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Legal Nutritional Boosting for Cycling

Jeukendrup, Asker; Tipton, Kevin D.

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Current Sports Medicine Reports: July 2009 - Volume 8 - Issue 4 - p 186-191
doi: 10.1249/JSR.0b013e3181ae9950
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Cycling events range from short, high-intensity workouts, lasting no more than a minute, to multi-day stage races where cyclists may spend 6 h or more per day on their bikes (23,26). The causes of fatigue and the factors determining optimal performance are quite different in these events. For sprint events on the track, muscle mass and peak power output are important whereas on the road maximal sustainable power output is a major determinant (23,26). In multi-day stage races, apart from maximal sustainable power output, the ability to recover is a major factor. Depending upon the discipline and the actual causes of fatigue, different nutritional strategies may be used to enhance performance (or at least prevent a decline in performance). Here we will review the evidence for a number of common nutritional strategies that have been employed by cyclists. There will be a focus upon strategies with strong evidence or where there is currently a lot of controversy. Only nutritional strategies that have seen significant developments in the last 5 yr will be discussed in more detail.


A great deal of recent attention has focused upon a potential new strategy to improve adaptations to endurance training. The technique is often referred to as Train-Low-Compete-High, where the high and low refers to glycogen in analogy to the altitude training strategy Live-High-Train-Low. In the late '60s, carbo-loading strategies were developed by scientists and applied by endurance athletes. A belief developed that training had to be performed in a glycogen-repleted state to maintain the quality of training and thereby optimize the adaptations to the training.

The background to the potential benefits of training with low glycogen stems from observations that a single bout of endurance exercise will increase translation transcription and/or mRNA content for various metabolic and stress-related genes. Typically, transcriptional activity peaks within the first few hours of recovery, returning to baseline within 24 h. These findings have led to the overall hypothesis that training adaptations in skeletal muscle may be generated by the cumulative effects of transient increases in gene transcription or translation during recovery from repeated bouts of exercise.

It is interesting to note that there are a number of studies reporting that altering substrate availability during exercise (e.g., by increasing dietary fat intake or commencing exercise with low muscle glycogen) can influence metabolic gene transcription, suggesting that modification of the training response may be possible via specific diet interventions. It has been shown that commencing endurance exercise with low muscle glycogen increases the activity of several metabolic genes and signaling proteins. In a study by Pilegaard et al. (35), six untrained male volunteers performed 2.5 h of cycling at 45% V˙O2max. One day prior to the experiment, subjects performed 90 min of one-legged cycling to reduce the muscle glycogen content in that leg. On the day of the experiment, muscle biopsies were taken from both legs at rest, post-exercise, and 2 and 5 h postexercise. Compared with the control leg, resting preexercise muscle glycogen content was 45% lower in the leg that had exercised the previous day. After 2.5 h of cycling at 45% V˙O2max, it was found that transcriptional activity of pyruvate dehydrogenase kinase 4 (PDK4), uncoupling protein 3 (UCP3), and hexokinase II (HKII) was significantly higher in the leg that had exercised with low muscle glycogen. Because both the control leg and the low glycogen leg were exposed to the same systemic concentrations of metabolites, hormones, catecholamines, and cytokines, it is reasonable to assume that increased transcriptional activity was in some way directly related to low muscle glycogen content.

The role of muscle glycogen could be explained by the fact that some signaling proteins (e.g., AMPK) possess glycogen binding domains, and when glycogen is low, these proteins are more active toward their specific targets. In support of this, Wojtaszewski et al. (43) reported that AMPK activity was elevated when a standardized bout of exercise (1 h of cycling at 70% V˙O2max) was undertaken with low muscle glycogen (160 compared with 900 mmol·kg−1 d.m.). Elevated AMPK activity with low muscle glycogen may be beneficial to individuals undertaking exercise training as AMPK is believed to play a critical role in regulating the adaptive response. Commencing endurance exercise with low muscle glycogen also has been shown to increase the activity of p38 mitogen-activated protein kinase (p38 MAPK), and like AMPK, p38 MAPK is thought to be a regulator of mitochondrial biogenesis and endurance training adaptations.

