Proposed Effect(s):* also falls under the category of stimulant, alkaloid and methylxanthine * increases endurance performance, spares glycogen, increases lipid oxidation, enhances neuromuscular function, and attenuates plasma potassium levels during exercise
The following is a scientific analysis of caffeine and its usage in exercise and performance. The primary objective of this analysis is to further educate health, fitness, and performance professionals on the potential effectiveness of this dietary supplement in daily activity as well as athletic performance, and also to determine health risks associated with caffeine if any exist.
Overview:
Caffeine is commonly consumed by people, including athletes, for various performance and or fitness related reasons. The short-term effects of caffeine on endurance and sprint performance have been studied in-depth, however the results of these studies remain controversial and inconclusive. The effects of caffeine on the performance of an athlete can be mediated by several factors that should be carefully considered. There are risks associated with caffeine supplementation and there are dietary alternatives. There is no recommended daily intake for caffeine.
Description:
Caffeine is a crystal-like substance found in many beverages (coffee, tea, and cola), medications, and foods. Caffeine is quickly absorbed into the bloodstream and attains maximum values within 15 to 120 minutes of consumption. Through the blood, caffeine is spread to many tissues in the body, including the brain. Enzymes in the liver breakdown caffeine, leaving very little to be cleared in urine.
Caffeine has both central and peripheral effects in the body. In the central nervous system caffeine affects parts of the brain and the spinal cord, while in the periphery it affects organs and tissues. At low doses (2-10 mg/kg), it can cause increased alertness, less fatigue, reduced reaction time, increased ventilation, and poorer performance of some fine motor skills. At higher doses (>15 mg/kg), caffeine can cause nervousness, insomnia, headaches, and unsteadiness. Caffeine also has inconsistent effects on the cardiovascular system. Depending on where it acts in the body, caffeine can either raise or lower heart rate and cause blood vessels to constrict or dilate. Caffeine can cause a mild increase in urine output from the kidneys and dilation of the bronchi. Caffeine causes the release of epinephrine from the adrenal glands, which causes lipolysis (break down of fat) in muscle and adipose tissues. This increased mobilization of free fatty acids can lead to glycogen sparing early in the exercise period because the body uses relatively more free fatty acids for energy. Caffeine also directly acts on muscle cells by enhancing the release of calcium from the sarcoplasmic reticulum in muscles cells, which improves muscle contraction.
There are a variety of possible mechanisms by which caffeine is proposed to enhance athletic performance, many of which are mentioned above. The most researched and widely acknowledged mechanism is by glycogen sparing via increased fat utilization, thus allowing the athlete to exercise longer at a given suBathmateaximal intensity. Other mechanisms include increased catecholamine release, increased calcium release from muscle cells, and reduced perception of effort. On a cellular level, caffeine inhibits adenosine, causing increased urine excretion, stimulation of the central nervous system, increased lipolysis in fat cells (adipocytes) and increased gastric secretion. Increased lipolysis in fat cells occurs because caffeine reduces the inhibitory influence of adenosine on lipolysis, thus increasing lipolysis. These methods of enhanced athletic performance and other possible mechanisms are examined further throughout the course.
Review of the Research:
Research on the ergogenic effects of caffeine was advanced by several studies in the late 1970s (Costill, Dalasky & Fink, 1978; Ivy, Costill, Fink & Lower, 1979). The effects of caffeine on exercise performance are controversial, with some studies finding an enhancing effect and others finding no effect at all. In general, these and other studies show that a dose of caffeine ranging from 5 - 9 mg/kg bodyweight ingested 1 hour before suBathmateaximal exercise (75-85% VO2 max) produced significant increases (28%-156%) in exercise time to exhaustion. In other words, subjects exercised significantly longer at a given intensity in the caffeine trials than in the placebo trials. While it is widely agreed upon that caffeine increases time to exhaustion, several research studies have reported differing results and mechanisms for this increase in time to exhaustion. Reported effects of caffeine include increased plasma epinephrine at rest and during exercise, increased serum and plasma free fatty acid (FFA) concentration, an attenuated decrease in blood glucose levels during exercise, decreased muscle glycogenolysis (i.e. muscle glycogen breakdown) especially during the first 15 minutes of exercise, decreased perceived exertion during the exercise trial, lower respiratory exchange ratios, increased use of muscle triglycerides, and significantly higher plasma glycerol levels. Furthermore, one study examining total work output over a two hour period, instead of time to exhaustion at a given exercise intensity, found that caffeine ingestion increased work output on a cycle ergometer by 7.4% compared to the control trial (Ivy et al., 1979).
The increased fat mobilization and glycogen sparing theory for increased time to exhaustion is based on the idea that caffeine increases fat mobilization for fuel and decreases glycogenolysis early in the exercise period. These two process combined allow the athlete to perform longer at a given intensity because they have spared glycogen early on in the exercise session. A decrease in perceived exertion in the caffeine trials can be explained by the stimulating effect of caffeine. Caffeine increases the excitability of neurons by lowering their threshold, thus permitting increased recruitment of motor units and improved nerve transmission.
