glucose e frutose durante exercicio fisico

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96:1277-1284, 2004. First published Dec 2, 2003; doi:10.1152/japplphysiol.00974.2003 J Appl PhysiolAsker E. JeukendrupRoy L. P. G. Jentjens, Luke Moseley, Rosemary H. Waring, Leslie K. Harding and

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Oxidation of combined ingestion of glucose and fructose during exercise

Roy L. P. G. Jentjens, 1 Luke Moseley, 1 Rosemary H. Waring, 2 Leslie K. Harding, 3 andAsker E. Jeukendrup 11 Human Performance Laboratory, School of Sport and Exercise Sciences, and 2 Schoolof Biosciences, University of Birmingham, Birmingham B15 2TT; and 3 Physics and Nuclear Medicine Department, City Hospital, Birmingham B18 7QH, United Kingdom

Submitted 9 September 2003; accepted in nal form 3 November 2003

Jentjens, Roy L. P. G., Luke Moseley, Rosemary H. Waring,Leslie K. Harding, and Asker E. Jeukendrup. Oxidation of com-bined ingestion of glucose and fructose during exercise. J ApplPhysiol 96: 12771284, 2004. First published December 2, 2003;10.1152/japplphysiol.00974.2003.The purpose of the present studywas to examine whether combined ingestion of a large amount of fructose and glucose during cycling exercise would lead to exogenouscarbohydrate oxidation rates 1 g/min. Eight trained cyclists (maxi-mal O 2 consumption: 62 3 ml kg 1 min 1 ) performed four exer-cise trials in random order. Each trial consisted of 120 min of cyclingat 50% maximum power output (63 2% maximal O 2 consumption),while subjects received a solution providing either 1.2 g/min of glucose (Med-Glu), 1.8 g/min of glucose (High-Glu), 0.6 g/min of fructose 1.2 g/min of glucose (Fruc Glu), or water. The ingestedfructose was labeled with [U- 13 C]fructose, and the ingested glucosewas labeled with [U- 14 C]glucose. Peak exogenous carbohydrate oxi-dation rates were 55% higher ( P 0.001) in Fruc Glu (1.260.07 g/min) compared with Med-Glu and High-Glu (0.80 0.04 and0.83 0.05 g/min, respectively). Furthermore, the average exogenouscarbohydrate oxidation rates over the 60- to 120-min exercise periodwere higher ( P 0.001) in Fruc Glu compared with Med-Glu andHigh-Glu (1.16 0.06, 0.75 0.04, and 0.75 0.04 g/min,respectively). There was a trend toward a lower endogenous carbo-hydrate oxidation in Fruc Glu compared with the other two carbo-hydrate trials, but this failed to reach statistical signicance ( P0.075). The present results demonstrate that, when fructose andglucose are ingested simultaneously at high rates during cyclingexercise, exogenous carbohydrate oxidation rates can reach peak values of 1.3 g/min.

substrate utilization; carbohydrate absorption; isotopic tracers; metab-olism

IT HAS BEEN SHOWN THAT CARBOHYDRATE (CHO) feedings duringprolonged moderate- to high-intensity exercise can postponefatigue and enhance exercise performance when the exerciseduration is 45 min or longer (2, 17, 41). The observedimprovements in performance with CHO ingestion have con-tributed to better maintenance of plasma glucose concentra-

tions and high rates of CHO oxidation late in exercise (3, 5),when muscle and liver glycogen levels are low.Studies that have used either stable (16, 21, 29, 36, 40) or

radioactive isotopes (3, 11) to quantify exogenous CHO oxi-dation during exercise have found peak oxidation rates of 1g/min (for review, see Refs. 10, 18, 21). Even when CHO wasingested at high rates (up to 3.0 g/min), oxidation rates did notexceed 1 g/min (16, 21, 29, 36, 40). In most of the above-citedstudies, glucose or glucose polymer was the type of CHO

ingested. Although direct evidence is lacking, it has beensuggested that the absorption capacity of glucose in the intes-tine (31) is a limiting factor for the oxidation of ingestedglucose (18, 21).

A number of studies have compared the oxidation rates of various types of ingested CHO with the oxidation of exogenousglucose during exercise (for review, see Ref. 18). From thesestudies, it appears that the rate of oxidation of ingested maltose(11), sucrose (27, 40), glucose polymer (26), and maltodextrin(32) is fairly similar to the oxidation rate of ingested glucose.However, signicantly lower exogenous CHO oxidation rateshave been reported for fructose ( 2025% lower) (1, 15, 25,26) and galactose ( 50% lower) (23) compared with glucose.There have been suggestions that the lower oxidation rate of fructose is due to a lower rate of absorption (1, 18). Further-more, both fructose and galactose have to be converted intoglucose in the liver before they can be oxidized, and this mayslow down the rate of oxidation.

