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Nutrition and Performance in Sport

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Christophe Hausswirth

Chapter 1. Nutrition: from training to competition

Topic 3. Nutrition and the brain

Romain Meeusen et Bart Roelands

Résumé

The brain and body are constantly exchanging to ensure that the former receives information on the energy status and metabolic requirements of the latter. Most nutrients influence the brain’s metabolic signal pathways. The constant interaction between the peripheral nervous system and the brain is controlled by the somatic, autonomic and neurohumoral pathways which are involved in the contribution, expenditure and storage of energy reserves. Brain cells are sensitive and responsive not only to fluctuations in blood sugar concentration, but also to metabolites that provide information on the body’s metabolic status. The constant interaction between the peripheral system and the brain is also present during prolonged exercise. In this context, disruptions to the supply of neurotransmitter precursors might be responsible for the occurrence of fatigue. The “central fatigue” theory is mainly based on an increase in the concentration of the neurotransmitter serotonin (5-HT). According to the scientific literature, physical performance would be little influenced, if at all, by the intake of tryptophan (TRP) or branched chain amino acid (BCAA) substrates. In contrast, the beneficial effect of carbohydrate intake during prolonged exercise is unquestionable and could be related to the increase (or maintaining of) the supply of substrates to the brain. Numerous studies indicate that hypoglycemia affects brain function and cognitive performance. The positive effect of glucose intake on athletic performance is clearly illustrated by several investigations using a carbohydrate mouth rinse compared to a placebo. Studies have clearly shown an improvement in performance even when the carbohydrate drink was not ingested. Interestingly, research has shown that a mouth rince activates multiple areas of the brain involved in the control of reward, emotion and motor output.

Texte intégral

1. Introduction

1Our human ancestors had to survive in very severe environment so that those most likely to reach reproductive age must have had a regulatory system that was efficient in procuring and metabolizing energy. The so-called “thrifty” genes were, and are still, involved in many aspects of this regulatory system, from a discerning perception of nutrients in the environment to an efficient transformation of calories into muscle work and body heat. These “intelligent” genes are thus not only controlling metabolic functions, but also cognitive and other roles of the central nervous system. At a given time in evolution, large portions of the nervous system have been dedicated to survival mechanisms such as procuring food. These metabolic signals will modulate brain circuits involved in finding food and its reward value.

2In this paper we will briefly explain how these signaling molecules will influence energy balance, explore how neurotransmitters, which have amino acid precursors, are involved in “central fatigue”, and how manipulation of these neurotransmitters can influence performance. The link between the positive incentive of food intake, and reward mechanisms that can be manipulated during prolonged exercise will be explained.

2. Energy balance and signaling from and to the brain

3Thinking about food can modulate neural activity in specific brain areas known to be involved in the cognitive controls of appetitive behaviors. This leads to saliva production, gastric acid, and insulin secretion (Berthoud, 2007). When food is encountered, smell and taste act as additional stimuli to recall memorial representations of experiences with particular food items. These memorial representations can be pleasant or unpleasant (e.g. conditioned food/taste aversion). Food intake regulation can be triggered by a period of fasting, and signals generated in proportion to body fat stores act in the brain to reduce food intake. Thus, when weight loss induced by caloric restriction reduces the level of inhibitory signals, food intake increases until the energy deficit is corrected. Signals generated during a meal (satiety factors), including peptides secreted from the gastrointestinal tract, provide information to the brain that inhibits feeding and leads to meal termination (Schwartz et al. 2000).

4Several signaling molecules that affect food intake and that are critical for normal energy homeostasis have been identified. Insulin, enters the brain from the circulation and acts there to reduce energy intake. Leptin, is a hormone secreted by adipocytes. Both hormones circulate at levels proportional to body fat content, and enter the CNS in proportion to their plasma level. Leptin receptors and insulin receptors are expressed by brain neurons involved in energy intake (Schwartz et al. 2000).