Most studies on the effects of caffeine on performance have examined its effects on suBathmateaximal continuous and intermittent endurance exercise on a treadmill or a cycle ergometer. Most of the studies using other exercise modalities examine time to exhaustion at a given intensity.
A study on the effects of caffeine ingestion (250 mg) on the performance of sprinters showed that caffeine improved the sprint performance of highly trained sprinters, but not untrained runners (Collomp et al., 1992). While caffeine increased maximal blood lactate concentrations in both trained and untrained sprinters, the trained subjects had significantly higher blood lactate levels after the sprint test than the untrained sprinters. The improved performance and greater blood lactate levels with caffeine ingestion in trained sprinters may reflect an increase in muscle glycogenolysis (the breakdown of glycogen to glucose) and buffering capacity of muscle. Furthermore, specific training may cause cellular adaptations, which are necessary to benefit from caffeine ingestion before sprint performance. Many studies have reported a glycogen sparing effect of caffeine during suBathmateaximal endurance exercise (Trice & Haymes, 1995; Spriet et al., 1992; Costill, Dalsky & Fink, 1978; Graham and Spriet, 1991; Graham and Spriet, 1995; Pasman, van Baak, Jeukendrup & de Haan, 1995). An increase in glycogenolysis with caffeine may appear to be contrary to these studies, however, caffeine has been shown to aid in calcium release, which then starts a cascade of events leading to catecholamine secretion.
Another study involving the effects of caffeine on swim performance showed that swimmers performed a 1,500m swim significantly faster with caffeine compared to without caffeine, while rating of perceived exertion was not significantly different (MacIntosh & Wright, 2005). In this study, caffeine ingestion (6 mg/kg bodyweight) 2 ½ hours before the swim trial also resulted in significantly lower pre-exercise plasma potassium levels and higher post-exercise blood glucose levels. Since a 1500m swim is usually performed in 18-25 minutes, it is unlikely that glycogen supplies would limit exercise capacity and therefore caffeine most likely exerts its ergogenic effect by mechanisms other than increased fat utilization. Since caffeine is known to enhance epinephrine release and catecholamines (i.e. epinephrine) stimulate gluconeogenesis (the conversion of amino acids to glucose), this may be the mechanism by which blood glucose was elevated post-exercise in the caffeine group. Lower pre-exercise plasma potassium levels are consistent with other studies showing that caffeine attenuates the exercise-related increase in plasma potassium. Since the accumulation of potassium may be related to fatigue, a lower starting point for plasma potassium may allow exercise at a higher intensity for a given distance before reaching the critical level of plasma potassium that causes fatigue. This suggests that electrolyte balance (potassium) and glucose availability may be important aspects of the performance enhancement effects of caffeine in this study.
While several of the above studies found similar effects of caffeine on exercise performance (increased time to exhaustion, increased plasma epinephrine, increased FFA concentration, decreased muscle glycogenolysis early in the exercise trial, etc.), several of the studies found results that are not in agreement with the above findings. These findings include no effect of caffeine on plasma FFA levels or respiratory exchange ratio, and no differences in oxygen consumption or heart rate between caffeine and placebo trials. It is interesting to note that a gender difference in the effects of caffeine on athletic performance was not discussed in the research studies used for this course.
It is important to note that research on the effects of caffeine on performance may be influenced by a number of factors: 1) dose, 2) time of caffeine ingestion before exercise, 3) form of caffeine, 4) pre-exercise glycogen stores, 5) prior caffeine habituation, and 6) intensity of exercise. Some of these factors or variables may be responsible for the conflicting results found in this area of research.
Dose-response effect of caffeine
Studies on the ergogenic effects of varying doses of caffeine on athletic performance were performed with doses ranging from 3 – 13 mg/kg (Kovacs, Stegen & Brouns, 1998; Pasman et al., 1995; Bruce et al., 2000; Graham & Spriet, 1995). These studies found that endurance performance (time to exhaustion), work output, and mean power improved significantly when caffeine was ingested in varying doses compared to a placebo. While caffeine enhanced endurance performance, most studies reported no dose-response of caffeine on time to exhaustion (i.e. lower doses were equally as effective in increasing time to exhaustion as moderate and high doses of caffeine). However, not all of the studies found similar results. For example, Kovacs, Stegen and Brouns (1998) reported a slightly greater improvement in performance with moderate (225 mg/l) compared to lower (150 mg/l) levels of caffeine. Furthermore, most studies reported that plasma FFA concentration increased equally or greater with increasing doses of caffeine, especially in the first 15 minutes of exercise. Graham and Spriet (1995) reported that the highest doses of caffeine (greater than 9 mg/kg bodyweight) had a greater effect on plasma epinephrine levels and plasma metabolites (free fatty acids and glycerol) compared to lower doses, but these doses had the same or less of an effect on endurance performance as lower doses.