Intestinal transport of glucose occurs via a sodium-depen-dent glucose transporter (SGLT1), which is located in thebrush-border membrane (8). It is likely that SGLT1-transport-ers are saturated at a glucose ingestion rate of 1 g/min, whichcould explain why higher glucose intake rates do not result in

oxidation rates higher than 1.01.1 g/min (21, 40). In contrastto glucose, fructose is absorbed from the intestine by GLUT-5,a sodium-independent facilitative fructose transporter (4, 8). Itis not unlikely that, when a mixture of glucose and fructose isingested, there is less competition for absorption comparedwith the ingestion of an isoenergetic amount of glucose (orfructose), and this may increase the availability of CHO intothe bloodstream for oxidation.

To our knowledge, only two studies have attempted toinvestigate the oxidation of combined ingestion of glucose andfructose (1, 33). The results of these studies are contradictory,which might be due to differences in study design or subjectselection. Riddell et al. (33) studied 12 children who ingested67.5 g of a mixture of glucose and fructose or an isoenergetic

amount of glucose during 90 min of exercise at 55% maximalO2 consumption (V O2 max ). No difference was found in exog-enous CHO oxidation between the two CHO trials, and peak oxidation rates did not exceed 0.36 g/min. In a study by Adopoet al. (1), six trained subjects cycled for 120 min at 61%VO2 max while ingesting 100 g of glucose or fructose or amixture of 50 g glucose and fructose. The addition of fructoseto the glucose drink increased total exogenous CHO oxidationby 27% compared with the isoenergetic glucose drink (0.61 vs.

Address for reprint requests and other correspondence: A. E. Jeukendrup,School of Sport and Exercise Sciences, Univ. of Birmingham, Edgbaston, B152TT, Birmingham, UK (E-mail: [email protected]).

The costs of publication of this article were defrayed in part by the paymentof page charges. The article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

J Appl Physiol 96: 12771284, 2004.First published December 2, 2003; 10.1152/japplphysiol.00974.2003.

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0.48 g/min). It should be noted that the amounts of CHOingested in the study of Adopo et al. were relatively small( 0.8 g/min), and, therefore, glucose (and fructose) transport-ers were probably not fully saturated. At present, there are nostudies available in the literature that have investigated whethercombined ingestion of large amounts of glucose and fructosecan result in exogenous CHO oxidation rates that exceed 1g/min. Furthermore, in the study of Adopo et al., it was notpossible to determine the oxidation rate of both glucose andfructose in one trial, because only one of the ingested CHO wasisotopically labeled. To measure the total oxidation rate of theingested glucose plus fructose mixture, two separate trials wereperformed, and this may have confounded the results.

We hypothesized that combined ingestion of a large amountof fructose (72 g) and glucose (144 g) during 2 h of exercisewould lead to exogenous CHO oxidation rates higher than 1g/min. The ingested fructose was labeled with [U- 13 C]fructose,and the ingested glucose was labeled with [U- 14 C]glucose,which enabled us to measure the oxidation rates of glucose andfructose when ingested simultaneously.

METHODS

Subjects. Eight trained male cyclists or triathletes, aged 29.0 2.7yr and with a body mass of 75.1 1.8 kg, took part in this study.Before participation, each of the subjects was fully informed of thepurpose and risks associated with the procedures, and a written,informed consent was obtained. All subjects were healthy, as assessedby a general health questionnaire. The study was approved by theSouth Birmingham Local Research Ethics Committee and the UKadministration of Radioactive Substance Advisory Committee.

Preliminary testing. At least 1 wk before the start of the experi-mental trials, an incremental cycle exercise test to volitional exhaus-tion was performed to determine the individual maximum poweroutput (W max) and V O2 max . This test was performed on an electro-magnetically braked cycle ergometer (Lode Excalibur Sport, Gro-ningen, The Netherlands), modi ed to the con guration of a racingbicycle with adjustable saddle height and handlebar position. After thesubjects reported to the laboratory, body mass (Seca Alpha, Hamburg,Germany) and height were recorded. Subjects then started cycling at95 W for 3 min, followed by incremental steps of 35 W every 3 minuntil exhaustion. Heart rate (HR) was recorded continuously by aradiotelemetry HR monitor (Polar Vantage, Kempele, Finland).Wmax was calculated from the last completed work rate, plus thefraction of time spent in the nal, noncompleted work rate, multipliedby the work rate increment. The results were used to determine thework rate corresponding to 50% W max, which was later employed inthe experimental exercise trials. Breath-by-breath measurements wereperformed throughout exercise by using an online automated gasanalysis system (Oxycon Alpha, Jaeger, Wuerzberg, Germany). Thevolume sensor was calibrated by using a 3-liter calibration syringe,and the gas analyzers were calibrated by using a 5.03% CO 2-94.97%N2 gas mixture. Oxygen consumption (V O2) was considered to bemaximal (V O2 max ) when at least two of the three following criteriawere met: 1) a leveling off of V O2 with increasing workload (increaseof no more than 2 ml kg 1 min 1), 2) a HR within 10 beats/min of predicted maximum (HR 220 minus age), and 3) a respiratory ex-change ratio (RER) 1.05. V O2 max was calculated as the averageoxygen uptake over the last 60 s of the test. The V O2 max and W maxachieved during the incremental exercise test were 62 3ml kg 1 min 1 and 374 12 W, respectively.