5The Hypothalamus is a brain area with an important regulation function on food intake and metabolism. Leptin was originally thought to selectively modulate activity of pro-opiomelanocortin (POMC) and neuropeptide-Y (NPY) neurons in the arcuate nucleus of the hypothalamus. Leptin can register and direct food related sensory input signals since it modulates the sensitivity of taste receptor cells in the oral cavity, vagal mechanoreceptors in the gut, olfactory detection in the olfactory bulb, and visual perception of food (Schwartz et al. 2000; Berthoud, 2007; Zhen & Berthoud, 2007).

6Other anabolic effector signalling molecules such as Agouti-related protein (AGRP), orexin, corticotropin-releasing hormone (CRH), thyrotropin-releasing hormone (TRH), cocaine-and amphetamine-regulated transcript (CART) and interleukin-1 are among a growing list of peptides that promote negative energy balance (Zhen & Berthoud, 2007).

7The gut hormone ghrelin has been shown to directly act on hippocampal neurons and induce formation of new synapses. The ghrelin-induced changes in synaptic density are correlated with enhanced spatial learning. Ghrelin is also involved in the appetitive phase of ingestive behavior when it is important to find food in the environment. It is also plausible that the ghrelin-induced changes in hippocampal function facilitate the recall of stored representations of prior experience with food (Zhen & Berthoud, 2007).

8Brain circuits have highly specialized roles in energy homeostasis. The ventromedial hypothalamic nucleus (VMN) is considered as the “satiety centre”, while the lateral hypothalamic area (LHA) can be considered as the “hunger centre”. NPY and AGRP are co-localized in arcuate nucleus neurons of the hypothalamus. POMC and CART are co-localized in arcuate nucleus neurons. A majority of both NPY/AGRP and POMC/CART neurons have been found to co-express leptin receptors and both types of neurons are regulated by leptin. NPY/AGRP neurons are inhibited by leptin, and consequently are activated in conditions where leptin levels are low.

9The above illustrates that looking for food and metabolizing nutrients, are basic brain mechanisms that are controlled by several mediators and located in specific brain areas.

3. Monoamine neurotransmitters and food intake

10Serotonin-containing neurons are present in the cells located along the midline of the brainstem. They are mostly clustered in the raphe nuclei and their axons innervate nearly every region of the central nervous system. The synthesis of serotonin (5-HT) requires two enzymatic steps. First the amino acid precursor tryptophan (TRP) is hydroxylized by TRP hydroxylase to L-5-hydroxytryptophan, and then decarboxilated to 5-Hydroxytryptamine (5-HT). Metabolization occurs via aldehyde dehydrogenase and monoamine oxidase to 5-hydroxyindoleacetic acid (Meeusen and De Meirleir, 1995). 5-HT is known to play an important role in various behavioral functions, such as sleep, fatigue, pain and arousal (Meeusen et al. 2001). Leptin increases serotonin turnover which raises the possibility that at least some of leptin’s weight-reducing effects are mediated through increased serotonin signaling.

11Noradrenalin (NA) is synthesized in the locus ceruleus. From here there are projections to the hypothalamus, thalamus and cortex. In some of these neurons, including those projecting to the PVN, noradrenaline is co-localized with NPY. Like NPY, injection of noradrenaline into the PVN increases food intake robustly. Leptin may inhibit noradrenaline release from terminals in this brain area. Increased noradrenaline signaling in hypothalamic areas may therefore contribute to hyperphagia induced by leptin deficiency, a hypothesis that implicates noradrenaline as an anabolic effector in the CNS control of energy homeostasis.

12Dopaminergic cells are primarily located in the mesencephalon, the diencephalon and the telencephalon. The main pathways include the nigrostriatal tractus, the ventral mesostriatal pathway and the tubero-infundibular system (Meeusen and De Meirleir, 1995). Tyrosine is converted to L-dihydroxyphenylalanine (DOPA) by the enzyme tyrosine hydroxylase. DOPA is then decarboxylated to Dopamine (DA) by DOPA decarboxylase. DA is implicated in arousal, motivation, reinforcement and reward, the control of motor behavior and mechanisms of addiction and can be reloaded in the synaptic vesicles for reuse. DA is enzymatically metabolized by monoamine oxidase to 3,4-dihydroxyphenylacetic acid which is further destroyed by catechol-O-methyltransferase to homovanillic acid, or can be converted into noradrenaline by dopamine β–hydroxylase. The catabolism of NA happens via monoamine oxidase and catechol-O-transferase. The main metabolite of NA is 3-methoxy-4-hydroxyphenylethyleneglycol (Meeusen and De Meirleir, 1995).