Time of caffeine ingestion before exercise
Most studies use a standard time interval of 60 minutes between time of caffeine or placebo ingestion and the start of the exercise trial. However, in a study by Weir, Noakes, Myburgh, and Adams (1987), serum free fatty acid levels actually peaked 3-4 hours after caffeine ingestion. If the mechanism by which caffeine enhances endurance performance depends on FFA utilization, this data shows that exercise should start at 3-4 hours post caffeine consumption instead of 1 hour. However, more research needs to be done in this area in order to more accurately determine when exercise should commence after ingesting caffeine in order to produce the greatest benefit.
Forms of caffeine
Many people consume caffeine on a daily basis in coffee, hot chocolate, caffeinated sodas, and many other drinks and foods. However, a large portion of the research studies on the ergogenic effects of caffeine involve using caffeine in a capsule or powder form in water, decaffeinated coffee or a glucose solution. A study by Graham, Hibbert, and Sathasivam (2002) examined whether caffeine administered independently of coffee would result in larger improvements in endurance performance. It was hypothesized that caffeine would exert the largest effect when ingested independently of coffee because coffee may have several effects that offset the ergogenic effects of caffeine. The study found that caffeine enhanced endurance performance and produced the greatest initial increase in plasma epinephrine only when it was consumed without coffee (i.e. in capsule form with water). Caffeine ingested in the form of coffee resulted in similar plasma caffeine levels as caffeine capsules, but the epinephrine response was much smaller (50% smaller) and it did not enhance endurance performance. This suggests that the physiological responses of the body to caffeine may be blunted or moderated by components in coffee other than caffeine.
Pre-exercise glycogen stores
Carbohydrate-loading is a popular pre-meet nutritional plan for many athletes. Consequently, many studies have investigated how caffeine ingestion affects athletic performance in carbohydrate-loaded subjects. Weir at al. (1987) found that serum FFA concentrations in carbohydrate-loaded subjects who also ate a high-carbohydrate meal before exercising were the same whether they ingested caffeine or not. Furthermore, the respiratory exchange ratio, heart rate, respiratory rate, and oxygen consumption were also not influenced by caffeine ingestion in the carbo-loaded subjects. This study shows that the combination of carbo-loading and eating a high-carbohydrate pre-exercise meal may inhibit the effect of caffeine on lipid mobilization and glycogen sparing. This may occur as a result of the insulin response to carbo-loading and a high-carbohydrate meal, since insulin inhibits lipolysis and stimulates lipid storage. Therefore, if the beneficial effect of caffeine is due only to its effect on lipid mobilization, then ingesting caffeine in a carbohydrate-loaded state before a race may not be helpful. Laurent et al. (2000) also found that caffeine ingestion in glycogen-supercompensated subjects did not affect the rate of glycogen utilization or FFA levels compared to caffeine-free trials. However, they did find that caffeine significantly increased plasma epinephrine, cortisol and ß-endorphin concentrations. They suggest that caffeine may improve exercise performance by reducing the threshold for ß-endorphin release, thereby lowering pain perception. Graham and Spriet (1991) reported that even though caffeine significantly improved endurance performance, caffeine did not produce significant changes in plasma FFA levels or respiratory exchange ratios relative to caffeine-free trials during exercise in carbohydrate-loaded subjects. Graham and Spriet (1991) postulate that the improvement in endurance performance may have been due to the higher dose of caffeine used in this study and most likely occurred by a mechanism other than glycogen sparing.
Prior caffeine habituation
The amount of caffeine that is ingested on a daily basis can vary greatly from one person to the next. Some people regularly ingest very high levels of caffeine, while others may consume very little caffeine. A study by Van Soeren and Graham (1998) examined the effect of caffeine ingestion on exercise performance and metabolic parameters in habitual caffeine users following a period of caffeine withdrawal. They reported that caffeine resulted in significant increases in plasma epinephrine and increased time to exhaustion in all caffeine trials regardless of withdrawal from caffeine. Therefore, they suggest that the caffeine-mediated improvement in endurance performance is not reduced by prior caffeine habituation. In other words, caffeine increased endurance performance equally in subjects that regularly ingested caffeine and those that did not regularly ingest caffeine.
Intensity of exercise
While a large majority of the research has examined the ergogenic effects of caffeine on endurance exercise, several recent studies have investigated the potential ergogenic effects of caffeine on high-intensity, sprint performance (Anselme et al., 1992; Collomp et al., 1991; Jackman, Wendling, Friars & Graham, 1996; Greer, McLean & Graham, 1998; Paton, Hopkins & Vollebregt, 2001). Unfortunately, the research on this topic is controversial and inconclusive. Some studies report an improvement in high-intensity, sprint performance with caffeine (Anselme et al., 1992; Jackman et al., 1996), while others report no effect of caffeine (Collomp et al., 1991; Greer, McLean & Graham, 1998; Paton, Hopkins & Vollebregt, 2001). Improvements in maximal anaerobic power and increased blood lactate levels with caffeine were reported by Anselme et al. (1992), while increased time to exhaustion (4.12 min to 4.93 min), increased muscle lactate levels, and increased catecholamine levels were reported by Jackman et al. (1996). These studies suggest that the ergogenic effect of caffeine on high-intensity exercise may occur via mechanisms other than glycogen sparing. Potential mechanisms include the caffeine-mediated direct action on muscle cells or the central nervous system (CNS) and a possible caffeine-induced release of lactate from muscle cells to the blood, thus allowing muscle cells to continue functioning without becoming too acidic. On the other hand, several studies (Collomp et al. 1991; Greer, McLean & Graham, 1998; Paton, Hopkins & Vollebregt, 2001) reported no change in maximum anaerobic capacity or power and no change in the speed of repeated sprints with caffeine. These studies strongly contradict the previously mentioned studies and suggest that there is no enhancement of high-intensity, sprint performance with caffeine ingestion.
