thermoregulation during exercise in

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DC\/IC\A/ ADTI/~I C ^ P ' ' ' '^^^ 2007; 37 (6); 649-682KCVICW MKII LC 0112-16d2/07/0008O669/S44.P5/0 2007 Adis Data Information BV. A ll r ig ti ts reserved .

Thermoregulation during Exercise inthe HeatStrategies for Maintaining Health and PerformanceDaniel YJendt}'^Luc J.C. van Loon^'^ a n d Wouter D. van Marken LichtenbeW^1 Dep artmen t of M ovement Sciences, Nu trition and Toxicology Research Institute Maastricht(NUTRIM), M aastricht U niversity, Maastricht, The N etherlan ds2 Dep artme nt of Hu m an Biology, Nu trition and Toxicology Research Institute Maastricht(NUTRIM), Maastricht University, Maastricht, The Netherlands

ContentsAb st ract 6691. Heat Exchange 6702. Physiology of Temperature Regulat ion 6712.1 The Role af the Hypafhalam us 671

2.2 Cutane ous Va sad i la t ion 6712.3 Sweating 6723. Factors Inf luen cing Thermo reguiat ion 6733.1 The Environm ent 6733.2 Dehydrat ion 6734. Heat iiiness 6735. interve ntion S trategies for Exercise in the Heat 6745.1 Whoie-Body P recooi ing 6755.2 Hyperhydrat ion 6755.3 Ciothing 6755.4 Heat Acci ima t isat ion 6765.5 P ract ica i Recom m end at ions for Heat Accl ima t isat ion 6765.6 Rehydraf ion 6775.7 P ract ica i Recom m end at ions for Rehydrat ion 6796. Conciusion 680

Abstract A S a result of the inefficiency of metabolic transfer, >75% of the energy that isgenerated hy skeletal muscle suhstrate oxidation is liberated asheat. Duringexercise, several powerful physiological mechanism s of heat loss are activated toprevent an excessive rise in body core temperature. However, ahot and humidenvironment can significantly add to the challenge that physical exercise imposeson the human thermoregulatory system, as heat exchange between body andenvironment is substantially impaired under these conditions. This can lead to


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acclimatisation, the temperature thresholds for both cutaneous vasodilation andthe onset of sweating are lowered, which, in combination with plasma volumeexpansion, improve cardiovascular stability. Effective nutritional interventionsinclude the optimisation of hydration status by the use of fluid replacementbeverages. The latter should contain moderate amounts of glucose and sodium,which improve both water absorption and retention.

It has been well established that exercise in theheat, especially if there is high humidity, can ad-versely affect performance and may even result inserious heat illness, such as heat exhaustion and heatstroke. Nevertheless, major championship eventsare often scheduled for the hottest part of the dayduring the summer. This article focuses on theproblems associated with exercise in the heat andthe strategies that athletes can use to minimise theimpact of environmental conditions on perform-ance. To provide the reader with a basic understand-ing of human thermoregulation, sections 1 and 2 ofthis article will describe heat transfer within thebody, heat exchange between the body and the envi-ronment, and the physiological mechanisms thatpromote heat loss.

1. Heat ExchangeDuring exercise, the release of energy as heat andthe concomitant rise in body core tem perature evoke

powerful physiological mechanism s to promote heatloss. However, for heat loss to occur, excess heatshould first be transported from the core to the skinwhere heat can be lost to the environment.''' As aresult of its relatively low metabolic rate and con-stant blood flow, the temperature of inactive skeletalmuscle tends to be between 33C and 35C. Conse-quen tly, at rest, heat is actually transferred from coreto skeletal m uscle tissue. The latter changes dramat-ically with the onset of exercise when the increase inheat production causes the muscle temperature torise, leading to a reversal of the temperature gradientbetween muscle and arterial blood. Heat is nowtransferred down this gradient from muscle to blood

the overall skin conductan ce. The latter is the suma fixed conductance by passive conduction acrthe subcutaneous fat and a variable conductance convective heat transfer to the cutaneous circution.i^l The ability to modulate skin blood flotherefore, constitutes a powerful defence mecnism against hyperthermia and will be discussedmore detail in section 2.2. On ce the m etabolic heatransferred to the skin, there are various ways which it can be lost to the surrounding environm eincluding radiation, conduction, convection aevaporation. The different mechanisms by whiheat can be gained or lost are defined by the hbalance equation: metabolism radiation condution convection - evaporation = heat storage.'^