The previously mentioned studies provide early evidence to suggest that training with low muscle glycogen might be a useful strategy to promote endurance training adaptations. However, further studies clearly are needed before this can be confirmed or dismissed.

Only one study has determined whether long-term training with low muscle glycogen can enhance the adaptive response to endurance training. Hansen et al. (11) recruited seven untrained males to undertake a 10-wk program of knee extensor exercise. Each of the subjects' legs was trained according to a different schedule, but the total amount of work performed by each leg was kept the same. One leg was trained twice a day every other day, whereas the other leg trained once daily. This meant that the leg that trained twice daily commenced half of the sessions with low muscle glycogen. Compared with the leg that trained with normal glycogen levels, the leg that commenced half of the training sessions with low muscle glycogen had more pronounced increases in resting muscle glycogen content and citrate synthase activity. Time to fatigue at 90% maximal power output increased in both legs after training. However, performance times were nearly twice as long in the leg that trained with low muscle glycogen (19.7 ± 2.4 vs 11.9 ± 1.3 min). These remarkable findings demonstrate that, under the specific conditions of the study, training with low muscle glycogen enhanced adaptations in skeletal muscle and improved exercise capacity. However, a number of details make it difficult to extrapolate these findings. First, the subjects recruited were untrained, and it is not yet known whether training with low muscle glycogen will translate into improved adaptations in already well-trained athletes. Second, subjects performed a fixed amount of work even though higher glycogen stores normally would allow for exercise to be performed at higher intensities and/or longer durations. Third, it is difficult to translate the results from single leg kicking exercise to that of real life sporting situations involving activities such as running, cycling, or swimming.

To take these findings to a more realistic sporting situation, researchers in Melbourne (Australia) and Birmingham (UK) investigated the effects of a 3-wk training program where all of the training was performed in the glycogen-loaded state or where half of the training was performed in a glycogen-depleted state (45). The performance during the self-paced training sessions in the glycogen-depleted state was impaired significantly. The subjects who trained always glycogen-loaded trained at higher absolute intensities. However, despite this, at the end of the training period, performance was improved equally in the low and high glycogen groups. Despite similarly enhanced performance, the metabolic adaptations between the two groups were very different. The low glycogen group did have a greater oxidative capacity, as evidenced by greater citrate synthase (TCA cycle enzyme) and β-hydroxyacyl dehydrogenase (rate limiting enzyme of β-oxidation) activities and greater COX IV content. Fat oxidation also was enhanced in the low glycogen group. So these findings partly confirm the findings of the single leg study by Hansen et al. (11). The difference is that even though adaptations were observed in metabolism, there were no differences in performance after 3 wk. It is of course possible that 3 wk is sufficient to see differences in metabolism but not quite long enough to see improvements in performance, and future studies should investigate longer training protocols.

It seems reasonable to conclude that endurance training in a glycogen-depleted state results in an improved capacity to use fat to fuel exercise. The mechanisms behind this are unclear but may involve activation of the peroxisome proliferator-activated receptors (PPAR). The PPAR are a group of nuclear receptor proteins that function as transcription factors regulating the expression of genes. PPAR play an essential role in the regulation of metabolism as well as many other processes.

Narkar et al. (33) recently showed that training rats on a treadmill, while at the same time giving them a drug that activated a transcription factor called PPAR∂, resulted in the same changes that occur when training in the glycogen-depleted state - namely increased capacity to use fat as a fuel. PPAR∂ seems to be activated by a byproduct of the breakdown of fat in muscle and increases the concentration of the enzymes that are required for oxidizing fatty acids (FA). The rats that got the drug and trained on the treadmill increased their ability to run at approximately 50% V˙O2max by 70% over those that ran on the treadmill, only. It is possible that exercising in a glycogen-depleted state activates PPAR∂ to a greater extent than training in the glycogen-loaded state. As discussed previously, a person exercising in the glycogen-depleted state increases circulating FA concentration and the oxidation of fat during exercise this result in more of the byproducts and more PPAR∂ activation.