The research studies discussed in this course have investigated the effect of caffeine on athletic performance. However, if an athlete decides to consume caffeine, it is very important for them to understand the associated health risks.
Recommended Intakes, Normal Values and Toxicity:
Many people believe that the requirements for athletes involved in heavy training are higher than the requirements for the rest of the population. While this may be true, there is no scientific evidence to support this hypothesis, and most nutrition experts/professionals agree that to correct deficiencies and/or to maintain optimal body functioning, the nutrient requirements for athletes do not exceed 200% of the recommendations (DRI, RDA, ESADDI, or otherwise) already established.
There is no DRI, RDA, or ESADDI for caffeine.
Previously certain levels of caffeine were prohibited in competition. It was removed from the prohibited list in 2004 and placed on the monitoring list. It could be returned to the prohibited list in the future. Urinary caffeine levels can depend on the caffeine dose, bodyweight, body composition (fat content), rate of caffeine metabolism in the liver, the timeframe during which the caffeine was ingested, hydration, exercise time, and other individual variables.
The negative effects of acute caffeine ingestion include sleep disturbances, diuresis (which can lead to dehydration), unsteadiness, gastrointestinal distress, and possible increases in blood pressure. The negative effects of chronic caffeine ingestion include withdrawal headaches, heart palpitations, and increased serum cholesterol. While it is difficult to achieve a lethal dose of caffeine by consuming coffee, tea or caffeinated sodas, deaths through the use of caffeine tablets have been reported.
Contraindications of caffeine use—Systemic
The medical considerations/contraindications included have been selected on the basis of their potential clinical significance. Risk versus benefit should be considered when the following medical problems exist
• Anxiety disorders, including agoraphobia and panic attacks (increased risk of anxiety, nervousness, fear, nausea, palpitations, rapid heartbeat, restlessness, and trembling )
• Cardiac disease, severe (high doses not recommended because of increased risk of tachycardia or extrasystoles, which may lead to heart failure )
• Hepatic function impairment (half-life of caffeine may be prolonged, leading to toxic accumulation )
• Hypertension or Insomnia (may be potentiated)
• Seizure disorders, in neonates (caution is recommended because seizures have been reported following toxic doses )
• Sensitivity to caffeine or other xanthines
In summary, there are three basic mechanisms by which caffeine may enhance athletic performance:
1. By causing a shift in muscle substrate metabolism from carbohydrates to fats especially during the first 15 minutes of exercise when glycogenolysis is normally very high. This is basically stating that fat utilization for energy during moderate intensity exercise is increased after caffeine intake, particularly in the early stages of exercise, which also means that glycogenolysis (the breakdown of glycogen to glucose for energy) is spared early so that more glycogen is available for energy later in the training session.
2. By stimulating the central nervous system via altering neurotransmitter function or increasing the recruitment of motor units because of a decrease in the activation threshold of neurons. This may be a factor in the decrease in perceived exertion that many studies found. Essentially, by decreasing the activation threshold of neurons, the caffeine is allowing the body to do the same work, but with a decreased perception of intensity and difficulty, which can lead to greater work potential.
3. By a direct effect on skeletal muscle homeostasis (i.e. attenuation of the accumulation of potassium). Seeing as it has been established that the accumulation of potassium may be related to fatigue, attenuating (decreasing) the potassium accumulation may invariably lead to increased work load due to delayed fatigue.
However, the research on the ergogenic effects of caffeine remains inconclusive.
TRAINER'S NOTE:
The research presented above states in most simple terms that caffeine can be effective in exercise by using more fat for energy than carbohydrates (glycogen), particularly at the beginning of exercise when normally, glycogen is the body’s primary fuel source. Caffeine can also sustain higher levels of energy and work potential for a longer period of time because it stimulates the nervous system by essentially blocking or holding back the activation threshold of neurons, which is what leads to a perception of fatigue. Lastly, caffeine has shown to decrease potassium accumulation, which as it states above may be related to fatigue, therefore once again delaying the perception of exhaustion, and increasing work load potential.
For the most current information on the Recommended Dietary Allowances (RDAs) and Dietary Reference Intakes (DRIs) for all nutrients, please visit this section of the US Department of Agriculture's Food & Nutrition Information Center:
http://fnic.nal.usda.gov/nal_displa...&tax_subject=256&topic_id=1342&level3_id=5140
Alternatives:
Below is the caffeine content of some common drinks and foods:
1 Cup of coffee 90-150 mg
1 Cup of tea 30-70 mg
1 can of Cola 30-45 mg
1 regular Chocolate bar 30 mg
1 Cold relief tablet 30 mg
The following is a scientific analysis of caffeine and its usage in exercise and performance. The primary objective of this analysis is to further educate health, fitness, and performance professionals on the potential effectiveness of this dietary supplement in daily activity as well as athletic performance, and also to determine health risks associated with caffeine if any exist.