13The role of DA in energy homeostasis is complex. Depletion of dopamine synthesis will cause feeding deficits. The feeding effects of DA vary with the brain region, for example, mesolimbic DA pathways (comprised of cell bodies in the substantia nigra and ventral tegmental area that project to the nucleus accumbens, striatum and cerebral cortex) seem to contribute to the “rewarding” aspects of consuming palatable foods. In contrast, DA signalling in the hypothalamus via neurons situated in the dorsomedial and arcuate nuclei seems to inhibit food intake.

4. What is Fatigue?

14Fatigue can be defined as an acute impairment of exercise performance which leads to an inability to produce maximal force output possible due to metabolite accumulation or substrate depletion (St Clair Gibson et al. 2003). It includes both an increase in the perceived effort necessary to exert a desired force or power output, and the eventual inability to produce that force or power output (Davis & Bailey, 1997). Fatigue will not only occur at the peripheral level, since there is ample evidence that also mechanisms at the central nervous system are implicated in the genesis of fatigue. These processes that lead to decrements in performance can occur at every level of the brain-muscle pathway (Noakes et al. 2004) and although literature made a distinction between peripheral and central fatigue, one should be aware that both pathways are integrated.

15Much research has been performed on the involvement of the motor pathways in fatigue. Neuromuscular fatigue occurs when a progressive exercise-induced failure of voluntary activation of the muscle exists together with a gradual failure to drive motorneurons. Taylor states that central fatigue can be demonstrated by an increase in the increment of force induced by nerve stimulation during a maximal voluntary contraction (Taylor et al. 2006). If extra force can be evoked by stimulating the motor neurons (superimposed twitch), central fatigue takes place possibly due to supraspinal mechanisms (Taylor et al. 2006). For an excellent review on this topic the authors would like to refer to the work by Gandevia (2001) and Taylor & Gandevia (2008).

16Brain neurotransmitter activity has not only been implicated in the regulation of cardiovascular (Ishide et al. 2000; Nauli et al. 2001), and endocrine (Chaouloff, 1993; Meeusen, 1999) responses during exercise, neurotransmitters and especially the central monoamines are strong candidates for inducing the centrally mediated effects of fatigue during exercise. The monoamines (5-HT, DA & NA) play a key role in signal transduction between neurons, and exercise-induced changes in the concentrations of these neurotransmitters (especially 5-HT & DA) have been linked to central fatigue. Initiated by Acworth et al. (1986), Newsholme and his co-workers (1987) developed the first hypothesis compromising changes in central neurotransmission to explain fatigue i.e. the “Central Fatigue Hypothesis”. This hypothesis is based on disturbances in brain 5-HT concentrations, as this neurotransmitter is involved in changes in sleep-wakefulness, emotion, sleep, appetite, the hypothalamic-pituitary axis, and numerous physiological functions (Meeusen et al. 2006). During exercise, the entry of tryptophan – precursor of 5-HT – into the central nervous system through the blood-brain-barrier is favored by increased muscle use of branched-chain amino acids (BCAA) and elevated plasma fatty acids as this elevates the ratio of unbound tryptophan to BCAA. This increases the amount of TRP crossing the blood-brain-barrier, consequently leading to higher 5-HT concentrations in the brain (Meeusen et al. 2006; Roelands & Meeusen, 2010; Davis et al. 2000). Events arising entirely from within the brain can influence an individual’s sensation of fatigue and thus potentially affect performance. This opens an opportunity to manipulate the central nervous system through changes in diet or supplementation with specific nutrients, including amino acids (BCAA, tyrosine), carbohydrates (CHO) and caffeine.

5. Nutrition to influence central fatigue

5.1 Branched Chain Amino Acids

17Fernstrom (2005) clearly indicated the importance of the BCAA. Leucine, isoleucine, and valine participate directly and indirectly in a variety of important biochemical functions in the brain such as protein synthesis, the production of energy, and the synthesis of the amine neurotransmitters 5-HT and the catecholamines DA and NA, which are derived from the aromatic amino acids TRP, phenylalanine, and tyrosine (Fernstrom, 2005). The ingestion of BCAA causes rapid elevation of their plasma concentrations, increases their uptake into brain.