Radiation is the loss or gain of heat in the forminfrared heat rays. All objects that are not at absolzero temperature emit such rays. The human bosimultaneously emits and receives radiant heWhen the body tem perature is higher than that ofsurroundings, a greater quantity of heat radiafrom the body than to it. When a nude person at ris placed in a thermal comfortable room, radiatiaccoun ts for app roxim ately 60% of total h eat loss.The transfer of heat from a body to an object (or vversa) or within an organism down a thermal graent is called conduction. At a comfortable rootemperature, only 3% of total body heat loss occby this mechanism. Heat transfer via moving gasliquid is called convection. A small amount of covection almost always o ccurs because of the tendcy of the air surrounding the skin to rise asbecom es heated. Consequently, an individual wh oplaced in a thermal comfortable room without csiderable air movement still loses about 15% of


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Thermoregulation during Exercise in Heat 671

prises the loss of water through ventilation anddiffusion, and there are no control mechanisms thatgovern the rate of insensible water loss for thepurpose of temperature regulation. The loss of heatby the evaporation of sweat, on the other hand, canbe controlled by regulating the rate of sweating, andsweating rates of up to 3.5 L/hour have been report-ed in trained athletes. For every mL of water thatevaporates from the body surface, 2.43kJ of heat islost. At rest in a comfortable environment, about25% of heat loss is due to evaporation. Of course,these percentages change with the onset of exercise,especially when the ambient temperature approach-es or is higher than an individual's core tempera-

nisms tend to bring the body temperature back tothis 'set-point'.'^1 This regulated level of core tem-perature varies =1C as a result of the circadianrhythm of body tem perature and the influence of themenstrual cycle and body temperature distribu-

2. Physiology of Tem perature Regulation2.1 The Role of the HypotholamusWhen the metabolic heat is eventually transport-

ed to the skin, heat loss is greatly accelerated bycutaneous vasodilation and sweating. Several lesionand stimulation studies on the brain have identifiedthe hypothalamus as the neural structure with thehighest level of thermoregulatory integration. Inves-tigators recorded a large number of heat-sensitiveneurons and about one-third as many cold-sensitiveneurons in the preoptic and anterior nuclei of thehypothalamus.t^l These thermosensitive neurons ef-fectively monitor the temperature of the blood flow-ing to the brain and can thus detect changes in coretemperature. In addition to sensing changes incore temperature, the preoptic-anterior hypothala-mus also receives afferent sensory input from ther-moreceptors throughout the body, including the spi-nal cord, abdominal viscera, the greater veins andthe skin. In this w ay, the thermosensitive neurons inthe hypothalamus compare and integrate the centraland peripheral temperature information. As a result,the hypothalamus is able to initiate the thermoregu-latory response mo st appropriate for any given ther-mal stress.'^'^l The critical threshold temperature in

2.2 Cutaneou s Voso dilationThe ability of the human body to adjust thecutaneous vasomotor tone provides an effective

means of modulating skin blood flow (SkBF) andtherefore heat flux from core to skin. As such, thecutaneous circulation can act as a major effector ofthe thermoregulatory response, but is also affectedby non-thermoregulatory responses, such as thebaroreflex and adjustments to dynamic exercise.During exercise, vasomotor reflexes have the effectof redistributing blood flow away from inactivetissue so that additional blood flow is provided tomeet the increased metabolic demands of skeletalmuscle. When thermoregulatory and non-thermo-regulatory responses occur simultaneously, as theydo during exercise, the cutaneous circulation is sub-jected to conflicting demands.'"^ This is illustratedby the fact that, although the net response of SkBFto exercise is eventually one of vaso dilation, there isnoticeable constriction of the cutaneous blood ves-sels even in the presence of significant hyperthermiawith the onset of exercise. Furthermore, the eleva-tion of SkBF that accompanies a rise in body tem-perature during rest is delayed until a higher bodytemperature is reached during exercise. Finally, ex-ercise places a limit on the capacity of the skin todilate and when the internal temperature approaches38C , the increase in SkBF is attenuated.t'2-'^J Fromthese observations, it can be concluded that themagn itude of SkBF during exercise is determined bycompeting vasoconstrictor and vasodilator influ-ences.