Overview:
Caffeine is commonly consumed by people, including athletes, for various performance and or fitness related reasons. The short-term effects of caffeine on endurance and sprint performance have been studied in-depth, however the results of these studies remain controversial and inconclusive. The effects of caffeine on the performance of an athlete can be mediated by several factors that should be carefully considered. There are risks associated with caffeine supplementation and there are dietary alternatives. There is no recommended daily intake for caffeine.
Description:
Caffeine is a crystal-like substance found in many beverages (coffee, tea, and cola), medications, and foods. Caffeine is quickly absorbed into the bloodstream and attains maximum values within 15 to 120 minutes of consumption. Through the blood, caffeine is spread to many tissues in the body, including the brain. Enzymes in the liver breakdown caffeine, leaving very little to be cleared in urine.
Caffeine has both central and peripheral effects in the body. In the central nervous system caffeine affects parts of the brain and the spinal cord, while in the periphery it affects organs and tissues. At low doses (2-10 mg/kg), it can cause increased alertness, less fatigue, reduced reaction time, increased ventilation, and poorer performance of some fine motor skills. At higher doses (>15 mg/kg), caffeine can cause nervousness, insomnia, headaches, and unsteadiness. Caffeine also has inconsistent effects on the cardiovascular system. Depending on where it acts in the body, caffeine can either raise or lower heart rate and cause blood vessels to constrict or dilate. Caffeine can cause a mild increase in urine output from the kidneys and dilation of the bronchi. Caffeine causes the release of epinephrine from the adrenal glands, which causes lipolysis (break down of fat) in muscle and adipose tissues. This increased mobilization of free fatty acids can lead to glycogen sparing early in the exercise period because the body uses relatively more free fatty acids for energy. Caffeine also directly acts on muscle cells by enhancing the release of calcium from the sarcoplasmic reticulum in muscles cells, which improves muscle contraction.
There are a variety of possible mechanisms by which caffeine is proposed to enhance athletic performance, many of which are mentioned above. The most researched and widely acknowledged mechanism is by glycogen sparing via increased fat utilization, thus allowing the athlete to exercise longer at a given suBathmateaximal intensity. Other mechanisms include increased catecholamine release, increased calcium release from muscle cells, and reduced perception of effort. On a cellular level, caffeine inhibits adenosine, causing increased urine excretion, stimulation of the central nervous system, increased lipolysis in fat cells (adipocytes) and increased gastric secretion. Increased lipolysis in fat cells occurs because caffeine reduces the inhibitory influence of adenosine on lipolysis, thus increasing lipolysis. These methods of enhanced athletic performance and other possible mechanisms are examined further throughout the course.
Review of the Research:
Research on the ergogenic effects of caffeine was advanced by several studies in the late 1970s (Costill, Dalasky & Fink, 1978; Ivy, Costill, Fink & Lower, 1979). The effects of caffeine on exercise performance are controversial, with some studies finding an enhancing effect and others finding no effect at all. In general, these and other studies show that a dose of caffeine ranging from 5 - 9 mg/kg bodyweight ingested 1 hour before suBathmateaximal exercise (75-85% VO2 max) produced significant increases (28%-156%) in exercise time to exhaustion. In other words, subjects exercised significantly longer at a given intensity in the caffeine trials than in the placebo trials. While it is widely agreed upon that caffeine increases time to exhaustion, several research studies have reported differing results and mechanisms for this increase in time to exhaustion. Reported effects of caffeine include increased plasma epinephrine at rest and during exercise, increased serum and plasma free fatty acid (FFA) concentration, an attenuated decrease in blood glucose levels during exercise, decreased muscle glycogenolysis (i.e. muscle glycogen breakdown) especially during the first 15 minutes of exercise, decreased perceived exertion during the exercise trial, lower respiratory exchange ratios, increased use of muscle triglycerides, and significantly higher plasma glycerol levels. Furthermore, one study examining total work output over a two hour period, instead of time to exhaustion at a given exercise intensity, found that caffeine ingestion increased work output on a cycle ergometer by 7.4% compared to the control trial (Ivy et al., 1979).
The increased fat mobilization and glycogen sparing theory for increased time to exhaustion is based on the idea that caffeine increases fat mobilization for fuel and decreases glycogenolysis early in the exercise period. These two process combined allow the athlete to perform longer at a given intensity because they have spared glycogen early on in the exercise session. A decrease in perceived exertion in the caffeine trials can be explained by the stimulating effect of caffeine. Caffeine increases the excitability of neurons by lowering their threshold, thus permitting increased recruitment of motor units and improved nerve transmission.
