Journal of the American College of Nutrition, Vol. 26, No. 90005, 604S-612S (2007)
Published by the American College of Nutrition
Exercise, Heat, Hydration and the Brain
R.J. Maughan,
S.M. Shirreffs and
P. Watson
School of Sport and Exercise Sciences, Loughborough University, Leicestershire, UNITED KINGDOM
Address correspondence to: Professor RJ Maughan, School of Sport and Exercise Sciences, Loughborough University, Leicestershire LE11 3TU, UNITED KINGDOM. E-mail: r.maughan{at}lboro.ac.uk
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ABSTRACT
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The performance of both physical and mental tasks can be adversely affected by heat and by dehydration. There are well-recognized effects of heat and hydration status on the cardiovascular and thermoregulatory systems that can account for the decreased performance and increased sensation of effort that are experienced in the heat. Provision of fluids of appropriate composition in appropriate amounts can prevent dehydration and can greatly reduce the adverse effects of heat stress. There is growing evidence that the effects of high ambient temperature and dehydration on exercise performance may be mediated by effects on the central nervous system. This seems to involve serotonergic and dopaminergic functions. Recent evidence suggests that the integrity of the blood brain barrier may be compromised by combined heat stress and dehydration, and this may play a role in limiting performance in the heat.
Key words: exercise, heat, hydration, fatigue
Key teaching points:
• Endurance exercise performance is impaired in the heat. Performance in most physical and cognitive tasks is impaired by dehydration. Peripheral factors, e.g. muscle glycogen depletion, can account for fatigue in endurance exercise in cool or temperature environments, but not in the heat.
• Fluid ingestion during exercise can decrease the subjective sensation of fatigue and enhance performance when exercise lasts more than about 40 minutes.
• A high core temperature, and especially a high brain temperature, seems to be associated with the onset of fatigue in endurance exercise in warm environments.
• Changes in brain neurotransmission, in particular dopamine, appear to be responsible for fatigue when exercising in the heat. Alterations to cerebral blood flow and/or metabolism may also be important mediators of fatigue during exercise in a warm environment.
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INTRODUCTION
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Humans have evolved to tolerate a wide range of environmental temperatures while keeping the body's core temperature within rather narrow limits. By adopting a combination of physiological and behavioral mechanisms, humans cope well with environmental extremes and successfully maintain core temperature at about 36 to 38°C in a wide range of environments and activity states. Excursions of deep body temperature above or below these limits demand greater involvement of the body's homeostatic mechanisms and a point may be reached where temperature must be allowed to drift. Loss of control of body temperature can result in impairments of physiological function and, if sufficiently severe, loss of consciousness and death. The signs and symptoms can be remarkably similar whether body temperature is high (hyperthermia) or low (hypothermia). Numerous strategies are available to limit the loss of function and to protect health in individuals exposed to high environmental temperatures or exercise stress; among the most effective of these strategies is maintenance of hydration status [1].
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EXERCISE IN THE HEAT: EFFECT ON THERMOREGULATION AND PERFORMANCE
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It is an everyday experience for athletes and those with physically demanding occupations that exercise feels harder when the ambient temperature is high and there is a corresponding reduction in exercise performance. This observation has been confirmed many times by well-controlled studies in laboratory conditions and by less well-controlled studies in the field. In the laboratory, exercise time to fatigue at constant power output (about 70% of VO2max) is longest at about 11°C, and is less at either higher or lower temperatures [2]. Parkin et al. also showed that exercise time to fatigue at an ambient temperature of 3°C was longer than at 20°C or 40°C [3]. A recent analysis of performance in marathon races taking place in varying environments concluded that there is an optimum temperature of about 10–12°C for marathon running [4].
Given the high rates of heat production sustained by faster marathon runners, it is not surprising that increasing the ambient temperature results in performance impairment. Any reduction in the rate of heat loss or addition of an external heat load, which occurs as soon as the environmental temperature exceeds the skin temperature, will clearly result in a more rapid rise in core temperature. This means that there must either be a faster rise in core temperature or a faster rate of sweat evaporation to increase the rate of heat loss. In turn, a faster sweat evaporation rate requires a faster sweat secretion rate and/or a higher skin temperature to achieve a higher evaporation rate. Maintaining a high skin temperature requires a high skin blood flow, diverting blood from the working muscles and/or increasing cardiac output that must be achieved [5].
