It is also apparent in Figure 1 and for the other sprints (data not shown) that the mean enhancements with caffeine arose partly through a reduction in fatigue as the test progressed. We quantified fatigue in the test by calculating the decline in the performance in the second half relative to the first. In the placebo condition, the declines were: 20-m sprint speed, 2.1% (90% confidence limits, ±1.4%); offensive sprint speed, 2.8% (±1.4%); Drive 1 power, 3.7% (±2.6%); Drive 2 power, 5.0% (±3.7%); defensive sprint speed, 0.9% (±1.2%); tackle sprint speed, 2.0% (±1.4%); passing accuracy, 9.0% (±4.7%); and 30-m sprint speed, 5.4% (±1.8%). The effects of caffeine on fatigue were decisive for all measures: possible through very likely reductions in fatigue for all but power in Drive 2, where a detrimental effect of caffeine was possible (Table 3).
For some measures, fatigue was not evident in the last circuit of the placebo condition relative to the first circuit. Indeed, for the 20-m sprint, there appeared to be an increase in performance of 5.5% (±3.2%) relative to the first circuit, and there were also substantial although less clear improvements for defensive, tackle and 30-m sprints. The other measures showed declines in performance, which were unclear for the offensive sprint and Drive 2, but possible for Drive 1 (6.5%; ±7.8%), and very likely for passing accuracy (18%; ±11%). It was only for these latter two measures that the effect of caffeine was clear in the last circuit: a likely benefit for the first drive (12%; ±11%) and an almost certain benefit for passing accuracy (28%; ±19%).
Plasma caffeine and epinephrine.
Figure 2 shows that 1 h after ingestion of caffeine, the plasma caffeine concentration increased to 8.2 μg·mL−1 (equivalent to 42 μmol·L−1) and then declined somewhat during the rugby test. The caffeine concentration before ingestion was below the level of detection in the assay for all subjects; the value is shown in the figure as 1 μg·mL−1. Caffeine concentration was also below the level of detection for all subjects at all time points in the placebo condition. Figure 2 also shows the plasma epinephrine concentration before, during, and after the rugby test for the caffeine and placebo conditions. Averaged over these three time points, the epinephrine concentration was 51% higher (90% confidence limits ±11%) in the caffeine condition than in the placebo condition.
There was a strong positive correlation (r = 0.59; 90% confidence limits −0.06 to 0.89) between plasma caffeine concentration during the caffeine condition and the change in epinephrine concentration between placebo and caffeine conditions; both concentrations were averaged in each subject over the pre-, mid-, and postexercise assays. Correlations between plasma caffeine and changes in performance were inconclusive, with the exception of a strong positive correlation with tackle sprint speed (r = 0.63) and a strong negative correlation with Drive 1 power (r = −0.80). All but one of the correlations of changes in epinephrine concentration before and during the test with changes in sprint speed were substantial and positive, and two were conclusive (range −0.03 through 0.64). All the correlations of changes in epinephrine with changes in drive power were substantial and negative, but none was conclusive (range −0.27 through −0.49). There was also a strong negative correlation between passing accuracy and epinephrine concentration before the performance test (r = −0.63), and the correlation during the test was negative but unclear (r = −0.27).
Effects of caffeine on exercise performance.
The present study is the first to report that caffeine has multiple beneficial effects on the physical and skill activities required in an intermittent high-intensity team sport. Such effects were demonstrated for five sprint tasks (high-speed requirement), a power task (high-force requirement), and an accuracy task performed rapidly (high motor skill requirement). The enhancements of performance were apparently not due to a placebo effect at the start of the rugby test because no subjects stated that they were confident about what treatment they had received.
Our conclusions are based on the approach to inferential statistics that emphasizes precision of estimation rather than null-hypothesis testing. To that end, we have followed recommendations to show and interpret the practical importance of confidence limits (e.g., Altman et al. (2) and Sterne and Smith (29)), which represent the uncertainty in the true value of each effect. We have built on these recommendations by enunciating a rule for deciding when an effect is clear or unclear and by making quantitative assertions about likelihood that the effect is beneficial or detrimental (20).
For the sprint tasks, most of the effects of caffeine averaged over the entire test were clear and all were positive (Table 3). The improvements of 0.5–2.9% were of similar magnitude to those effects reported for endurance exercise (9,15,24) or high-intensity exercise of 4- to 10-min duration (4,14,21). The positive effects in the present study cannot be compared with those of other studies on repeated sprints (17,27) because the duration of the test was considerably longer. This point is important because the influence of caffeine on the sprints was more apparent in the second half of the test (Fig. 1). We demonstrated that caffeine protects against fatigue during sprints, first from our caffeine versus placebo analysis of the first versus second half sprint performances (Table 3), and second because caffeine was without substantial effect when there was no apparent fatigue, as seen during the efforts for the sprints of the last circuit (Fig. 1).
