Caffeine is consumed in many beverages and foods throughout the world.
It is the most commonly used drug in North America and, probably, in
many other countries. The short term consumption of caffeine may resul
t in increased urination, gastrointestinal distress, tremors, decrease
d sleep, and anxiety symptoms in certain individuals. The long term co
nsumption of caffeine at < 5 cups/day does not appear to increase the
risk of cancer, cardiovascular disease, peptic ulcer disease or cardia
c arrhythmias. At the cellular level, caffeine is a competitive antago
nist of adenosine receptors and probably acts directly on the ryanodin
e receptor (Ca++ release channel) to potentiate Ca++ release from skel
etal muscle sarcoplasmic reticulum. As a result of these 2 cellular me
chanisms of action, caffeine causes increased lipolysis, a facilitatio
n of central nervous system transmission, a reduction in plasma potass
ium during exercise, an increased force of muscle contraction at lower
frequencies of stimulation, and a sparing of muscle glycogen (partial
ly or wholly due to an increase in free fatty acid oxidation). These m
echanisms of action would predict that caffeine should be of ergogenic
benefit during endurance exercise performance, especially when glycog
en depletion would be rate limiting to performance. A review of the li
terature suggests that caffeine at doses of approximately 6 mg/kg is n
ot of ergogenic benefit to high intensity exercise performance, but si
milar doses are ergogenic in endurance exercise performance. These dos
es (approximately 6 mg/kg) would result in urinary caffeine concentrat
ions less than the current International Olympic Committee restricted
level of 12 mg/L, and consideration should be given to lowering this l
evel.