Even at moderate ambient temperatures, the reduced skin-to-environment temperature gradient results in performance decrements. For instance, Galloway and Maughan showed that performance is reduced when ambient temperature is increased from 11°C to 21°C [2]. Nielsen calculated that this effect's magnitude was such that it would not be possible for a well-trained marathon runner to complete the distance in less than 3 h 20 min in the hot and humid conditions predicted for the Atlanta Olympic Games held in 1996 [6]. Although increasing ambient temperature's effect on performance in competitive situations is less than might be predicted from theoretical considerations or from laboratory studies, the decrement is nonetheless real.
A change in body temperature may be regarded as a failure of homeostasis or as a re-setting of the point around which regulation occurs. Small fluctuations are normal: over the course of the day, core temperature varies by about 1°C [7]. During exercise, some degree of core temperature elevation is normal with the increase proportional to the absolute and relative (expressed as a fraction of VO2max) power output [8]. Rise in body temperature is also influenced by the environment. Core temperature rises faster in hot environments when power output is maintained at a constant rate, and a higher core temperature is observed at the point of fatigue (Fig. 1).
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Fig. 1. Effects of ambient temperature on (a) endurance capacity and (b) core temperature (adapted from [2]). Data in (b) are shown for all time points for which data are available for all subjects.
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When skin temperature exceeds environmental temperature, heat can be lost to the environment through radiation, convection, and evaporation. Heat loss by conduction is negligible for exercise in air, but becomes significant when immersed in water. Once environmental temperature exceeds skin temperature, evaporation is the only mechanism by which the body can lose heat. Sweating is evoked when core temperature rises and increases in proportion to core temperature, but the sweating rate is also influenced by skin temperature. Sweat evaporation will depend on the water vapor pressure gradient at the skin surface: this in turn depends on skin and environmental temperature and the relative humidity at the skin surface.
Although a rise in body temperature is commonly perceived to indicate a failure of the body's thermoregulatory function, there may well be a regulated increase in core temperature during exercise. Effective heat loss by evaporation of sweat demands adequate rates of sweat secretion onto the skin surface to maintain a wet skin and a high skin temperature to allow for evaporation before the sweat drips from the skin surface. Humans are provided with abundant sweat glands distributed over the body surface and have a high capacity for sweat secretion: trained athletes can sustain sweating rates of more than 2 L/h over prolonged periods [9]. Evaporation of all this sweat from the body surface would remove heat at a rate of 2.4 MJ/h (1160 kcal/h). This approximates the average rate of metabolic heat production for a 70 kg runner who completes a marathon in about 2 h 30 min. If all this sweat could be evaporated from the skin surface and the latent heat of vaporization was contributed from the body rather than from the environment, this runner would be able to maintain body temperature rather well. A faster runner, however, would require a greater rate of evaporative heat loss to prevent a rise in core temperature, unless he or she has a better running economy that allows the faster pace to sustained with a lower metabolic rate.
At these high rates of sweat secretion, it is possible that a significant fraction will simply drip from the skin surface once the evaporative capacity of the environment is exceeded. This will increase loss of water and solutes without making any contribution to body temperature maintenance. To prevent this and ensure the sweat evaporates, a high skin temperature, and therefore a high skin blood flow, is required; this is a major limitation to exercise performance. Heat convection from the active muscles to the skin surface requires a cutaneous blood flow that is inversely proportional to the temperature gradient from the core to the skin: the smaller that temperature gradient, the greater the blood flow to be diverted to the skin to lose heat, and this may lead to a fall in perfusion of skeletal muscle, brain, and other tissues in the case of prolonged, strenuous exercise in the heat [10]. If body temperature is allowed to rise, the gradient from core to skin is increased and the cutaneous blood flow necessary to maintain thermal balance is reduced. Some increase in core temperature may therefore be beneficial, and even necessary to maintain thermoregulatory function, when the heat production rate is high and the environment does not favor heat loss. This may account for the observation from field studies that faster runners normally have the highest post-race core temperatures [11].
