Potential ergogenic effects of caffeine at the cellular level are mediated by three main mechanisms of action which are: intracellular mobilization of calcium from sarcoplasmic reticulum and increased sensitivity of myofibrilles to calcium; inhibition of phosphodiesterases leading to an increase in cyclic-3',5'-adenosine monophosphate (cAMP) in various tissues including muscle; and the antagonism at the level of adenosine receptors, mainly in the central nervous system. The main mechanism of action of caffeine at the level usually encountered in vivo after the ingestion of a few cups of coffee is undoubtedly linked to the antagonism of caffeine at adenosine receptors. Caffeine also increases production of plasma catecholamines that allow the body to adapt to the stress created by physical exercise. Catecholamine production increases probably, in turn, the availability of free fatty acids as muscle substrates during work, thus allowing glycogen sparing. Caffeine is able to increase muscle contractility, has no ergogenic effect on intense exercise of brief duration, but can improve the time before exhaustion. Caffeine is also able to improve physical performance and endurance during prolonged activity of submaximal intensity. Glycogen sparing resulting from increased rate of lipolysis could contribute to the prolonged time to exhaustion. Finally, tolerance to the methylxanthine should be taken into account when an athlete wants to draw any benefit from caffeine absorption prior to a sports event.