Caffeine is a drug that is commonly accepted around the world as part of a normal eating pattern, with around 90 of adults consuming it daily (Burke, 2008). Caffeine has been used for consumption since the sixteenth century and has now become the fuel for modern society (Stamford, 1989). Caffeine has become so popular due to its benefits of improving alertness, mood and behaviour via the central nervous system (Williams et al., 1987). Williams (1991) found it is one of the most widely consumed drugs in the world and is most commonly found the beverages tea and coffee. Jacobson (1987) suggests caffeine has been associated with enhancing performance and physiological capabilities for a long time, more importantly it is consumed by people in sport specifically to improve performance (Desbrow & Leveritt, 2006, Keisler & Armsey, 2006).
Athletes for many years have used caffeine to improve performance showing that it can be used as an ergogenic aid (Graham et al., 1994). In the world of sport, The World Anti-Doping Agency (WADA) have removed caffeine from their banned substance list and instead replaced it on their monitoring programme during competition (WADA, 2009). Athletes have used caffeine to enhance strength, improve reaction times and increase prolonged exercise proving that caffeine is effective as an ergogenic aid (Graham, Rush & Van Soren, 1994).
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Whilst the effects of caffeine on aerobic performance have been well established (Costill, Dalksy, & Fink, 1978; Falk et al., 1989; Ivy, Costill, Fink, & Lower, 1988; Trice & Haymes, 1995, Van Soeren & Graham, 1998), the effects on anaerobic performance aren't as well researched. This article is focusing and discovering the effects of caffeine in anaerobic performance.
1.2 Aims of Study
The aim of this study is to determine the effect of caffeine on an anaerobic 1km Time Trial Cycle. The results of this study will be able to prove and support previous research that caffeine does improve high intensity anaerobic performance.
1.3 Research Hypothesis
"150-300 mg/kg of caffeine ingested prior to performance will significantly decrease the time to perform the 1km Time Trial"
"150-300 mg/kg of caffeine ingested prior to performance will not significantly decrease the time to perform the 1km Time Trial"
Review of Literature
Caffeine is an ingredient of tea, coffee, chocolate and soft drinks consumed far and wide in modern society (Drewnowski 2001). Caffeine is alkaloid structurally identified as 1,3,7 trimethylxanthine (Williams, Barnes & Gadberry 1987). The three trimethylxanthine derivatives - which give off similar physiological reactions, are all found naturally in plants such as coffee beans, cocoa beans, tea leaves and kola nuts (Graham, 1978). Therefore in coffee, tea and chocolate, cola drinks and energy drinks there are high levels of caffeine, in an average cup of coffee there is on average 83mg of caffeine (Burg, 1976). Caffeine levels can be seen in Table 1.
Table 1: Caffeine levels in food/drink used in sport.
Energy drinks contain amounts of caffeine that exceed the amounts found in soft drinks and the concentration levels are similar to those found in coffee (Mandel, 2002). Caffeine is usually digested orally and within minutes it is enters all the organs and tissues of the body. It is distributed throughout the water in the body with the greatest concentration in the skeletal muscle making this the highest depot of water (Williams, 1991). The half life of caffeine after absorption can last from 4-6 to two days depending on a person's individual age, weight, sex or hormonal status (Jacobson and Kulling, 1989). Caffeine has diuretic (elevated urination rates) properties when administered to people with low tolerance (Maughan and Griffin, 2003). Most people (90% of adults who consume it daily (Burke, 2008)) have built a strong tolerance to this effect and studies have failed to confirm the common belief that caffeine does indeed cause dehydration (Armstrong et al., 2005, Armstrong et al., 2007).
2.2 Ergogenic Effects
The effectiveness of caffeine on the body as an ergogenic aid made caffeine hard to deal with for governing bodies in the past (Spriet, 1995). For this reason in 1962, the evidence against caffeine caused the International Olympics Committee to place it on their banned substances list for high consumption of the drug for athletes in competition only to take it off again in 1972. Caffeine had been limited in all sports as it has the power to enhance performance to the extent where it could gain an unfair advantage (Spriet, 1995). Since caffeine is found in many foods that are considered to be part of a "normal eating pattern" when the IOC test for the drug, the banned level was set above 12 ug ml-1 (International Olympic Committee, 2003) which Jacobson and Kulling (1989) suggest is the equivalent of 5-6 cups of coffee (500-600mg of caffeine) in a 1-2 hour period. Van der Merwe et al. (1998) found that realistically, this high dosage allowance would only be exceeded through injections, tablets, suppositories or the deliberate ingestion of high amounts. This law came into effect as the IOC wanted to keep the integrity of sport and prevent abuse by athletes as caffeine may be the most abused drug in the world (Spriet, 1995). Recently in 2003 the IOC did remove caffeine from their banned substance list however the IOC still monitor caffeine levels in competitive athletes (World Anti-doping Agency, 2005). In America the National Collegiate Athletic Association (NCAA) requires that athletes have a urinary caffeine concentration under 15 ug ml-1. Graham and Spriet (1991) suggest that urinary caffeine concentration as low as 10 ug ml-1 could improve performance. Therefore caffeine can still be used as an aid by competitive and recreational athletes.