It has been known for a long time that carbohydrate feeding can improve endurance cycling performance. Performance in events lasting 2 h or longer usually is improved when carbohydrate is ingested during exercise (20,22,25). More recently, it also was demonstrated that carbohydrate can improve exercise performance during time trials (∼40 km) that last approximately 1 h (21). This fact is interesting because carbohydrate availability is not thought to be limiting during these events. In fact, the same improvements were seen when subjects rinsed their mouths without ingesting the carbohydrate solution (4). However, no effects upon performance were seen when glucose was infused at relatively high rates (5). The current thinking is that carbohydrate works via a central mechanism having an effect upon the brain after binding to carbohydrate receptors in the oral cavity or intestinal tract (4,5). At the Olympic Games in Beijing, track athletes were seen rinsing their mouths with a carbohydrate drink, and some athletes were sucking on lollypops before their events. It is interesting to note that when the exercise duration is shorter and the intensity higher (16-20 km time trials), there may be no effect of the ingested carbohydrate (24). This lack of effect is likely because other factors overrule the possible central effects of carbohydrate. We will now focus upon the longer-distance events where carbohydrate availability is a limiting factor.

The Search for the Optimal Carbohydrate

To determine the most effective type of carbohydrate, studies have compared the oxidation rates of various types of carbohydrate to the oxidation of ingested glucose during exercise (20,22,25). The results of a relatively large number of studies can be summarized quite easily: there are carbohydrates that are oxidized at high rates (up to approximately 1 g·min−11) and carbohydrates that are oxidized at lower rates. Glucose is oxidized at relatively high rates, whereas the other two monosaccharides, fructose and galactose, are oxidized at much lower rates because they have to be converted into glucose in the liver before they can be metabolized. The oxidation rates of maltose, sucrose, and glucose polymers (maltodextrins) and even high molecular weight glucose polymers with a relatively large amount of amylopectin are comparable to glucose.

It has been suggested that by feeding a single carbohydrate source (e.g., glucose, fructose, or maltodextrins) at high rates, the specific transporter proteins that aid absorption of that carbohydrate from the intestine become saturated. Once these transporters are saturated, feeding more of that carbohydrate will not result in greater intestinal absorption and increased oxidation rates. In 1995, Shi et al. (39) suggested that the ingestion of carbohydrates that use different transporters might increase total carbohydrate absorption. Subsequently, a series of studies was conducted at the University of Birmingham in the United Kingdom using different combinations of carbohydrates to determine their effects upon exogenous carbohydrate oxidation during exercise. In the first study, subjects ingested a drink containing glucose and fructose (16). Glucose was ingested at a rate of 1.2 g·min−1 and fructose at a rate of 0.6 g·min−1. In the control trials, the subjects ingested glucose at a rate of 1.2 g·min−1 and 1.8 g·min−1 (matching glucose intake or energy intake). It was found that the ingestion of glucose at a rate of 1.2 g·min−1 resulted in oxidation rates of about 0.8 g·min−1. Ingesting glucose at 1.8 g·min−1 did not increase the oxidation rate. However, after ingesting glucose plus fructose, the rate of total exogenous carbohydrate oxidation increased to 1.23 g·min−1, an increase in oxidation of 45% compared with a similar amount of glucose. In subsequent studies, different combinations and amounts of carbohydrates were evaluated in an attempt to determine the maximal rate of oxidation of mixtures of exogenous carbohydrates (15,17-19,28,42). Very high oxidation rates were observed with combinations of glucose plus fructose, with maltodextrins plus fructose, and with glucose plus sucrose plus fructose. The highest rates were observed with a mixture of glucose and fructose ingested at a rate of 2.4 g·min−1. With this feeding regimen, exogenous carbohydrate oxidation peaked at 1.75 g·min−1. This is 75% greater than what was previously thought to be the absolute maximum. It must be noted that these rates of carbohydrate ingestion are very high and are much higher than current practice by athletes. The results of these studies are summarized in the Figure.

Graphical depiction of exogenous carbohydrate from glucose and glucose:fructose mixtures at varying intake rates. Graph is based upon various studies (15,17-19,28,42) summarized in (20). It can be seen that with increasing intake, the oxidation from glucose plateaus, whereas the oxidation of glucose:fructose continues to increase.

