Two questions that have intrigued sports scientists for 25 years are: does caffeine ingestion prior to exercise cause an improved performance, and if it does, what mechanisms are responsible for that improvement? Early research indicated that caffeine ingestion increased time to exhaustion in endurance exercise because it caused a metabolic response in humans. The reason for this was thought to be that the presence of caffeine in the blood appeared to stimulate the release of the catecholamines adrenaline and noradrenaline, which in turn brought about an increase in the availability of fat as fuel for the working muscles; the effect of this was thought to be a sparing of muscle glycogen, or carbohydrate stores.

Other possible explanations for caffeine's action - for instance, that it may result in more forceful muscular contractions by affecting the action of calcium in the muscle - have been discounted because of the unfeasibly large (probably toxic) amount of caffeine needed to promote such actions. This leaves the stimulation of catecholamine release as the most likely explanation for caffeine's ergogenic effect, and, for this reason, most studies investigating caffeine's effect on performance have concentrated on endurance exercise. There would appear to be little point in studying its effect on short-term (ie, less than five minutes), intense (90-100% VO2max) exercise, where the provision of glycogen is not a limiting factor.

Nevertheless, some research has shown that caffeine does improve short-term performance (see, for instance, PP, December 1993, pp 5-6) although the results have not always been statistically significant. In such exercise, it is believed that caffeine must act directly on the muscle or on the central nervous system if it is to alter performance.


Withdrawal symptoms
In a recent study at the University of Brighton, a group of undergraduate sports scientists took part in an experiment which was designed to test whether caffeine does affect short-term performance. The subjects were given a gelatine capsule containing either a placebo or caffeine (5mg/kg body mass) one hour prior to a 1500m time-trial performed on a friction-braked cycle. Each subject chose his own strategy to cover the 1500m as quickly as possible. Subjects were asked to refrain from caffeine ingestion for two weeks prior to the first test and until after the second test had been completed. The second test was carried out by all subjects one week after the first trial at the same time of day.

The potency of caffeine as a drug was initially illustrated by the fact that many of the students experienced quite powerful withdrawal symptoms. When the placebo and caffeine capsules were given out, 81 per cent of the subjects correctly identified that they had taken caffeine and 94 per cent correctly identified that they had taken the placebo. Caffeine ingestion did not cause any significant changes in heart rates during the warm-up, or after a recovery period, and it did not alter the time taken to reach half-distance. It also did not significantly change the time taken to complete the 1500m, or mean VO2 (oxygen uptake). It did, however, result in a significantly increased mean and peak exercise heart rate.

The conclusion from all this? Caffeine did not cause an improvement in this type of performance but it did cause a significant increase in exercise heart rate. That being said, the fact that the mean time to complete the trial was 1.2 secs quicker during the caffeine trial than during the placebo initially looked exciting. This is because the level of improvement required by an athlete may be smaller than the level of scientific significance. Does this therefore suggest that caffeine ingestion would be a worthwhile tactic before competing in events of this nature? No, for the following reason.


The learning effect
Although no significant differences were found between the performance times when expressed by trial order, mean performance during the second trial was 1.3 secs quicker. Similarly, mean time taken to perform the last 750m was 2.6 secs quicker during the second trial. This implies that there was a learning effect, or, more simply, the subjects got better at performing the task once they got used to it.

The results from this experiment suggest that the most likely cause of caffeine's ergogenic effect in endurance events is that it does stimulate catecholamine release. This was borne out by the significant increase in the exercise heart rate found in this experiment, because catecholamines accelerate the depolarisation of the sinus node and cause the heart to beat faster. The increase in the warm-up and recovery heart rates in this experiment were not significant, though they were clearly elevated during the caffeine trial. The greater increase in heart rates during the exercise may have been caused by additional catecholamine release stimulated by physical performance.

This experiment suggests that there is no benefit in using caffeine as an ergogenic aid in short-term, high-intensity exercise. In addition, the changes in heart rates during the experiment, together with some of the comments from the students about how they actually felt (ranging from 'profoundly sick' to 'weird') did show that caffeine is a very potent drug even when only a moderate dose (5mg/kg) is taken. This dosage would result in urinary caffeine levels below the limit set by the International Olympic Committee for competition. The unpleasant side-effects might cause even endurance athletes to have second thoughts about using caffeine.

Lee Oliver