Experimental design. Each subject performed four exercise trials,which consisted of 120 min of cycling at 50% W max, while ingestingan 8.7% glucose drink (Med-Glu), a 13.1% glucose drink (High-Glu),an isoenergetic fructose plus glucose drink (Fruc Glu) (the ingested

fructose-to-glucose ratio was 1:2), or plain water (Wat). To quantifyexogenous CHO oxidation, the ingested fructose was enriched with[U- 13 C]fructose, and the ingested glucose was labeled with[U- 14 C]glucose. The order of the experimental drinks was counter-balanced in a crossover design. Experimental trials were separated byat least 7 days.

Diet and activity before testing. Subjects were asked to record theirfood intake and activity pattern 2 days before the rst exercise trialand were then instructed to follow the same diet and exercise activitiesbefore the other three trials. In addition, 5 7 days before eachexperimental testing day, they were asked to perform an intensetraining session ( glycogen-depleting exercise bout) in an attempt toempty any 13 C-enriched glycogen stores. Subjects were further in-structed not to consume any food products with a high naturalabundance of 13 C (CHO derived from C4 plants: corn, sugar cane) atleast 1 wk before and during the entire experimental period to reducethe background shift (change in 13 CO 2 ) from endogenous substratestores.

Protocol. Subjects reported to the Human Performance Laboratoryin the morning (between 7:00 and 9:00 AM) after an overnight fast(10 12 h) and having refrained from any strenuous activity or drink-ing any alcohol in the previous 24 h. For a given subject, all trials

were conducted at the same time of the day to avoid any in uence of circadian variance. On arrival in the laboratory, a exible 21-gaugeTe on catheter (Quickcath, Baxter BV, Norfolk, UK) was inserted inan antecubital vein of an arm and attached to a three-way stopcock (Sims Portex, Kingsmead, UK) to allow for repeated blood samplingduring exercise. The catheter was kept patent by ushing with 1.0 1.5ml of isotonic saline (0.9% Baxter) after each blood sample collection.After voiding, subjects were weighed in cycling shorts to the nearest0.1 kg by using a platform scale (Seca Alpha, Hamburg, Germany).

The subjects then mounted a cycle ergometer, and a resting breathsample was collected in 10-ml Exetainer tubes (Labco Brow Works,High Wycombe, UK), which were lled directly from a mixingchamber in duplicate to determine the 13 C-to- 12 C ratio ( 13 C/ 12 C) inthe expired air. A second resting breath sample was collected for laterdetermination of 14 CO 2-speci c activity. The expired air of each

second breath sample was collected in a 6-liter anesthetic gas bag byusing a two-way Hans Rudolph valve and subsequently passedthrough a CO 2 trapping solution, containing 1 ml of hyamine hydrox-ide in 1 M methanol (Zinsser Analytic, Berkshire, UK), 2 ml of 96%ethanol (BDH Laboratory Supplies, Poole, UK), and one to two dropsof phenolphthalein (Riedel-de Hae n, Seeize, Germany). The expiredair was bubbled for 2 3 min through the pink-colored CO 2 trappingmixture until the solution became clear, at which point exactly 1 mmolof CO 2 was trapped (37). Seventeen milliliters of liquid scintillationcocktail (Ready Gel, Beckman Coulter, High Wycombe, UK) wasthen added to the solution, and 14 CO 2 radioactivity in disintegrations/ min (dpm, later converted to dpm/mmol) was subsequently counted ina liquid scintillation counter (Beckman, LS 1800).

Next, a resting blood sample (10 ml) was taken and stored on iceuntil centrifugation. Subjects then started a 120-min exercise bout at

a work rate equivalent to 50% W max (63 2% V O2 max ). Additionalblood samples were drawn at 15-min intervals during exercise. Ex-pired breath samples were collected every 15 min until the end of exercise. V O2 , carbon dioxide production (V CO2), and RER weremeasured every 15 min for periods of 4 min by using an onlineautomated gas analysis system, as previously described.