18It was hypothesized that by reducing the production of serotonin in the brain, feelings of fatigue could be attenuated and performance enhanced. Supplementation of BCAA has been proposed as a possible strategy to limit the development of central fatigue. BCAA compete with TRP (the precursor of serotonin) for transport across the blood brain barrier. If more BCAA are available in the circulation, then more will be transported across the blood brain barrier at the cost of TRP. This would imply that with increased BCAA availability, less TRP will be available in the brain, less 5-HT would be formed, and consequently fatigue would be reduced. Meeusen and co-workers (1996) using in vivo brain microdialysis demonstrated that increased TRP availability resulted in an elevation in extracellular 5-HT and 5-hydroxyindoleacetic acid concentrations in 24-hour fasted rats. Exercise for one hour further increased extracellular levels of 5-HT. Good evidence for the role of BCAA in limiting TRP entry into the CNS and attenuating the increase in 5-HT has also been reported (Gomez-Merino et al. 2001). During the placebo trial (saline infusion) a progressive increase in extracellular 5-HT was apparent in the hippocampus as exercise continued, but this elevation was abolished when exercise was preceded by an infusion of valine.

19Although this is a very attractive theory, there is limited or only circumstantial evidence to suggest that exercise performance in humans can be altered by nutritional manipulation through BCAA supplements. Madsen et al. (1996), Struder et al. (1998) and van Hall et al. (1995) all attempted to influence the plasma free TRP to BCAA ratio by BCAA supplementation but failed during exercise in normal ambient temperature (Watson et al. 2004). BCAA have also been given in combination with carbohydrates during exercise. It is a well-known fact that ingestion of carbohydrates during prolonged exercise can delay fatigue, which is often suggested to be due to the maintenance of blood glucose levels and the supply of energy when muscle glycogen levels are low. While there is some evidence of BCAA ingestion influencing ratings of perceived exertion and mental performance, the results of several well-controlled laboratory studies have failed to demonstrate a clear positive effect on exercise capacity or performance during prolonged fixed intensity exercise to exhaustion, prolonged time trial performance, incremental exercise or intermittent shuttle-running (Meeusen & Watson, 2007).

5.2 Tyrosine

20Tyrosine, or 4-hydroxyphenylalanine can be synthesized in the body from phenylalanine, and is found in many high-protein foods such as soy products, chicken, turkey, fish, peanuts, almonds, avocados, milk, cheese, yogurt and sesame seeds. Acute consumption of tyrosine increases the ratio of tyrosine to other large neutral amino acids such as leucine, isoleucine, valine and TRP. Tyrosine shares a common transport molecule with large neutral amino acids at the blood-brain barrier; therefore an increase in the tyrosine ratio causes an increase in brain tyrosine and a decrease in large neutral amino acids concentration. Consequently, this would lead to an increase in brain DA and NA concentration (Tumilty et al. 2011). A review by Lieberman (2003) states that tyrosine is a leading candidate for use as a cognitive performance enhancer in military operations (Committee on Military Nutrition, 1994). A series of pre-clinical, animal studies have been conducted that clearly indicate that tyrosine reduces many of the adverse effects of acute stress on cognitive performance in a wide variety of stressful environments. Given this unique potential use, it is not surprising that tyrosine has been the focus of considerable military interest for its cognitive “anti-stress” effects (Lieberman, 1994). Although it has been difficult to conclusively demonstrate that tyrosine has beneficial effects in humans, in part due to ethical concerns, the preponderance of evidence, suggests that tyrosine has utility as an acute treatment to prevent stress related declines in cognitive function.