Caffeine increased the peak power of Drive 1 over the entire test by 5% (Table 3, Fig. 1). Specifically, this involved enhancement in the first circuit and diminished fatigue as shown over the two halves and in the last circuit. Caffeine has also been shown to improve other activities requiring high force production such as competitive rowing (4) and maximum isometric voluntary contractions (MVC) (22,23). The peak MVC force for the quadriceps can increase by 5% (23), but such effects are only detected in situations where there is submaximal voluntary activation (23,25,31). The only clear detrimental effect with caffeine in the present study was for Drive 2, which showed increased fatigue in the second half compared with the first half. Similar detrimental effects have been shown for the latter sprints during repeated Wingate testing (17).
The largest and possibly most exciting new finding with caffeine was a 10% improvement in the ability to pass balls accurately while pressured to pass rapidly (simulating game conditions). This was observed both early in the test and later when the subjects were fatigued (Table 3, Fig. 1). The importance of this observation is that over the course of a game, the subjects would deliver a pass successfully 90% of the time with caffeine compared with 83% in the placebo condition or a difference of about five passes out of 70. This supplement-induced improvement in a skill task requiring coordinated movements of several muscle groups is not found in current literature.
Ingestion of 6 mg·kg−1 caffeine produced a peak plasma concentration of approximately 8 μg·mL−1, which is similar to that previously reported for the same dose of caffeine (15,17). Before administration of treatments, the subjects showed levels of caffeine below the 2 μg·mL−1 threshold of detection for the assay. For the average subject, who weighed 98 kg, the dose was 600 mg of caffeine, which is equivalent to approximately six cups of coffee (30). The detection threshold is therefore equivalent to approximately 1.5 cups of coffee consumed 1 h before the assay. The assay was therefore not sensitive enough to confirm rigorous compliance with the instruction to abstain from caffeine-containing products. In a meta-analysis of the effects of caffeine on performance (G. R. Stuart and W. G. Hopkins, unpublished observations), abstention from caffeine-containing food and drink for at least several days produced an additional performance enhancement of approximately 1.5%. The effects we have observed on performance could therefore be underestimates of the full effect expected with abstention.
Mechanisms for the effects of caffeine on performance.
Caffeine exerted its beneficial effects by causing obvious reductions in fatigue and in some cases by enhancement in the first circuit. However, apart from the first station in the first circuit (the 20-m sprint), all bouts were performed after prior exercise and therefore some fatigue could be involved. We discuss first the extent and nature of fatigue for the different activities and then how caffeine may exert its performance enhancing effects by reducing fatigue or enhancement when the subjects were fresh.
The nature of the rugby test was one of repeated high-intensity exercise, with fatigue being apparent in every type of activity in the placebo condition (Fig. 1). The rugby test involved a much greater volume of supramaximal exercise (~14 min) compared with other studies on intermittent exercise, yet compared with typical endurance studies the volume was much less. The etiology of fatigue in repeated intermittent exercise could in principle involve several factors (16). It should also be noted that fatigue during any one activity in the rugby test is likely to depend on the cumulative effects imposed by all other previous physical activities. Fatigue mechanisms that are plausible for rugby include changes of muscle high-energy phosphates (16), acidosis (13,16), lowered muscle glycogen levels (16,17), rundown of electrolyte gradients such as for potassium (K+) (17,24), and/or a reduced motor drive from the CNS, i.e., central fatigue (11,22).
With the sprint tasks, an astounding finding was that in the very last circuit the subjects were able to restore sprint times relative to that of the first circuit (or even improve the time). This observation (Fig. 1) strongly suggests that the working muscles could still function maximally and therefore the slowing of sprints over the course of the test resulted from a diminished motor drive from the CNS. The slowing may be related to an inability to sustain exercise at the high levels of perceived exertion that occur in the latter stages of intermittent high-intensity shuttle running (10,14,26) or with endurance exercise (9).