Most studies on the effects of caffeine on performance have examined its effects on suBathmateaximal continuous and intermittent endurance exercise on a treadmill or a cycle ergometer. Most of the studies using other exercise modalities examine time to exhaustion at a given intensity.
A study on the effects of caffeine ingestion (250 mg) on the performance of sprinters showed that caffeine improved the sprint performance of highly trained sprinters, but not untrained runners (Collomp et al., 1992). While caffeine increased maximal blood lactate concentrations in both trained and untrained sprinters, the trained subjects had significantly higher blood lactate levels after the sprint test than the untrained sprinters. The improved performance and greater blood lactate levels with caffeine ingestion in trained sprinters may reflect an increase in muscle glycogenolysis (the breakdown of glycogen to glucose) and buffering capacity of muscle. Furthermore, specific training may cause cellular adaptations, which are necessary to benefit from caffeine ingestion before sprint performance. Many studies have reported a glycogen sparing effect of caffeine during suBathmateaximal endurance exercise (Trice & Haymes, 1995; Spriet et al., 1992; Costill, Dalsky & Fink, 1978; Graham and Spriet, 1991; Graham and Spriet, 1995; Pasman, van Baak, Jeukendrup & de Haan, 1995). An increase in glycogenolysis with caffeine may appear to be contrary to these studies, however, caffeine has been shown to aid in calcium release, which then starts a cascade of events leading to catecholamine secretion.
Another study involving the effects of caffeine on swim performance showed that swimmers performed a 1,500m swim significantly faster with caffeine compared to without caffeine, while rating of perceived exertion was not significantly different (MacIntosh & Wright, 2005). In this study, caffeine ingestion (6 mg/kg bodyweight) 2 ½ hours before the swim trial also resulted in significantly lower pre-exercise plasma potassium levels and higher post-exercise blood glucose levels. Since a 1500m swim is usually performed in 18-25 minutes, it is unlikely that glycogen supplies would limit exercise capacity and therefore caffeine most likely exerts its ergogenic effect by mechanisms other than increased fat utilization. Since caffeine is known to enhance epinephrine release and catecholamines (i.e. epinephrine) stimulate gluconeogenesis (the conversion of amino acids to glucose), this may be the mechanism by which blood glucose was elevated post-exercise in the caffeine group. Lower pre-exercise plasma potassium levels are consistent with other studies showing that caffeine attenuates the exercise-related increase in plasma potassium. Since the accumulation of potassium may be related to fatigue, a lower starting point for plasma potassium may allow exercise at a higher intensity for a given distance before reaching the critical level of plasma potassium that causes fatigue. This suggests that electrolyte balance (potassium) and glucose availability may be important aspects of the performance enhancement effects of caffeine in this study.
While several of the above studies found similar effects of caffeine on exercise performance (increased time to exhaustion, increased plasma epinephrine, increased FFA concentration, decreased muscle glycogenolysis early in the exercise trial, etc.), several of the studies found results that are not in agreement with the above findings. These findings include no effect of caffeine on plasma FFA levels or respiratory exchange ratio, and no differences in oxygen consumption or heart rate between caffeine and placebo trials. It is interesting to note that a gender difference in the effects of caffeine on athletic performance was not discussed in the research studies used for this course.
It is important to note that research on the effects of caffeine on performance may be influenced by a number of factors: 1) dose, 2) time of caffeine ingestion before exercise, 3) form of caffeine, 4) pre-exercise glycogen stores, 5) prior caffeine habituation, and 6) intensity of exercise. Some of these factors or variables may be responsible for the conflicting results found in this area of research.
Dose-response effect of caffeine
Studies on the ergogenic effects of varying doses of caffeine on athletic performance were performed with doses ranging from 3 – 13 mg/kg (Kovacs, Stegen & Brouns, 1998; Pasman et al., 1995; Bruce et al., 2000; Graham & Spriet, 1995). These studies found that endurance performance (time to exhaustion), work output, and mean power improved significantly when caffeine was ingested in varying doses compared to a placebo. While caffeine enhanced endurance performance, most studies reported no dose-response of caffeine on time to exhaustion (i.e. lower doses were equally as effective in increasing time to exhaustion as moderate and high doses of caffeine). However, not all of the studies found similar results. For example, Kovacs, Stegen and Brouns (1998) reported a slightly greater improvement in performance with moderate (225 mg/l) compared to lower (150 mg/l) levels of caffeine. Furthermore, most studies reported that plasma FFA concentration increased equally or greater with increasing doses of caffeine, especially in the first 15 minutes of exercise. Graham and Spriet (1995) reported that the highest doses of caffeine (greater than 9 mg/kg bodyweight) had a greater effect on plasma epinephrine levels and plasma metabolites (free fatty acids and glycerol) compared to lower doses, but these doses had the same or less of an effect on endurance performance as lower doses.
Time of caffeine ingestion before exercise
Most studies use a standard time interval of 60 minutes between time of caffeine or placebo ingestion and the start of the exercise trial. However, in a study by Weir, Noakes, Myburgh, and Adams (1987), serum free fatty acid levels actually peaked 3-4 hours after caffeine ingestion. If the mechanism by which caffeine enhances endurance performance depends on FFA utilization, this data shows that exercise should start at 3-4 hours post caffeine consumption instead of 1 hour. However, more research needs to be done in this area in order to more accurately determine when exercise should commence after ingesting caffeine in order to produce the greatest benefit.