2.2.1 Rate of Perceived Exertion
Always on Time
Marked to Standard
Several studies have proved caffeine to lower RPE in exercise (Costill et al. 1978; Fisher et al. 1986; Falk et al. 1990; Doherty and Smith 2005; Norager et al. 2005). Tarnopolsky (2008) suggests that a reduction in RPE after the consumption of caffeine during exercise could be due to factors other than metabolic efficiency. Factors include a reduction in central fatigue and the afferent pain output, an attenuation of neuromuscular conduction block and a potentiation of force output for a given neural point.
2.2.2 Central Nervous System Stimulation
Williams (1991) suggests Caffeine can have a direct effect on the central nervous system and along with Coffee is responsible for increasing wakefulness (Levy and Zylber-Katz 1983;Yanik et al. 1987; Walsh et al. 1990; Landolt et al. 1995). Syed (1976) states that caffeine passes the blood/barrier eagerly and therefore can affect the central nervous system directly acting as a powerful stimulant at all levels. Stimulation therefore can effect motor-coordination, behaviour, mood, sleeping pattern and overall output (effort). Caffeine stimulates the central nervous system by the release of epinephrine which could inhibit the depressant actions of adenosine (Williams, 1991). After the ingestion of caffeine plasma catecholamine production is increased, the actions of catecholamine are essential as they let the body adapt to stress caused by physical exercise (Nehlig & Debry, 1994). Caffeine is also know to stimulate the medullary, respiratory, vasomotor, and vagul centres and therefore could effect blood pressure, heart rate and respiratory rate (Jacobson and Kulling, 1989).
2.2.3 Camp Levels
Caffeine is responsible for the inhibition of the enzyme Phosphodiesterase (PDE) which degredates adenosine 3'5' cyclic monophosphate (cyclic AMP) (Williams, 1991). Nehlig and Debry (1994) suggest that by inhibiting PDE, the levels of cyclic AMP are increased which therefore increases neurotransmitter release. As a result of this release there will be increase in motor neuron recruitment. With the increasing levels of cyclic AMP, lipases that are hormone sensitive are activated which promote lipolysis. With the increased lipolysis there is an increased availability of free fatty acids as substrates (Dodd, Herb & Powers 1993). The free fatty acid available increases muscle fat oxidation which decreases carbohydrate oxidation (Spriet, 1995). When exercising glycogen is the primary source of energy, Stamford (1989) suggests that caffeine preserves the glycogen, as fat is promoted as a fuel source. Costill et al,. (1978) found that caffeine increased the rate of lipolysis which spared the rate of glycogen depletion from the liver and skeletal muscle.
2.2.4 Muscle Calcium
Nehlig & Derby (1994) state that caffeine can start and prolong the duration of active muscle contractions through an increased release of calcium from the sarcoplasmic reticulum. Myofilament sensitivity to calcium can also be increased due to the ingestion of caffeine. Also twitch development within the muscles will increase due to the increased calcium and myofilament sensitivity (Dodd et al,. 1993).
2.2.5 Adenosine Receptor Inhibition
Adenosine is a large component of ATP, which acts as an energy source for chemical reactions in cells (Zhang & Wells, 1990). Caffeine, by blocking adenosine receptors, increases neuronal activity by increasing neurotransmitter release and lowering the threshold for activation. The increase in neuronal activity could cause the facilitation of additional motor units therefore there is a chance of decrease in the time required for recruitment (Williams, 1991).
2.2.6 Neuromuscular Transmission
Okoro (1982) found that the compound muscle potentials elicited by electrical stimulation of the muscle afferent and efferent neurons are increased in amplitude. Following caffeine ingestion the stimulus thresholds required for elicitation of the reflexes are reduced. This suggests that the transmission of the electrical impulse between the motor neuron and the muscle must be improved to increase muscle activation (Williams, 1991)
2.2.7 Muscle Contractility
Williams (1991) found that the direct application of caffeine has an effect on skeletal muscle. In low concentrations, caffeine potentiates twitches of directly stimulated rest and fatigued muscle by 10-200%. Concentrations of 0.01 to 2.5 milimoles have a small or no measurable effect upon contractility. However, higher concentrations (levels above 2.5 milimoles) can potentially cause spontaneous contracture of the muscle. This occurs due to the development of tension without any membrane potential until it is equal or greater than peak titanic tension. The muscles then start to relax after several minutes of caffeine exposure.