Manipulation of body temperature prior to exercise can have profound effects on performance. Lee and Haymes showed clear effects on performance when subjects exercised to exhaustion at 82% VO2max at an ambient temperature of 24°C when this was preceded by 30 min rest at either 5°C or 24°C followed by 10–16 min at 24°C [12]. Although core temperature at the end of exercise was the same during both trials, exercise time to fatigue was greater (26.2 ± 9.5 min) after cold exposure than after resting in the warmer environment (22.4 ± 8.5 min). Similarly, Gonzalez-Alonso et al. immersed seven subjects in water at 17, 36, or 40°C for 30 min prior to exercise [13]. Subjects then exercised to exhaustion at 60% of VO2max on a cycle ergometer at an ambient temperature of 40°C. Exercise times to fatigue are shown in Table 1.
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Table 1. Effects of Prior Immersion in Water at Different Temperatures on Time to Fatigue in a Cycle Ergometer Test at 60% of VO2max [13]
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Similar results have been demonstrated in many other studies. Prior heating can also dramatically increase the subjective sensation of effort during exercise (Fig. 2), potentially indicating a role of body temperature in the development of fatigue during hyperthermia. There is some evidence to support the idea that fatigue during prolonged exercise in a warm environment may coincide with the attainment of a critical core temperature [13,14]. These data suggest there may be a thermal limit to exercise performance that serves as a protective mechanism to prevent potential damage to the body by limiting further heat production. Nonetheless, it is clear that many individuals reach the point of fatigue during exercise in the heat long before attaining values of 39.5°C [15], and there are many studies where there is no consistency in the core temperature at the point of fatigue.
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Fig. 2. Effect of prior warming on (a) core temperature during subsequent exercise and recovery and (b) the subjective rating of perceived exertion (RPE) during exercise. Redrawn from Watson et al. [36].
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It is possible that the concept of a critical core temperature, where individuals fatigue upon attaining a particular core temperature, is not as straightforward as originally proposed, with feedback from other factors likely to play a role in developing fatigue under heat stress. It must, of course, be remembered that rectal temperature was the measure of core temperature used in most of these studies, while some studies have also used oesophageal temperature. This may be inappropriate as the relationship between rectal temperature and brain temperature has not been clearly established in humans, unlike some of the various animal models that have been used where rectal and brain temperature can be measured simultaneously [16]. It is easier to believe that important events related to fatigue may be taking place in the brain than in the rectum.
There is also some evidence that the beneficial effects of repeated exposures to exercise in a hot environment are due to a lowering of the pre-exercise resting core temperature, with the rate of rise of body temperature during exercise being little affected [14]. This is contrary to the commonly held view that acclimation benefits exercise performance in the heat by promoting heat loss through a greater evaporative heat loss that results from more profuse sweating and a more effective distribution of sweat secretion over the body surface [17].
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HYDRATION, THERMOREGULATORY FUNCTION AND EXERCISE PERFORMANCE
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There is a well-recognized interaction among hydration status, thermoregulation and exercise tolerance, and some of the consequences of hypohydration are shown in Table 2.
In exercise of short duration there is not sufficient time for sweat loss to cause significant reductions in body water content. However, an individual who begins such exercise in a state of hypohydration may perform less well. This was clearly demonstrated by Armstrong et al. who showed that inducing hypohydration by administering a diuretic agent prior to simulated races at distances of 1500 m, 5 km and 10 km reduced performance by 3.1%, 6.7%, and 6.3% respectively [18]. The theoretical advantage of a reduction in body mass that has to be carried does not therefore compensate for the negative effects of a reduced body water content. In a field situation, measures of cardiovascular function are not possible, but it seems likely that there may be no reduction in the maximum cardiac output that can be achieved, despite the reduced blood volume [19]. In the short time scale of the 1500 m run (about 4 min), it seems very unlikely that thermoregulation plays a significant role, though muscle temperature is likely to rise rapidly in the active muscle groups.
Evidence for the effects of hydration status in prolonged exercise performance comes from many different lines of investigation. When exercise lasts more than about 40–60 min, performance can be improved by ingesting water or carbohydrate, and the effects of the two are independent and additive [20]. Many other studies, often less well-controlled, have produced similar results. The evidence that ingesting plain water is effective is, perhaps, less conclusive than the evidence for a beneficial effect of dilute carbohydrate-electrolyte drinks [21]. It is not easy to be sure, however, that the carbohydrate in this case is playing a metabolic role, though some of it is undoubtedly oxidized [22]. An alternative explanation may be that adding small amounts of carbohydrate can promote water absorption in the small intestine, thus providing more effective rehydration. When the time scale is short, as in exercise lasting less than a couple of hours, ingested fluid will be effective only if it is emptied rapidly from the stomach and absorbed rapidly in the small intestine. For this reason, concentrated carbohydrate solutions may be ineffective as they may promote transient net secretion in the small intestine, resulting in a temporary loss of body water into the small intestine [21].