In subsequent studies, more practical but still quite large amounts of carbohydrate were ingested by the subjects (1.5 g·min1) and it was observed that the subjects' ratings of perceived exertion (RPE) tended to be lower with the mixture of glucose and fructose compared with glucose alone (28). More recently it was demonstrated that a glucose and fructose blend of carbohydrate can improve performance significantly more than a glucose only drink (8). In that study subjects performed 2 h of steady-state exercise followed by a time trial that lasted approximately 60 min. Glucose ingestion improved time trial performance by 11%. Glucose and fructose ingestion improved performance by another 8% (19% faster compared with placebo).

The term oxidation efficiency was introduced to describe the percentage of the ingested carbohydrate that is oxidized (25). High oxidation efficiency means that smaller amounts of carbohydrate remain in the gastrointestinal tract, reducing the risk of causing gastrointestinal discomfort that frequently is reported during prolonged exercise. Therefore, compared with a single source of carbohydrate, ingesting multiple carbohydrate sources results in a smaller amount of carbohydrate remaining in the intestine, and osmotic shifts and malabsorption may be reduced. Reduction of malabsorption probably means that drinks with multiple transportable carbohydrates are less likely to cause gastrointestinal discomfort. It is interesting to note that this has been a consistent finding in studies that have attempted to evaluate gastrointestinal discomfort during exercise (20). Subjects tended to feel less bloated with the glucose plus fructose drinks compared with drinking glucose-only solutions. A further advantage of the carbohydrate blend (glucose plus fructose) is that gastric emptying and fluid delivery seem to be improved compared with glucose only (27).


The excitement of protein added to carbohydrate drinks stems from a small number of studies that suggest that adding a small amount of protein (∼2% whey protein or approximately 20 g·L−11) to a carbohydrate drink produced improvements in endurance capacity compared with a carbohydrate drink alone (14,36,37). It has been speculated that increased endurance capacity with CHO + protein may be caused by increased protein oxidation when muscle glycogen is depleted (29) or as a result of attenuations in central fatigue (3). Neither of these explanations seems very plausible, and evidence for these mechanisms to be involved is lacking. The few studies that report positive effects also have been criticized, and others have not been able to show any performance effects. In fact, no study using time-trial time as the measure of performance has reported increased performance with additional protein. For example, in a study by van Essen et al. (41), athletes performed an 80-km cycling time trial on three occasions and drank either a 6% carbohydrate blend, a 6% carbohydrate + 2% whey-protein blend, or a sweetened placebo. All of the subjects consumed the solutions at a rate of 1 L·h−1. It was found that the average performance time was identical for the CHO and CHO + protein trials (roughly 135 min) and both were significantly faster (by approximately 4%) than the placebo trial (141 min). This study demonstrated that when athletes ingest a carbohydrate during exercise at a rate considered optimal for CHO delivery, protein provides no additional performance benefit during an event that simulates real-life competition. Therefore at present there is no reason to advise athletes to ingest protein during endurance exercise.


Caffeine has been used for a long time as a performance-enhancing substance. Although it is present in our daily diet, it also is regarded as a drug. Therefore caffeine falls within a grey category of substances that are sometimes treated as drugs and sometimes as nutrition. This confusion is illustrated by the fact that caffeine has been on and off the list of banned substances. However, because it is so abundant in our diet, and only small doses of caffeine are needed to see an ergogenic effect, it is difficult to control.

The evidence for its ergogenic properties is convincing. Although not all studies show effects of caffeine upon endurance performance, a large number of well-conducted studies have shown improved endurance capacity after ingesting caffeine at a dose of 3-9 mg·kg−1 b.w. (6,10,34,40). More recently, studies have used smaller doses of caffeine (as little as 1-3.2 mg·kg−1 b.w.) and still observed the positive effects upon performance (7,30). At exercise intensities around 85% V˙O2max, improvements of 10% to 20% typically are found in time to exhaustion. A recent metaanalysis of published studies on caffeine and exercise performance (9) suggests that the magnitude of the performance-enhancing effect increases as the duration of exercise increases. In most of these studies, caffeine also decreased perceived ratings of exertion.