21One study has measured a net brain uptake of tyrosine during prolonged exercise in humans (Nybo et al. 2003); however, acute tyrosine supplementation did not improve either prolonged exercise capacity (Struder et al. 1998) or performance (Chinevere et al. 2002) in temperate conditions. Exercise in the heat on the other hand, represents a specific demand on brain DA which is not apparent in temperate conditions (Watson et al. 2005; Roelands et al. 2008). Therefore, brain tyrosine requirement may be greater with the cumulative demands of exercise and heat stress, and may become limiting to dopamine synthesis and release. Tumilty et al. (2011) assessed the effects of acute tyrosine supplementation on exercise capacity in the heat. Although this first study indicated that supplementing a nutritional dopamine precursor 1 hour pre-exercise was associated with increased exercise capacity in the heat (Tumilty et al. 2011), several recent studies clearly showed that oral tyrosine administration was not able to influence exercise performance in the heat, (Tumilty et al. 2013, 2014; Watson et al. 2012). Further studies are needed to identify the influence of regular supplementation of large amounts of tyrosine (5 g to 10 g) on health due to chronic changes in sympathetic nervous system activity.

5.3 Carbohydrate

22Another nutritional strategy that may influence the development of central fatigue is CHO feeding. Nybo (2003) showed that the average force production during a sustained maximal muscle contraction was decreased after 3 hours of exercise at 60% VO2max in endurance-trained subjects. Blood glucose levels significantly decreased from 4.5 to 3 mmol/L after exercise and a diminished activation drive from the CNS was apparent. This central fatigue was reversed when euglycaemia (4.5 mmol/L) was maintained with the ingestion of 200 g of CHO. In addition, it was easier for the subjects to retain power output at the end of prolonged exercise when hypoglycaemia was prevented (Karelis et al. 2010). The beneficial effect of CHO supplementation during prolonged exercise could also relate to increased (or maintained) substrate delivery for the brain, with a number of studies indicating that hypoglycemia affects brain function, and cognitive performance. Carbohydrate feeding has been shown to improve higher intensity exercise performance lasting approximately 60 min even though the estimated amount of glucose delivered to the muscle during this period was estimated to be very small (Jeukendrup et al. 1997). The same research group infused glucose during a time trial to study the performance effects with increased carbohydrate availability. Failure to observe a benefit of glucose infusion on time trial performance (Carter et al. 2004a), prompted this group to suggest an alternative mechanism for the ergogenic effect of CHO centered around the activation of CHO receptors found in the mouth. Carter et al. (2004b) reported a 3% (PLA 61.37 min; CHO 59.57 min) increase in performance following the rinsing of a maltodextrin solution around the mouth before and during exercise. No solution was actually ingested during the protocol, suggesting that this performance benefit may have been mediated through direct communication between receptors present in the mouth and the brain. Other groups have also looked into the effects of a CHO mouth rinse on performance. Also Pottier et al. (2010) found a performance improvement on a 60 min time trial rinsing with a CHO-electrolyte solution, while Rollo et al. (2008, 2010, 2011) showed ergogenic effects on different time trials. Interestingly, most studies that found an effect were carried out in the fasted state. When a CHO mouth rinse was performed in a fed state, no effect on performance in a 45 min (Whitham & McKinney, 2007) and 60 min time trial was observed (Beelen et al. 2009). The authors suggested that oral perception of carbohydrates perhaps only plays a role when muscle and liver glycogen stores are reduced. This finding was, however, not replicated in a very recent study by Fares & Kayser (2011). In this study a mouth rinse with a maltodextrin solution increased time until exhaustion in both a fed and fasted state in non-athletic male subjects (Fares & Kayser, 2011). Sinclair et al. (2014) investigated the effect of different durations of CHO mouth rinse on cycling performance. In a placebo controlled study they found that both 5 seconds and 10 seconds mouth rince improved performance compared to placebo, but only in the 10 seconds trial this was statistically significant. This could indicate that a longer rinse period is superior to short periods. The concept of the CHO mouth rinse has been supported by work investigating brain activity following the ingestion of a bolus of glucose (Liu et al. 2000), and research demonstrating activation of several brain regions after rinsing CHO solutions within the mouth (Chambers et al. 2009). These studies highlight a marked increase in brain activation, occurring immediately after CHO enters the mouth, with a second spike in activity observed 10 minutes following ingestion, presumably occurring as the substrate enters the circulation. Turner et al. (2014) used functional magnetic resonance imaging to investigate the possible brain regions involved in CHO sensing. They combined oral exposure to CHO with a motor task. Areas of activation associated with CHO were over the primary sensory motor cortex, and regions within the limbic system connected with reward. These findings are very novel and suggest an interesting mechanism of action. Further investigation of CHO receptors in the mouth is certainly warranted.