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HYDRATION STATUS AND COGNITIVE FUNCTION
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The absence of specific reliable tests of different aspects of cognitive function aspects has contributed, in large part, to the limited amount of information available. There are few reports on the effects of hypohydration on mental performance and cognitive function, but some negative effects have been recorded. Gopinathan et al. reported a reduction in a variety of tasks involving arithmetic ability, short-term memory, and visual tracking after dehydration (2–4% of body mass) induced by exercise in the heat and water restriction; the decrement in performance was roughly proportional to the extent of the water deficit, but there was no measurable loss of performance with a 1% reduction in body mass [23]. This may reflect the relative insensitivity of the tests used. The effects of hydration status are discussed in detail by Lieberman [24].
Much of the popular press on drinking and hydration status suggests that a conscious effort is required by individuals if they are to drink sufficient fluid to maintain a state of body water balance. While many physiological responses to hypohydration have been studied extensively, the perceived subjective responses to hypohydration have been largely ignored. This is particularly relevant if it is possible that it is "easy" for people to inadvertently restrict their fluid intake over a number of days and thus become hypohydrated. One recent study described the physiological responses and subjective feelings resulting from 13, 24 and 37 h of fluid restriction and compared these with a euhydration trial of the same duration [25]. Body mass decreased by 2.7% after 37 h with fluid restriction. The subjects reported that their thirst increased during the first 13 h of fluid restriction and then did not significantly increase further. They also reported headache with fluid restriction and that their ability to concentrate and alertness were reduced. They also indicated they felt more tired when restricting their fluid intake. However, what was clear from these subjects was that they all greatly desired something to drink during the later stages of the study and had to make a conscious effort to abstain from drinking and to continue eating dry foods. These subjects therefore would not have become dehydrated to this extent "by accident."
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THE ROLE OF THE BRAIN
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The thermoregulatory responses to exercise and heat stress occur without conscious action by the brain, but this does not mean the brain is not aware of what is occurring or that it is not essential for conservation of function when exposed to these stresses. All animals seek to escape environmental extremes to more comfortable zones, except when there is a compelling reason, such as a need for food, to risk the thermal stress. The primary human response to thermal stress is to change the environmental conditions, and where this is not possible to adjust the amount of insulation or type of clothing. A further option is to alter the rate of metabolic heat production: this involves increasing activity levels when subjected to cold stress or reducing effort in warm weather. People are more inclined to walk briskly on cold days and to dawdle on hot ones. Only when these strategies are not successful in preventing a change in thermal comfort are the physiological mechanisms invoked.
Noakes and colleagues have recently made much of the possible role of the brain in maintaining thermal homeostasis in exercise and stressed the importance of a "central governor" that prevents a failure of homeostasis by causing a voluntary cessation of effort (or a reduction in exercise intensity) when homeostasis is challenged [26,27]. The concept of a "governor" that limits exercise performance to prevent a catastrophic failure of physiological function has been ascribed by Noakes to AV Hill [26]. The central nervous system's role in the fatigue that accompanies exercise was widely recognized much earlier than the work of Hill, however. In 1919, Bainbridge [28] wrote, "It has long been recognized that the main seat of fatigue after muscular exercise is the central nervous system. Mosso long ago stated that "nervous fatigue is the preponderating phenomenon and muscular fatigue is also at bottom an exhaustion of the nervous system.’ There appear, however, to be two types of fatigue, one arising entirely within the central nervous system, the other in which fatigue of the muscles themselves is superadded to that of the nervous system."
The above is a remarkably elegant description of a phenomenon that most would take for granted, but its failure lies in the absence of any reference to the physiological mechanisms involved. In that sense, the "central governor" described at length in recent publications remains a "black box" and has not increased our understanding. The key role of the central nervous system (CNS) in setting the limits to exercise performance and in anticipating demands is taken for granted by those involved in sport and is manifested in the pacing strategies adopted by runners, cyclists, and other athletes.