Forms of caffeine
Many people consume caffeine on a daily basis in coffee, hot chocolate, caffeinated sodas, and many other drinks and foods. However, a large portion of the research studies on the ergogenic effects of caffeine involve using caffeine in a capsule or powder form in water, decaffeinated coffee or a glucose solution. A study by Graham, Hibbert, and Sathasivam (2002) examined whether caffeine administered independently of coffee would result in larger improvements in endurance performance. It was hypothesized that caffeine would exert the largest effect when ingested independently of coffee because coffee may have several effects that offset the ergogenic effects of caffeine. The study found that caffeine enhanced endurance performance and produced the greatest initial increase in plasma epinephrine only when it was consumed without coffee (i.e. in capsule form with water). Caffeine ingested in the form of coffee resulted in similar plasma caffeine levels as caffeine capsules, but the epinephrine response was much smaller (50% smaller) and it did not enhance endurance performance. This suggests that the physiological responses of the body to caffeine may be blunted or moderated by components in coffee other than caffeine.
Pre-exercise glycogen stores
Carbohydrate-loading is a popular pre-meet nutritional plan for many athletes. Consequently, many studies have investigated how caffeine ingestion affects athletic performance in carbohydrate-loaded subjects. Weir at al. (1987) found that serum FFA concentrations in carbohydrate-loaded subjects who also ate a high-carbohydrate meal before exercising were the same whether they ingested caffeine or not. Furthermore, the respiratory exchange ratio, heart rate, respiratory rate, and oxygen consumption were also not influenced by caffeine ingestion in the carbo-loaded subjects. This study shows that the combination of carbo-loading and eating a high-carbohydrate pre-exercise meal may inhibit the effect of caffeine on lipid mobilization and glycogen sparing. This may occur as a result of the insulin response to carbo-loading and a high-carbohydrate meal, since insulin inhibits lipolysis and stimulates lipid storage. Therefore, if the beneficial effect of caffeine is due only to its effect on lipid mobilization, then ingesting caffeine in a carbohydrate-loaded state before a race may not be helpful. Laurent et al. (2000) also found that caffeine ingestion in glycogen-supercompensated subjects did not affect the rate of glycogen utilization or FFA levels compared to caffeine-free trials. However, they did find that caffeine significantly increased plasma epinephrine, cortisol and ß-endorphin concentrations. They suggest that caffeine may improve exercise performance by reducing the threshold for ß-endorphin release, thereby lowering pain perception. Graham and Spriet (1991) reported that even though caffeine significantly improved endurance performance, caffeine did not produce significant changes in plasma FFA levels or respiratory exchange ratios relative to caffeine-free trials during exercise in carbohydrate-loaded subjects. Graham and Spriet (1991) postulate that the improvement in endurance performance may have been due to the higher dose of caffeine used in this study and most likely occurred by a mechanism other than glycogen sparing.
Prior caffeine habituation
The amount of caffeine that is ingested on a daily basis can vary greatly from one person to the next. Some people regularly ingest very high levels of caffeine, while others may consume very little caffeine. A study by Van Soeren and Graham (1998) examined the effect of caffeine ingestion on exercise performance and metabolic parameters in habitual caffeine users following a period of caffeine withdrawal. They reported that caffeine resulted in significant increases in plasma epinephrine and increased time to exhaustion in all caffeine trials regardless of withdrawal from caffeine. Therefore, they suggest that the caffeine-mediated improvement in endurance performance is not reduced by prior caffeine habituation. In other words, caffeine increased endurance performance equally in subjects that regularly ingested caffeine and those that did not regularly ingest caffeine.
Intensity of exercise
While a large majority of the research has examined the ergogenic effects of caffeine on endurance exercise, several recent studies have investigated the potential ergogenic effects of caffeine on high-intensity, sprint performance (Anselme et al., 1992; Collomp et al., 1991; Jackman, Wendling, Friars & Graham, 1996; Greer, McLean & Graham, 1998; Paton, Hopkins & Vollebregt, 2001). Unfortunately, the research on this topic is controversial and inconclusive. Some studies report an improvement in high-intensity, sprint performance with caffeine (Anselme et al., 1992; Jackman et al., 1996), while others report no effect of caffeine (Collomp et al., 1991; Greer, McLean & Graham, 1998; Paton, Hopkins & Vollebregt, 2001). Improvements in maximal anaerobic power and increased blood lactate levels with caffeine were reported by Anselme et al. (1992), while increased time to exhaustion (4.12 min to 4.93 min), increased muscle lactate levels, and increased catecholamine levels were reported by Jackman et al. (1996). These studies suggest that the ergogenic effect of caffeine on high-intensity exercise may occur via mechanisms other than glycogen sparing. Potential mechanisms include the caffeine-mediated direct action on muscle cells or the central nervous system (CNS) and a possible caffeine-induced release of lactate from muscle cells to the blood, thus allowing muscle cells to continue functioning without becoming too acidic. On the other hand, several studies (Collomp et al. 1991; Greer, McLean & Graham, 1998; Paton, Hopkins & Vollebregt, 2001) reported no change in maximum anaerobic capacity or power and no change in the speed of repeated sprints with caffeine. These studies strongly contradict the previously mentioned studies and suggest that there is no enhancement of high-intensity, sprint performance with caffeine ingestion.