The cutaneous circulation is controlled by twobranches of the sympathetic nervous system: anoradrenergic active vasoconstrictor system and an


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transmitter from cholinergic nerves is the primarymechanism of cutaneous active vasodilation. Al-though the precise mechanisms remain to be eluci-dated, it is clear that this system plays a vital role inthe control of SkBF as its activation can fully dilatecutaneous arterioles, increasing whole-body SkBFto levels approaching 8 L/min, or 60% of cardiacoutput during heat stress.''^' The fact that SkBF iscontrolled by two different branches of the sympa-thetic nervous system raises the question of whichpathway(s) actually sets the limitations of cutaneousvasodilation. In an attempt to separate the vasocon-strictor and vasodilator control of the cutaneousvasculature, a series of experiments was conductedthat used a combination of laser-Doppler flowmetryand the local iontophoresis of the anti-adrenergicagent bretylium tosylate.^"'^'^' This technique al-lows the selective blockade of the active vasocon-strictor system in a small area of skin without affect-ing the active vasodilator system. The observationthat the reductions in cutaneous vascular conduc-tance that are normally seen with the onset of exer-cise were completely abolished at the bretylium-treated sites led to the conclusion that the cutaneousvasoconstriction that accompanies the onset of exer-cise is solely mediated by an increased active vaso-constrictor tone.f"^ On the other hand, the exercise-induced elevation in the internal temperature thresh-old for cutaneous vasodilation appears to be theresult of a delayed vasodilator response b ecause theshifts in temperature threshold were identical bothwith and without vasoconstrictor system block-ade.'"^ The third non-thermoregulatory effect ofexercise on SkBF, the attenuation of the rate of risein SkBF during the later stages of prolonged dynam -ic exercise, is due to a similar attenuation of activevasodilator activity.t'^^

As mentioned earlier in this section, besides be-ing an efferent arm of the thermoregulatory re-sponse, SkBF is also known to respond to non-thermoregulatory responses, including baroreflexes.

sents a significant fraction of the total vascular coductance. To test the hypothesis that baroreceptunloading during dynamic exercise limits cutaneovasodilation, several investigators had subjects peform dynamic exercise with and without barorecetor unloading induced by lower body negative presure (LBNP).t'*-'5] During exercise with LBNP, tbody core temperature required to elicit cutaneovasodilation was significantly elevated, indicatithat SkBF responses during exercise can be modlated by baroreceptor unloading. The finding ththe limitation in cutaneous vasodilation was quickreversed when LBNP was removed clearly suppothe view of a neurally mediated interaction such the baroreflex instead of a time-dependent factsuch as a circulating vasoactive hormone.''^^

2.3 Sv\/eating

Activation of eccrine sweat glands causes sweto be secreted onto the skin surface, thereby proming heat loss by evaporation of the water content the sweat. These eccrine glands cover most of tbody and are innervated by sym pathetic cholinergnerve fibres. Cholinergic stimulation of the swegland elicits the secretion of a so-called precursfluid, the composition of which resembles that plasma, except that it does not contain the plasmproteins. Therefore, sodium chloride is the primaelectrolyte in sweat, with potassium, calcium amagnesium present in smaller amounts. As the prcursor fluid runs through the duct portion of tsweat gland, its composition is modified by actireabsorption of the sodium and chloride."''*' Asresult, sweat is hypotonic compared with plasmand sweat sodium concentration typically rangfrom 10 to 70 mm ol/L, whereas that of chloriranges from 5 to 60 mmol/L, depending on disweat rate and degree of heat acclimatisation.'^Athletes performing high-intensity exercise in t


