Caffeine and Endurance Performance
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abstract
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 result in increased urination, gastrointestinal distress, tremors, decreased sleep, and anxiety symptoms in certain individuals. The long term consumption of caffeine at < 5 cups/day does not appear to increase the risk of cancer, cardiovascular disease, peptic ulcer disease or cardiac arrhythmias. At the cellular level, caffeine is a competitive antagonist of adenosine receptors and probably acts directly on the ryanodine receptor (Ca++ release channel) to potentiate Ca++ release from skeletal muscle sarcoplasmic reticulum. As a result of these 2 cellular mechanisms of action, caffeine causes increased lipolysis, a facilitation of central nervous system transmission, a reduction in plasma potassium during exercise, an increased force of muscle contraction at lower frequencies of stimulation, and a sparing of muscle glycogen (partially or wholly due to an increase in free fatty acid oxidation). These mechanisms of action would predict that caffeine should be of ergogenic benefit during endurance exercise performance, especially when glycogen depletion would be rate limiting to performance. A review of the literature suggests that caffeine at doses of approximately 6 mg/kg is not of ergogenic benefit to high intensity exercise performance, but similar doses are ergogenic in endurance exercise performance. These doses (approximately 6 mg/kg) would result in urinary caffeine concentrations less than the current International Olympic Committee restricted level of 12 mg/L, and consideration should be given to lowering this level.
