' hypothesis is the foundation of a new study to determine the effects of intracerebroventricular injection of caffeine and the adenosine A1 and A2 receptor agonist 5'-N-ethylcarboxamidoadenosine (NECA) on treadmill run time to fatigue in rats. NECA was chosen for the study because caffeine is a nonselective adenosine receptor antagonist, and it is not known which of the four subtypes of adenosine receptors may be involved in an effect of caffeine on fatigue. However, A2b and A3 receptors are relatively less active than A1 and A2a receptors under normal physiological conditions.
Contact: Donna Krupa
American Physiological Society