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3. Factors Influencing Thermo regulafion3.1 The EnvironmentHeat loss by radiation and convection d epends onthe maintenance of a large temperature gradientbetween the skin and the surrounding air. When thetemperature of the air exceeds 36C , the gradient forheat exchange is reversed and the body now gainsheat by radiation and convection instead of losing it.Heat loss by evaporation of sweat then becom es theprimary means of heat dissipation. As sweat canonly be effective for cooling if it evaporates, thepotential for evaporative heat loss is determined bythe water vapour p ressure gradient between the skinand the environment and the movement of air overthe skin. This means that when the relative hum idityin the air is low (dry air), sweat will evaporaterelatively fast. On the other hand, if the relativehumidity of the surrounding air is high, the evapora-tion of sweat will be hindered and sweat will accu-

mulate with little loss of body heat.'^' Therefore,exercise in a hot, humid environment may requirelevels of evaporative heat loss that exceed the capac-ity of the environment to accommodate more watervapour, resulting in a critical heat load that limitsfurther exercise and increases the risk of developingheat3.2 Deh ydrationWhen sweating becomes the primary means ofheat dissipation, sweat loss must be matched by

fluid consumption to avoid dehydration. This isoften difficult because the stimulus to drink is notinitiated until an individual has incurred a waterdeficit of approximately 2% of body mass.'^' ' Con-sequently, when water intake during exercise in theheat is ad libitum, some dehydration is likely tooccur. The physical work capacity for aerobic exer-cise is reduced when a person is dehydrated bymarginal (1-2% total body water [TBW]) waterdeficits. Dehydration resulted in much larger decre-

reduced exercise performance mediated by a bodywater deficit. It has been shown that dehydrationreduces both skin blood flow and sweating re-sponses during exercise.'^'-^-'' Because sweat is hy-potonic compared w ith plasma, thermal dehydrationresults in a hyperosmotic, hypovolaemic condition.Therefore, both the singular and combined effects ofplasma hyperosmolality and hypovolaemia havebeen proposed to mediate the reduced heat losseffector responses.t^^' Although it has been shownthat both conditions can adversely affect thermoreg-ulation, core temperature responses are usually morestrongly correlated with tonicity than with bloodvolume.!^''! Several investigators have reported thathyperosmolality elevates core temperature by in-creasing the threshold temperature for both the initi-ation of skin vasodilation and sweating without af-fecting sensitivity (response per unit change in bodytemperature).l^^'^^'^*] These shifts in threshold tem-perature are often interpreted as indicative of a CNSchange in the thermoregulatory effector signal.Studies on single neurons in hypothalamic slicepreparations suggest that osmotic effects on thermo-regulation could be mediated by a direct influence ofextracellular fluid osmolality on thermosensitivecells as almost half of the thermosensitive neuronsdecrease their firing rates in a hypertonic medi-urr, [27,28] Besides affecting the CNS, tonicity couldalso exert a peripheral effect via a high interstitialosmotic pressure, which inhibits fluid availability tothe sweat gland.'^"*' When, during exercise, an ath-lete 's core tem perature is raised as a result of hot andhumid weather conditions or (severe) dehydration,there is an increased risk of developing heat illness.

4. Heaf IllnessIn the literature, three exercise-related heat ill-nesses are described: heat cramps, heat exhaustion

and heat stroke. The term 'heat cramps' stems fromthe original description of the condition by Tal-bot,f ^ who reported muscle cramping in personsperforming physical work in hot, humid environ-


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competitors. Two strategies that have proven to beparticularly effective in reducing health problemsand performance decrements associated with exer-cise in the heat are heat acclimatisation and rehydra-tion, and they are therefore given special attention.Some basic ou tlines of a number of additional strate-gies including whole-body precooiing, hyperhydra-tion and clothing selection are discussed in sections5.1-5.3.