The relationship between speed and distance in athletic events was well described by AV Hill in 1925 [29], and by many others before and since. Given that a fairly uniform pace is maintained in most athletic events, the pace adopted at the outset is based on experience of what the maximum tolerable pace is likely to be. This is then subject to modulation by signals arising in the peripheral tissues as described by Bainbridge [28] and by a conscious decision based on environmental conditions, tactical considerations and other factors. Every elementary coaching manual published in the last century or more has emphasized the need for the inexperienced athlete to be cautious in the early stages of a race and set off at a pace more modest than might feel appropriate. Every athlete also knows that there are "good days" and "bad days" when performance is above or below what is expected, and that these appear to be unrelated to peripheral factors.
Marino et al. suggest the brain is able to calculate the rate of heat storage allowable under the prevailing environmental conditions and that this information, along with knowledge of the exercise duration, will determine motor unit recruitment at different times during the exercise [30]. This system is proposed to limit the rate of heat production during exercise, thus allowing a task to be completed prior to catastrophe (fatigue). Unless one subscribes to the belief that some higher being controls the destiny of the human race, there must be a physical basis for the CNS limitations to performance that clearly exist. The physical mechanisms involved in the "central governor" are not well understood, but are likely to have a neurological basis which ultimately means there must be a neurochemical mechanism, or more likely, a number of mechanisms acting in concert. Various pharmacological interventions have been applied to test this hypothesis and the outcomes are generally consistent with a role for key central neurotransmitters, specifically dopamine, serotonin and noradrenaline in the fatigue process.
Perhaps the most convincing evidence for the brain's role in the fatigue process comes from pharmacological interventions. Amphetamines, which act on central dopamine (DA) receptors, are well known to enhance exercise performance and are prohibited under the rules of the World Anti-Doping Agency [31]. Various studies demonstrated a marked increase in exercise capacity following administration of amphetamines to both rodents [32] and humans [33, 34]. Amphetamines are thought to enhance exercise performance through the maintenance of DA release late in exercise, as an elevation in catecholaminergic neurotransmission is typically linked to arousal, motivation, and reward. Changes in regional dopamine metabolism have also been implicated in the control of locomotion and posture in moving animals, which may also be an important aspect of DA's role in fatigue [35].
Many different psychotropic drugs that act through changes to central dopaminergic and noradrenergic neurotransmission with varying degrees of receptor specificity to treat/manage psychiatric disorders are now available. Bupropion, which acts on central dopamine and noradrenaline receptors, was recently shown to enhance endurance performance in the heat (Fig. 3), but this effect was not seen when exercise was undertaken in temperate conditions [36]. Even though a higher power output was maintained during exercise in the heat after administration of this drug, the subjects’ perception of effort and thermal discomfort was the same on both the treatment and placebo trials. Rectal temperature at the end of the trial was, however, higher during the treatment trials than the placebo trials, which is consistent with the higher mean power output. It is possible that dopaminergic drugs may dampen or override inhibitory signals arising from the CNS, to cease exercise due to hyperthermia and enable an individual to maintain a high power output despite an elevated core temperature.
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Fig. 3. Effects of administration of an acute dose of Paroxetine (a selective serotonin reuptake inhibitor); Figure 3A: and Bupropion (a dopamine/noradrenaline reuptake inhibitor); Figure 3B: on subsequent exercise (redrawn from [31] and [36] respectively). Note: Figure 3A shows a reduction in exercise capacity with Paroxetine, whereas Figure 3B demonstrates an increase in time trial performance following Bupropion administration.
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Traditional views of neurotransmission's role in the development of fatigue during prolonged exercise have centered on the neurotransmitter serotonin (5-hydroxytrypamine; 5-HT). Work by Newsholme and colleagues suggested that changes in substrate mobilization occurring during prolonged exercise would result in an increased uptake of the amino acid tryptophan into the CNS [37]. As serotonin synthesis is largely dependent on tryptophan's availability, researchers postulated that central serotonergic synthesis, and therefore activity, would increase as a consequence of the metabolic changes occurring as exercise continued. Serotonergic neurotransmission has been linked to feelings of lethargy and tiredness, and Newsholme proposed that this response could contribute to the fatigue process. The evidence for drugs acting on serotonin receptors is perhaps less convincing than the work on dopamine, with some studies showing a reduction in exercise capacity following the administration of 5-HT agonists [38,39] (Fig. 3) while others have shown no effect [40–42]. An attraction of this hypothesis was the possibility of altering central 5-HT activity via nutritional supplements, including branched-chain amino acids, tryptophan, and carbohydrate. Attempts to influence performance by nutritional interventions designed to manipulate the availability of neurotransmitter precursors, however, have generally been unsuccessful [43–46], with only a few exceptions [47].