2.3 Anaerobic Studies
Still after intensive research the effects of caffeine consumption on exercise performance is still unclear (Graham, Hibbert, & Sathasivam, 1998; Nehlig, Daval, & Derby, 1992). When it comes to caffeine on "aerobic" performance, the effects have been well established (Costill, Dalksy, & Fink, 1978; Falk et al., 1989; Ivy, Costill, Fink, & Lower, 1988; Trice & Haymes, 1995, Van Soeren & Graham, 1998), where as the effects on "anaerobic" performance are still unclear. Earlier studies haven't found improvement in performance; Greer, McLean and Graham (1998) found that caffeine ingestion didn't improve performance during four 30 second sets of cycling with 4 minute rests between each. These findings were more recently supported by Bell, Jacobs and Ellerington (2001) as they found no improvement in a 30 second Wingate performance after the ingestion of caffeine. However most recently Wiles et al,. (2006) found caffeine did improve performance in a 1km time trial on an electronically braked cycle ergometer. These results were similar to the findings of Collomp et al (1992) who found improvements in 100m swimming performance in trained swimmers. Unlike Wiles et al (2006) who found an mean improvement of 2.4 s or 3.1% in a 1km cycling time trial (however finding practical significance in context of real-life), Collomp et al,. (2006) measured blood lactate concentration which had a significant increase after ingestion in both trained and untrained participants. Bell et al,. (2001) found that caffeine did improvement performance (time to exhaustion) in a maximum accumulated oxygen deficit (MOAD) test which was performed at 150% V02 peak and lasted 2 minutes. This finding was supported by Doherty (1998) and Doherty, Smith, Davison and Hughes (2002) who found during a treadmill MOAD test that a dose of 5mg of Caffeine improved time to exhaustion by 10% in trained athletes. Bruce et al,. (2000) found that caffeine improved performance on a 7 minute 2000m rowing performance by competitive oarsmen. Jenkins et al,. (2008) also found improvements in performance for a 15 minute cycling time trial where work done was improved by 4% through the ingestion of 2 and 3 mg.kg of caffeine.
2.4 Time Trial Cycling (quotes needed)
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Time trialling is a test of the cyclist against the watch instead of other cyclists. Riders are not allowed to ride with each other and are often separated appropriately in performance levels. The order of the race is set so the fastest cyclists are spaced apart so they don't pass one another. The slower cyclists aren't affected as the faster cyclists will pass them quickly so that neither of them will be helped or hindered. Races can be organised over any distance and the winner is the fastest over the course.
For sprinters (1km cyclists) the most important source of energy is the breakdown of ATP (adenosinetriphosphate) and PC (phosphocreatine), the most available energy source in the muscle. 1km sprinters after using their immediate high-energy sources, obtain energy from the anerobic (nonoxidative) breakdown of carbohydrates (Burke, 1986). From Figure 1, it is easy to see that with work up to 2 minutes, anaerobic power is most important. At around 2 minutes, a 50:50 ratio exists; as the time increases, aerobic power becomes more important (Burke, 1986).
Anaerobic metabolism relies on the muscle glycogen and blood glucose as its fuel in order to work, with lactic acid being the end product of this system. The stored glycogen or glucose without the presence of oxygen breaks down into lactic acid. The breakdown of glucose would then continue into aerobic metabolism if there was a presence of oxygen. When there are high levels of lactic acid, the contraction of the muscles are repressed, this is due to the proteins being only able to function with a certain amount of acidity.
For the amount of caffeine to be consumed, each subject's average daily caffeine intake was estimated using a questionnaire (appendix whatever) as it has been known that habitual ingestion can result in a tolerance and therefore influence the results (Armstrong et al., 2005, Armstrong et al., 2007, Robertson et al,. 1981, Stamford, 1989)
Talk about amounts used in other research.
150-200mg of caffeine was used in this investigation (3 grams of coffee) as it realistically represents what an athlete may use before an event (Wiles et al., 1992).
Throughout this investigation all subjects were requested to continue with their normal dietary habits for consistency. They were also asked to not ingest any food or drink that contained caffeine for a period of at least 24 hours before the time trial. An hour before the time trial the subjects were asked to consume either a cup (350ml) of caffeinated coffee in hot water or a cup (350ml) of decaffeinated coffee in hot water. Pilot studies in the past have shown decaffeinated coffee to be an excellent placebo as subjects are unable to tell between the two forms of coffee (Wiles et al., 1992). The coffee - caffeinated and decaffeinated were administrated an hour before the 1km time trial as this time period is the optimal absorption window for caffeine as Jacobson (1987) and Robertson et al,. (1981) suggest.
An indoor electric cycle was used for however many times trials, think 3 for each drink. Each time before testing each subject declared themselves fit and that they haven't undertaken any exercise that could affect the outcome of the testing. To make sure that circadian rhythm didn't affect the outcome, subjects were asked to fast and the testing was performed at the same time (Winget et al,. 1985).
Each subject was asked to perform a self performed warm-up on the cycle for 5-10 minutes. The intensity of each warm was closely monitored for consistency for each subject. After each Time Trial the subjects were asked straight away their Rate of Perceived Exertion based on a scale of 1-10.
A recovery time of 5 minutes was selected as various studies have indicated this to be the peak time for blood lactate levels to be recorded (Cortes CW et al,. 1988). The blood sample was then taken and analysed using need name and model.