5.1 Whole-Body PrecooiingA number of studies reported that subjects exer-

cising in the heat reached the point of voluntaryexhaustion at similar and consistent body core tem-peratures despite different starting core tempera-tures or rates of heat storage.''^^ Therefore, it hasbeen proposed that a critical body tem perature existsthat directly accelerates exhaustion. Although theunderlying mechanisms are not well understood,evidence is emerging that hyperthermia directly af-fects the functioning of the brain through alteringcerebral blood flow and metabolism and decreasingthe level of central cognitive or neuromusculardrive, which may in turn decrease muscle functionor a lter the percep tion of effort. ^ Given the p re-sumed im portance of body core temperature on elic-iting exhaustion, the basis of whole-body precooiingis to reduce the heat content of the body by coolingthe periphery before exercise, thereby increasing themargin for metabolic heat production and increasingthe time to reach the critical limiting temperaturewhen a given exercise intensity can no longer bemaintained. Whole-body precooiing can beachieved by a variety of m ethods, including cold aircooling, cold water immersion and the use of awater-cooled garment.'^'^ The current body of evi-dence suggests that precooiing is able to increasecapacity for prolonged exercise at various ambienttemperatures. However, regardless of the method

5.2 HyperhydrationThe observation that dehydration adversely af-

fects thermoregulation gave rise to the idea thatgreater than normal body water (hyperhydration)might have thermoregulatory advantages. Althoughmany studies have examined the effects of hyperhy-dration on thermoregulation in the heat, a largenumber have had serious design problems that con-found their results (e.g. the control condition repre-sents dehydration rather than euhydration). Someinvestigators reported lower core temperatures andhigher sweating rates during exercise afterhyperhydration, while others did not.'^" Althoughhyperhydration was often induced by having sub-jects overdrink plain water, it is now thought thatglycerol solutions are more effective as a hyperhy-drating agent as they reduce the rate of eliminationof water.f""' Lyons et al.''*^l gave subjects 2L of waterwith and without glycerol over a 2.5-hour periodprior to treadmill walking in a hot, dry environm ent.Compared with the water trial, glycerol ingestionshowed a substantially lower core temperature(0.7C), a reduction in urine output and a highersweating rate (33%). Montner et al.t''^^ reported thatglycerol hyperhydration increased exercise time-to-exhaustion in temperate climates, but found no sig-nificant thermoregulatory advantages. These resultsare in accordance with a study by Latzka et al.,'''^)who found that glycerol hyperhydration extendedendurance time (from 30 to 34 minutes) in subjectsexposed to unco mp ensable heat stress, but that it hadno beneficial effect on thermoregulation comparedwith maintenance of euhydration. In summ ary, thereare some indications that hyperhydration reducesthermal strain during exercise, but data supportingthis notion are not very robust.

5.3 ClothingThe type and am ount of clothing worn can have a

major impact on heat dissipation during exercise.f'* ^Clothing generally represents a layer of insulationthat imposes a barrier to heat transfer from the skin


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efficiency are observed.t"**^ Considering that evapo-ration of sweat is the most important mechanism ofheat loss during exercise in the heat, clothing thatposes the least amount of resistance to evaporationmay prove beneficial. In practice, this would meanrelatively m inimal clothing, which can range from abasic swimsuit to a short-sleeve t-shirt and mid-thigh shorts. For a more detailed description of therelationship between clothing and thermoregu lation,the reader is directed to a review by Gavin.^^'

5.4 Heat AcclimatisationIt has been well established that regular exposure

to hot environments results in a number of physio-logical adaptations that reduce the negative effectsassociated with exercise in the heat. These adapta-tions include a decreased body core temperature atrest, decreased heart rate during exercise, increasedsweat rate and sweat sensitivity, decreased sodiumlosses in sweat and urine, and an expanded plasmavolume (PV).['''l The effect of acclimatisation on PVis extremely important in terms of cardiovascularstability as it allows for a greater stroke volume anda lowering of the heart rate. There remains somedebate whether the expansion of PV is selective orrather refiects a generalised expansion of the ex-tracellular fiuid volume (ECF).'''*^ Recently, Patter-son et al.''*' tried to solve this uncertainty by simu l-taneously measuring PV, ECF, interstitial fiuid vol-ume (ISF) and TBW in subjects that followed anexercise-heat acclimatisation protocol. They report-ed a simultaneous exp ansion of the resting PV , EC F,ISF and TBW following either short- or long-termheat acclimatisation and concluded that the increasein PV is part of a ubiquitous expansion of the entireECF. The mechanism for the expansion of ECF andthe subsequent increase in PV remains speculative;however, it has been suggested that the infiux ofprotein from the cutaneous interstitial space to thevascular compartments causes an elevated colloid-osmotic pressure that will draw fluid into the in-travascular compartment, thereby inducing a selec-