The research studies discussed in this course have investigated the effect of caffeine on athletic performance. However, if an athlete decides to consume caffeine, it is very important for them to understand the associated health risks.
Recommended Intakes, Normal Values and Toxicity:
Many people believe that the requirements for athletes involved in heavy training are higher than the requirements for the rest of the population. While this may be true, there is no scientific evidence to support this hypothesis, and most nutrition experts/professionals agree that to correct deficiencies and/or to maintain optimal body functioning, the nutrient requirements for athletes do not exceed 200% of the recommendations (DRI, RDA, ESADDI, or otherwise) already established.
There is no DRI, RDA, or ESADDI for caffeine.
Previously certain levels of caffeine were prohibited in competition. It was removed from the prohibited list in 2004 and placed on the monitoring list. It could be returned to the prohibited list in the future. Urinary caffeine levels can depend on the caffeine dose, bodyweight, body composition (fat content), rate of caffeine metabolism in the liver, the timeframe during which the caffeine was ingested, hydration, exercise time, and other individual variables.
The negative effects of acute caffeine ingestion include sleep disturbances, diuresis (which can lead to dehydration), unsteadiness, gastrointestinal distress, and possible increases in blood pressure. The negative effects of chronic caffeine ingestion include withdrawal headaches, heart palpitations, and increased serum cholesterol. While it is difficult to achieve a lethal dose of caffeine by consuming coffee, tea or caffeinated sodas, deaths through the use of caffeine tablets have been reported.
Contraindications of caffeine use—Systemic
The medical considerations/contraindications included have been selected on the basis of their potential clinical significance. Risk versus benefit should be considered when the following medical problems exist
• Anxiety disorders, including agoraphobia and panic attacks (increased risk of anxiety, nervousness, fear, nausea, palpitations, rapid heartbeat, restlessness, and trembling )
• Cardiac disease, severe (high doses not recommended because of increased risk of tachycardia or extrasystoles, which may lead to heart failure )
• Hepatic function impairment (half-life of caffeine may be prolonged, leading to toxic accumulation )
• Hypertension or Insomnia (may be potentiated)
• Seizure disorders, in neonates (caution is recommended because seizures have been reported following toxic doses )
• Sensitivity to caffeine or other xanthines
In summary, there are three basic mechanisms by which caffeine may enhance athletic performance:
1. By causing a shift in muscle substrate metabolism from carbohydrates to fats especially during the first 15 minutes of exercise when glycogenolysis is normally very high. This is basically stating that fat utilization for energy during moderate intensity exercise is increased after caffeine intake, particularly in the early stages of exercise, which also means that glycogenolysis (the breakdown of glycogen to glucose for energy) is spared early so that more glycogen is available for energy later in the training session.
2. By stimulating the central nervous system via altering neurotransmitter function or increasing the recruitment of motor units because of a decrease in the activation threshold of neurons. This may be a factor in the decrease in perceived exertion that many studies found. Essentially, by decreasing the activation threshold of neurons, the caffeine is allowing the body to do the same work, but with a decreased perception of intensity and difficulty, which can lead to greater work potential.
3. By a direct effect on skeletal muscle homeostasis (i.e. attenuation of the accumulation of potassium). Seeing as it has been established that the accumulation of potassium may be related to fatigue, attenuating (decreasing) the potassium accumulation may invariably lead to increased work load due to delayed fatigue.
However, the research on the ergogenic effects of caffeine remains inconclusive.
TRAINER'S NOTE:
The research presented above states in most simple terms that caffeine can be effective in exercise by using more fat for energy than carbohydrates (glycogen), particularly at the beginning of exercise when normally, glycogen is the body’s primary fuel source. Caffeine can also sustain higher levels of energy and work potential for a longer period of time because it stimulates the nervous system by essentially blocking or holding back the activation threshold of neurons, which is what leads to a perception of fatigue. Lastly, caffeine has shown to decrease potassium accumulation, which as it states above may be related to fatigue, therefore once again delaying the perception of exhaustion, and increasing work load potential.
For the most current information on the Recommended Dietary Allowances (RDAs) and Dietary Reference Intakes (DRIs) for all nutrients, please visit this section of the US Department of Agriculture's Food & Nutrition Information Center:
http://fnic.nal.usda.gov/nal_displa...&tax_subject=256&topic_id=1342&level3_id=5140
Alternatives:
Below is the caffeine content of some common drinks and foods:
1 Cup of coffee 90-150 mg
1 Cup of tea 30-70 mg
1 can of Cola 30-45 mg
1 regular Chocolate bar 30 mg
1 Cold relief tablet 30 mg