5.4 Caffeine

23Caffeine (1,3,7-trimethylxanthine) is found in varying quantities in the seeds, leaves and fruit of some plants, where it acts as a natural pesticide that kills certain insects feeding of the plants. It is most often consumed as coffee or tea, but can also be found in energy drinks, chocolate bars and soft drinks. After oral ingestion, caffeine is rapidly an almost completely absorbed from the gastrointestinal tract into the bloodstream. Caffeine has long been recognized as an ergogenic aid. For a while caffeine use was restricted for athletes, and it was only removed from the list of banned substances in January 2004 and to be put on the monitoring list. The mechanism of action of caffeine is still elusive. In the past it has been attributed to an increased availability of free fatty acids (Spriet et al. 1992), resulting in a glycogen sparing effect. However, this finding is far from conclusive and there is now evidence that the mechanism of action of caffeine is not due to muscle glycogen sparing (Graham et al. 2000). Current research supports a CNS effect mediated by antagonism of adenosine receptors as most likely cause (Davis et al. 2003). Adenosine inhibits the release of DA, logically, caffeine will induce higher brain DA concentrations (Davis et al. 2003). Human studies using a variety of protocols have shown performance improvements after caffeine intake (Jackman et al. 1996; McNaughton et al. 2008; Glaister et al. 2008; Walker et al. 2008). Warren et al. (2010) recently conducted a systematic review and meta-analysis of the research literature assessing the effect of caffeine ingestion on maximal voluntary contraction MVC). They concluded that overall, caffeine improves MVC strength and muscular endurance.

24Glade (2010) states that besides ergogenic effects, caffeine also increases resting energy expenditure, mental energy, cognitive function, neuromuscular coordination, elevates mood and relieves anxiety. Caffeine may thus reduce perception of effort and pain during exercise, thereby allowing subjects to perform at higher workloads for a longer period of time (Motl et al. 2003). Caffeine has been shown to be effective in relatively low doses (3 mg/kg) and its effect seems to level off at 6 mg/kg, and therefore it should not be recommended to take very high doses. Given the widespread use of caffeine by many, the level of habitual intake may be an important factor to consider when undertaking caffeine supplementation with the view to enhance performance. In some naïve individuals, caffeine can produce several side effects, such as tachycardia and palpitations, nervousness, dizziness and gastrointestinal symptoms that may be detrimental to performance. The positive (and possible negative) effects of caffeine seem very individually determined so prior experience with doses and timing is essential before using supplementation in competitive environments.

6. Conclusion

25Originally fatigue was attributed solely to peripheral factors, such as muscular and cardiovascular factors. Since a few decades there is proof that fatigue can also occur at the level of the brain. This so-called ‘central fatigue’ compromises specific alterations in the functioning of the central nervous system. It seems that although the rationale for the central fatigue hypothesis is solid, but the largely inconsistent findings of nutritional manipulation studies with BCAA and tyrosine make it difficult to draw any firm conclusions regarding the role of central neurotransmission in the fatigue process. Both CHO and caffeine have already shown to be ergogenic in different exercise protocols. The mechanism by which this happens is, however, not entirely clear and might very well be a combination of both central and peripheral aspects. Although recent studies have already started incorporating new technologies such as transcranial magnetic stimulation, in vivo microdialysis and other dynamic imaging technologies to better understand what happens in the brain, the search for the central mechanisms of fatigue, and the role of nutrition in the development of fatigue, remains to be unraveled!

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Auteurs

PhD. Dept Human Physiology and Sports Medicine, Vrije Universiteit Brussel, Brussels, Belgium. School of Public Health, Tropical Medicine and Rehabilitation Sciences, James Cook University, Queensland, Australia. Corresponding author: Prof Dr Romain Meeusen Pleinlaan 2 – 1050 Brussels – Belgium rmeeusen@vub.ac.be

PhD. Dept Human Physiology and Sports Medicine, Vrije Universiteit Brussel, Brussels, Belgium. Fund for Scientific Research Flanders (FWO)

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