exhibited similar relative expansions and thatgeneralised ECF expansion was the primary mecnism for the PV enlargement. Therefore, it is pposed that electrolyte retention, rather than the fiux of protein, mediates the early PV expansiThere is indirect evidence from the literature support this view, for example, the observation tacclimatisation-induced PV expansions are reducin subjects who are fed a low-salt diet comparwith subjects receiving a moderate- or high-sdiet.'^^l A close relationship has also been observbetween dietary sodium intake and the PV expsion that occurred in response to 3 days of endurancycling.^"] Furthermore, when spironolactone, aldosterone inhibitor, was administered to subjeduring endurance training, the exercise-induced expansion was also restricted.'^-^l Therefore, it cowell be that elevated plasma aldosterone levepossibly in combination with other fiuid-regulathormones, result in an increased sodium and waretention by the kidney after heat acclimatisation.Moreover, it is well established that heat accmatisation improves the reabsorption of sodifrom sweat, resulting in a greater amount of solremaining in the plasma. This will result in a fiushift from the intra- to the extracellular compament, thereby causing a better maintenance PV.[20] Another consistent finding after heat acmatisation is the lowering of the temperature threolds for both sweating and cutaneous vasodilatwithout the occurrence of a significant change in slope of the relations. It is postulated that reguexposure to high temperatures results in a lowerof the set-points in the hypothalamus at whsweating and vasodilation are initiated.'^'"

5.5 Practical Recommendations forHeat AcclimatisationThe process of acclimatisation to exercise in

heat begins within a few days, and full adaptattakes 7-1 4 days for m ost individuals. It is clear frtable I that the systems of the human body adap


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Table I. Range of days required for different adaptations to occurduring fieat acciimatisationAdaptation Days of heat

acciimatisationDecrease in heart rate during exercise 3- 6Plasma volume expansion 3-6Decrease in sweat Na+ and C|- 5-1 0concentrationsincrease in sweat rate and sweat sensitivity 7-1 4increase in cutaneous vasodilation 7-14

cular function through an expansion of PV and areduction in heart rate. An increase in sweat rate andcutaneous vasodilation are seen during the laterstages of heat acclimatisation.^'''l

Endurance-trained athletes exhibit many of thecharacteristics of heat-acclimatised individuals andare therefore thought to be partially ad apted; how ev-er, full adaptation is not seen until at least a week isspent training in the heat.'^^' It is not necessary totrain every day in the heat, as it has been shown thatexercising in the heat every third day for 30 daysresults in the same degree of acclimatisation asexercising every day for 10 days.'^^^ As the mainte-nance of an elevated body core temperature and thestimulation of sweating appear to be the criticalstimuli for optimal heat acclimatisation, it has beenrecommended that strenuous interval training orcontinuous exercise should be performed at an in-tensity exceeding 50% of an athlete's maximal oxy-gen u ptake . I""' There is ev idence that exercise b outsof about 100 minutes are most effective for theinduction of heat acclimatisation and that there is noadvantage in spending longer periods exercising inthe heat.I^^l Unfortunately, heat acclimatisation is atransient process and will gradually disappear if notmaintained by repeated exercise-heat exposure. Itappears that the first physiological adaptations tooccur during heat acclimatisation are also the first tobe lost.['"J There is considerable variability in theresults of studies concerning the rate of decay ofheat acclimatisation, as some authors report signifi-cant losses of heat acclimatisation in less than a

matisation is better retained than humid-heat accli-matisation and that high levels of aerobic fitness arealso associated with a greater retention of heat accli-matisation.'^^'5.6 RehydrationAlthough athletes may be tempted to believe thatthe need for fluid replacement will decrease as theybecome adjusted to the heat, heat acclimatisationwill actually increase the requirement for fiuid re-

placement because of the earlier onset of sweat-ing.l*''' In addition, core temperature responses afterdehydration are the same for unacclimatised andacclimatised individuals, indicating that the advan-tages conferred by heat acclimatisation are abol-ished by dehydration.12'1 Rehydration during exer-cise in the heat should therefore be made a clearpriority. However, there is little agreement on theformulation of an optimal fiuid replacement bever-age. Factors that influence the effectiveness of abeverage as a fiuid replacement include its rate ofgastric emptying, intestinal absorption and how wellthe fiuids are retained in the intra- and extracellularfiuid compartments.''^'