To further emphasize the potential involvement of dopaminergic neurons in the fatigue process, there is some recent evidence that rats selectively bred for either high or low running capacity show differences in the expression of genes related to dopaminergic function in some regions of the brain [48]. Attempts to find a genetic basis for the success of specific athletic populations, such as the East African distance runners, have generally been unsuccessful [49], perhaps because researchers have studied the wrong variables.
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POTENTIAL MECHANISMS LINKING HEAT, HYDRATION, AND PHYSIOLOGICAL FUNCTION
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It is not easy to see an immediate mechanism that links fluid balance, thermoregulatory function, and central serotonergic or dopaminergic function. However, it was recently shown that prolonged exercise performance in the heat may be associated with an increased permeability of the blood brain barrier (BBB) [50]. This conclusion was based on an increased concentration of a brain specific protein (S-100ß) in the circulation after exercise in the heat, but not after a similar exercise bout performed in cool conditions. The BBB's function is to protect the brain by preventing pathogens and small molecules that may disrupt CNS function from accessing it. It also acts to prevent escape of valuable nutrients from the brain. The BBB is normally impermeable to S-100ß, though it can escape from the brain in various stress situations that disrupt barrier function [51]. If S-100ß can escape from the CNS during exercise, it seems likely that other compounds can leave or enter the brain. The fact that increased permeability is observed when core temperature is elevated by exercise in the heat may not be significant, but may be a factor in the early fatigue that occurs in this situation.
Further circumstantial evidence to support this suggestion comes from the observation that the rise in serum S-100ß with exercise in the heat is at least partially abolished by water ingestion [52]. This may be associated with the better control of osmotic equilibrium across the BBB, limiting the structural changes responsible for the increased permeability that would otherwise take place. While there is evidence that relatively mild dehydration can negatively influence cognitive performance [23], little is known about the mechanisms affecting the brain. These data suggest that changes in whole body fluid balance can directly influence the CNS, and this may potentially play a role in the mental and physical performance deterioration seen with dehydration.
High cerebral temperature may lead to alterations in motor drive that affect the ability to recruit sufficient muscle fibers to meet the demands of exercise [53]. This effect may be mediated, at least in part, by blood flow changes occurring in response to redistribution of cardiac output due to exercise-heat stress. During exercise in temperate conditions, cerebral blood flow is markedly increased during exercise [54], but a decline in blood flow to the brain has been reported during exercise with hyperthermia [55]. It is clear that exercise, coupled with heat stress, results in a significant number of metabolic and circulatory perturbations within the brain. At present, it is impossible to single out a key factor that is ultimately responsible for development of central fatigue and reduction in exercise performance in the heat, but this likely involves interplay between these responses, to varying degrees.
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SUMMARY
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Performance of both physical and mental tasks is significantly reduced by heat and dehydration. The cardiovascular and thermoregulatory systems are particularly stressed under these conditions and provision of fluids can prevent dehydration and greatly reduce the adverse effects of heat stress. There is growing evidence that the effects of high ambient temperature and dehydration on exercise performance may be mediated by effects on the CNS. Hyperthermia results in changes in the brain's electrical activity, a marked reduction in the ability to maintain voluntary contractions, and an increase in perceived exertion. While the precise role of the CNS in the development of fatigue is yet to be determined, preliminary evidence supports a neurotransmission role in the fatigue process. A number of circulatory perturbations, including a reduction in cerebral blood flow and increased permeability of the blood-brain barrier, may also influence performance when exercise is undertaken in high ambient temperatures, particularly in the presence of significant levels of dehydration.
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FOOTNOTES
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Conflict of Interest Disclosure: RJ Maughan is a member of the Gatorade Sports Science Institute Sports Medicine Advisory Board but does not believe this to be a conflict of interest. The other authors have no conflicts of interest to declare in relation to this work.
Received July 16, 2007.
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ABSTRACT
INTRODUCTION