The improvement in performance originally was explained by the increased availability of plasma fatty acids, which supposedly resulted in a suppression of carbohydrate metabolism and consequently to a decrease in glycogen use. However, a number of studies did see performance improvements without changes in the rate of fat oxidation, and it is highly unlikely that this is the mechanism behind the observed effects. It has become very clear in recent years that the effects of caffeine are caused by its stimulant properties.

It seems that the main factor limiting the oxidation of carbohydrate from a drink is the absorption. In a recent study it was suggested that caffeine might increase glucose absorption. This result led to the idea that caffeine added to a carbohydrate drink not only might increase absorption but also may lead to greater delivery of carbohydrate to the muscle and higher exogenous carbohydrate oxidation rates. Yeo et al. (44) tested this hypothesis and found that exogenous carbohydrate oxidation was increased by 17% when relatively large amounts of caffeine were added. So caffeine not only may have a direct effect upon exercise performance, it also may aid the absorption and oxidation of carbohydrates. The exact dose of carbohydrate and caffeine required is still unclear because a follow-up study with a low dose of caffeine did not find a significant increase (13).

Caffeine use has side effects. Individuals who normally avoid caffeine may experience gastrointestinal distress, headaches, tachycardia, restlessness, irritability, tremor, elevated blood pressure, psychomotor agitations, and premature left ventricular contractions, all caused by the effect of caffeine upon the central nervous system. It often is stated that caffeine is a diuretic and, therefore, should not be consumed in the hours before exercise when hydration is required. However, recent studies have demonstrated that moderate intakes of caffeine do not affect urine losses or hydration status (1,2). Very high intakes of caffeine have been associated with peptic ulcer, seizures, coma, and even death.


Sodium bicarbonate, sodium citrate, and other alkalinizers may help to buffer some of the lactic acid that is produced during very high-intensity exercise. Especially in track cycling, this could have some benefits, although this has not been tested directly. Various studies suggest that a minimal dose of bicarbonate ingestion is needed to improve performance, and there is a dose-response relationship between the amount of bicarbonate ingested and the observed performance effect (12,31). A dose of 200 mg·kg−1 b.w. ingested 1-2 h before exercise seems to improve performance in most studies, whereas 300 mg·kg−1 b.w. seems to be the optimum dose (with tolerable side effects for most athletes). Doses of less than 100 mg·kg−1 b.w. do not affect performance. Intakes greater than 300 mg·kg−1 b.w. tend to result in gastrointestinal problems (bloating, abdominal discomfort, and diarrhea). Bicarbonate seems to be effective during maximal exercise lasting approximately between 1 and 7 min. However, a study by McNaughton et al. (32) showed improved performance in a 1-h time trial, which was accompanied by a higher blood pH throughout the exercise. In another study, these findings were not confirmed (38).

The side effects of sodium bicarbonate intake in such large doses can be quite severe. At doses of 300 mg·kg−1 b.w., many athletes experience diarrhea, gastrointestinal discomfort, bloating, and cramps 1 h after loading. These side effects are dose dependent and have a high prevalence. The main cause of these problems is the large amount of sodium that is ingested with the bicarbonate and the reaction of bicarbonate with the HCl in the stomach, which generates a large volume of CO2 that distends the stomach wall. Drinking large amounts of water during the loading is likely to alleviate some of the problems.


Many supplements have been claimed to improve endurance performance or recovery. However, very little evidence exists that any of these supplements actually work. Some of the strategies discussed here have been proven to be effective. Strategies that are not discussed here lack evidence to conclude confidently that they would result in a beneficial effect upon cycling performance. In all situations the possible ergogenic effect should be balanced against the possible negative effects: high costs of a supplement, negative (ergolytic) effects, adverse health effects, or positive drugs test. Evidence should be collected on both sides of the equation, and only when the possible benefits outweigh the possible negative effects should a decision be made in favor of the supplement.


The most promising, relatively new nutritional strategy to improve endurance performance is the ingestion of relatively large amounts of multiple transportable carbohydrates during exercise. Although much is written about ingesting protein with carbohydrate during exercise, the evidence is equivocal, at best. There also has been much interest in training with low glycogen to maximize training adaptations, but the longer-term effects upon performance are still unclear, and more research is needed. Various supplements have been suggested to improve endurance performance, but most of these nutrition supplements lack the scientific support that would warrant the recommendation.


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