The rate of gastric emptying is closely related togastric volume. The larger the volume consumed,the greater the gastric emptying rate, up to at least600m L. Therefore, when a high rate of gastric emp-tying is desirable, this can be accomplished by keep-ing gastric volume high by repeated drinking.f^^lHow ever, this volume effect can be overruled by thechemical composition of a drink. For example, theaddition of carbohydrate to sports drinks can slowthe rate of gastric emptying by its effect on energycontent and osmolality, which are believed to exerttheir control of gastric emptying via the activity ofreceptors in the small intestine.'*"' In an attempt todetermine the separate effects of osmolality andenergy content on gastric emptying, investigatorsused mixtures of free glucose and glucose polymersso that they could vary energy density and osm olali-ty independently. The results of this study clearly


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different rates, but where the energy content wassimilar, even large differences in osmolality hadrelatively little effect on the emptying rate.'*"

Once the gastric contents are emptied into thesmall intestine, fiuids must be absorbed before anybeneficial effects of rehydration can occur. Absorp-tion of water is mainly a passive process caused bythe creation of local osmotic gradients that promotenet movement of water out of the intestinal lumen.Most sports drinks contain moderate amounts ofcarbohydrate, which, besides providing an energysource for the working muscles, will improve waterabsorption by producing favourable osmotic gradi-ents.'*^' Glucose and sodium are absorbed by a com -mon membrane carrier in the brush border of theproximal small intestine and this carrier appears totransport two sodium molecules for each moleculeof glucose. The transport of glucose and sodium intothe cell via this membrane carrier mechanism andthe subsequent extrusion of sodium by the Na+-K+pump in the basolateral membrane produces theosmotic gradient for fiuid absorption.'*^'

On the basis of the role of sodium in activenutrient transport, it might be hypothesised that theaddition of sodium in sports drinks will improve theabsorption of water and glucose by activating agreater number of intestinal carrier proteins. How-ever, a study by Gisolfi et al.'^*' showed that theaddition of sodium in concentrations of 0, 25 and 50mmol/L in a 6% carbohydrate solution producedsimilar effects on the absorption of water, sodiumand glucose in the duodenum. It seems that theglucose in the solution was the more importantfactor for enhancing intestinal water absorptioncompared with plain water, as glucose alone wasjus t as effective as glucose plus sodium. An explana-tion for this lack of effect comes from the observa-tion that within only 10cm of the duodenum , intesti-nal and perhaps pancreatic secretions produce aluminal sodium concentration of 40 mmol/L, whichis twice the amount included in most sportsdrinks.'^*' Furthermore, in addition to transcellular

are transported by a process known as 'solutidrag' through the paracellular pathway. Resufrom an animal model suggest that the presence glucose in the intestinal lumen opens the tight juntions between brush border cells by activating ctoskeletal elements within the enterocyte.'*^' Tpermits maximal uptake of fiuid and solutes, espcially when glucose concentrations are well abothose required to saturate the membrane carrier.'*

Although the study by Gisolfi and Duchman'showed that sodium up to 50 mmol/L in a 6carbohydrate solution did not significantly alter fid or glucose absorption, there are other considetions for the inclusion of sodium in sports drinFirst, moderate amounts of sodium will impropalatability for most individuals, which increavoluntary consumption. More importantly, the adtion of sodium to a fiuid replacement beverage wdramatically improve the retention of water afexercise-induced dehydration. This is especially iportant in events where athletes have to perforepeated bouts of exercise. The importance of addition of sodium to rehydration beverages been systematically evaluated by Maughan aLeiper.'**' They dehydrated subjects by equivalent of 2% of body mass by intermittent excise in the heat after which the subjects had to inga test drink w ith a volume equal to 150% of the filost. These test drinks contained sodium 0, 2 5, 50100 mmol/L. It was evident that urine output in hours after exercise was inversely proportionalthe sodium content of the ingested fiuid. The sjects only remained in positive fiuid balance whthe amount of sodium in the test drink exceededmm ol/L. These results w ere confirmed in a studyShirreffs et al.'*^' who showed that even whenvolume equal to twice the amount lost in sweaingested, subjects could not remain in po sitive fibalance when a low sodium drink (23 mmol/L) wconsumed. A positive fiuid balance was eventuamaintained when drinks containing 61 mmol/Lsodium were consumed in amounts >] .5 times