The magnitude of fatigue in the drives (Fig. 1) is comparable to the reduction in peak MVC force (~10%) seen for leg muscles after a soccer test (28). Indeed, the drives are likely to require near maximal recruitment of motor units in the working muscles as is necessary for MVC. Several neural or muscular mechanisms already alluded to could be involved in fatigue of the drives but the present study cannot discriminate between the possibilities. The fact that peak power for Drive 2 was always less than for Drive 1 (by 10–15%) throughout the test and even in the last circuit (Table 1, Fig. 1), could be explained by a substantial contribution from processes in muscle and may involve high-energy phosphates that had not recovered in the 5-s rest period between drives (16).
Impairment of the ball-passing accuracy task (Fig. 1) could involve either a loss of concentration or another effect via the CNS that diminishes coordinated motor drive to the muscle groups involved in passing the ball. Other studies involving intermittent high-intensity exercise tests have revealed a loss of ground-stroke hitting accuracy in a tennis performance test (10) or diminished ability to dribble a soccer ball quickly (26). However, the impaired performance in both of these tests may have been due to players moving more slowly, which did not contribute to the skill impairment in the present study.
Caffeine is known to influence many processes that could explain performance enhancement. These processes include several aspects of excitation–contraction coupling in skeletal muscles (1,5), attenuation of the rundown of the K+ gradient during exercise (18,24), mobilization of free fatty acids from adipose tissue (4,9), slowing of muscle glycogen depletion (15), and modifications to CNS activity (11,22). Moreover, caffeine may act indirectly via inhibition of adenosine receptors (11,15,22), inhibition of cyclic AMP phosphodiesterase activity (15), elevation of the plasma epinephrine concentration (9,24), or via theophylline or paraxanthine the breakdown products of caffeine (15,18). The only unlikely mechanisms include some of the excitation contraction coupling processes (1,5) and phosphodiesterase inhibition (15), which require much higher concentrations of caffeine than in the present study.
We looked for a possible role of epinephrine but did not systematically investigate other mechanisms. In the placebo condition, the plasma epinephrine concentration exceeded 2 nmol·L−1 throughout the rugby test (Fig. 2), which is comparable to that seen with intense exercise (17,21). Also, in the caffeine condition, plasma epinephrine was elevated both at rest and throughout the test (Fig. 2), making it a potential mediator for the enhancements. However, the correlation analysis revealed that epinephrine could be a mediator of performance improvement but only for the sprint activities. On the contrary, the higher epinephrine levels tended to dampen the beneficial effects of caffeine with the drives and the passing accuracy task.
We attributed the fatigue during repeated sprints to impaired motor drive. Caffeine could act either by attenuating this central fatigue or by acting directly on muscle. However, because the sprint time in the last circuit showed no fatigue in the placebo condition and caffeine did not improve this performance measure (Fig. 1), we propose that the entire effect of caffeine on the earlier sprints is mediated via the CNS. If this is the case, then one explanation could be that caffeine inhibits the binding of adenosine to adenosine receptors in the brain (11,15) and thereby reduces perception of exertion (9,14). Another possibility, based on the positive correlation between changes in plasma epinephrine and sprints speed, is that a restoration of motor drive to the exercising leg muscles with caffeine may actually be mediated by epinephrine acting on the CNS.
Caffeine may have improved Drive 1 performance through increased motor drive (23), changes in metabolism (9,15), or direct effects on muscle (24,25,31). This effect is unlikely to be mediated via epinephrine acting on muscle to potentiate excitation-contraction coupling (5) because the correlation analysis suggested that elevated epinephrine is, if anything, detrimental for this response. The mechanism for the decline in performance of Drive 2 with caffeine is uncertain. Nevertheless, this negative effect is of minor concern given the notable gain in power output with caffeine during Drive 1.
It is difficult to imagine that the improved passing accuracy with caffeine would involve anything other than an effect somewhere in the motor control areas in the CNS. This effect could involve an increased level of attention (19) or arousal (15). The negative correlation between change in epinephrine concentration and change in performance suggests that epinephrine attenuates this effect. This effect of caffeine is likely to be important in competitive sports where the ability to perform skills like passing balls, hitting balls, or shooting goals with accuracy late in the event is a key to successful performance.
Caffeine provides several valuable performance-enhancing effects on simulated intermittent high-intensity team-sport performance, making it a potentially useful supplement for games such as rugby, football, soccer, hockey, basketball, and tennis. Although the mechanisms for the effects of caffeine are not fully understood, we speculate that caffeine influences several processes in the CNS to reduce fatigue with repeated sprint and permit a higher level of motor drive and motor skills throughout games.
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Keywords:©2005The American College of Sports Medicine
EPINEPHRINE; ERGOGENIC; FATIGUE; RUGBY; SPRINT