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5.7 Practical Recommendationsfor RehydrationTo maintain adequate hydration, it is generally

recommended that athletes consume fluids at a ratethat closely matches their loss of water throughswea ting and urine losses.'^^^ This generally requiresthe ingestion of 200-300mL of fluid every 10-20minutes.'^" However, as it takes 20-30 minutes foringested fluids to he distrihuted throughout the bodyafter gastric emptying, intestinal absorption and os-motic flow, the beneficial effects of fluid intakeduring events lasting 30 minutes are advised to drink200-300mL of their preferred sports drink justbefore exercise and to continue drinking the samesports drink throughout the event until there are 20minutes remaining, after which little extra fluid isingested. As mentioned in section 5.6, an importantfactor with regard to the effectiveness of a sportsdrink is its rate of gastric emptying and maintaining400-600mL of fluid in the stomach will optimisegastric emptying.t''^' However, drinking highervolumes of fluid can negatively affect performancebecause of the time lost in obtaining and drinkingmore fluid together with gastric discomfort that maybe encountered. Therefore, from a performancepoint of view, athletes may allow themselves todrink less than what is needed for full rehydrationand finish with up to 2% of body m ass loss. How ev-er, when safety is the main concern, there is noquestion that the closer the rate of drinking canmatch the rate of dehydration, the better.'^'^

Although it is clear that the addition of carbohy-drate to a sports drink can improve intestinal waterabsorption, there clearly appears to be an upp er limitto the amount of carbohydrate that can be addedwithout limiting fiuid availability. Sports drinks thatcontain >7% carbohydrate are associated with a

Table II. Overview of principles regarding heat acciimatisalion andrehydrationHeat acclimatisationFuil adaptation takes 7-14d to be completedHeat acciimatisation is best achieved by strenuous intervaltraining or continuous exercise at 550% ot maximai oxygenuptal


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A commonly used and safe technique to deter-mine the acute loss of body water is the measure-ment of body mass change. The loss of body massover the course of exercise essentially equals waterloss because no other body constituent is lost at sucha high rate. When body mass measurements aremade with an interval of >4 hours, the body massdifference should be corrected for the net utilisationof endogenous glycogen and fat stores.''^! Table IIsummarises some basic principles regarding heatacclimatisation and rehydration.

6. ConclusionDuring exercise, large amounts of energy are

liberated as heat. To prevent a continuous rise inbody core temperature, physiological mechanismssuch as cutaneous vasodilation and sweating areactivated to promo te the loss of excess heat. How ev-er, several factors such as a hot and humid environ-ment and thermal dehydration can negatively influ-ence thermoregulation and may even result in seri-ous heat illness. Fortunately, athletes can minimisethe risks associated with exercise in the heat throughheat acclimatisation and rehydration. The completeprocess of heat acclimatisation takes 7-14 days formost individuals. Strenuous interval training or pro-longed moderate intensity exercise in the heat seemto be most effective in promoting heat acclimatisa-tion. With respect to rehydration, it is recomm endedthat athletes consume fluids at a rate that closelymatches sweat and urine losses. This generally re-quires the ingestion of 200-300mL of fluid every10-20 minutes, starting just before exercise andcontinuing until 20 minutes of exercise are remain-ing. It has been shown that the addition of carbohy-drate solutions (


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2005; 63 : S40-54C o r res p o n d en ce : Dr Wouter D. van Marken Lichtenbelt, Dpartment of Human Biology, Maastricht UniversiPO Box 616, Maastricht, 6200 MD , The N etherlan ds.E-mail: [email protected]


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