During the rst 3 min of exercise, subjects drank an initial bolus(600 ml) of one of the four experimental drinks: Med-Glu, High-Glu,Fruc Glu, or Wat. Thereafter, every 15 min, a beverage volume of 150 ml was provided. The total uid provided during the 120-minexercise bout was 1.65 liters. The average rate of glucose intake in theMed-Glu and High-Glu trial was 1.2 and 1.8 g/min, respectively. Inthe Fruc Glu trial, subjects ingested, on average, 0.6 and 1.2 g/minof fructose and glucose, respectively.

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Subjects were asked every 30 min to ll in a questionnaire to rate(possible) gastrointestinal (GI) problems. Immediately after exercise,subjects voided and were weighed again wearing cycling shorts only.All exercise tests were performed under normal and standard envi-ronmental conditions (20 23C dry bulb temperature and 50 60%relative humidity). During the exercise trials, subjects were cooledwith standing oor fans in order minimize thermal stress.

Experimental drinks. The fructose used in the Fruc Glu trial wasa corn-derived crystalline fructose (Krystar 300, A. E. Staley Manu-facturing), which has a high natural abundance of 13 C [ 11.9 vs.Pee Dee Bellemnitella (PDB)]. To increase the 13 C content of thefructose even further, a trace amount of uniformly labeled 13 Cfructose was added { 0.083 g [U- 13 C]fructose/l ( 99%; CambridgeIsotope Laboratories)}. The fructose provided to the subjects in theFruc Glu trial had a 13 C enrichment of 134.7 vs. PDB. The 13 Cenrichment of the corn-derived fructose and the experimental fructosesolution was determined by elemental analyzer-isotope ratio massspectrometry (Europa Scienti c GEO 20 20, Crewe, UK).

In all three CHO trials, a wheat-derived glucose (Amylum, London,UK) was used that has a 13 C enrichment of 27.5 vs. PDB. Theglucose ( fructose) beverages were labeled with a trace amount of 0.45 MBq [U- 14 C]glucose/l (Amersham Pharmacia Biotech, LittleChalfont, UK), leading to a dose rate of 0.37 MBq/h. Furthermore, toall drinks, 20 mmol/l of sodium chloride were added to stimulate uidabsorption.

Questionnaires. Subjects were asked to ll out a short question-naire every 30 min during the exercise trials. The questionnairecontained questions regarding the presence of GI problems at thatmoment and addressed the following complaints: stomach problems,GI cramping, bloated feeling, diarrhea, nausea, dizziness, headache,belching, vomiting, and urge to urinate or defecate. While subjectswere on the cycle ergometer and continued their exercise, eachquestion was answered by simply ticking a box on the questionnairethat corresponded to the severity of the GI problem addressed. Theitems were scored on a 10-point scale (1 not at all, 10 very, verymuch). The severity of the GI symptoms was divided into twocategories, severe and nonsevere symptoms, as was previously de-scribed by Jeukendrup et al. (20). Severe complaints included nausea,stomach problems, bloated feeling, diarrhea, urge to vomit, andstomach and intestinal cramps, because these are symptoms thatcommonly impair performance and may bring with them health risks.The above symptoms were only registered as severe symptoms whena score of 5 out of 10 was reported. When a score 5 was given,they were registered as nonsevere. All other symptoms were regis-tered as nonsevere, regardless of the score reported.

Analyses. Blood samples were collected into prechilled tubes con-taining potassium oxalate and sodium uoride (Beckton Dickinson,Plymouth, UK) and were centrifuged at 2,300 g and 4 C for 10 min.Aliquots of plasma were immediately frozen in liquid nitrogen andstored at 70C until analyses of glucose and lactate. Glucose(glucose HK kit, Sigma-Aldrich, Dorset, UK) and lactate (lactate kit,Sigma-Aldrich) were analyzed on a COBAS BIO semiautomaticanalyzer (La Roche, Basel, Switzerland).

Breath samples were analyzed for 13 C/ 12 C by gas chromatographycontinuous ow isotope ratio mass spectrometry (Europa Scienti c,Crewe, UK). Furthermore, a second series of breath samples wasmeasured for 14 CO 2 radioactivity. These breath samples were countedfor 10 min in a liquid scintillation counter, and all counts werecorrected for differences in quench and background. From indirectcalorimetry (V O2 and V CO 2), stable isotope measurements (breath13 CO 2 / 12 CO 2), and radioactive isotope measurements (breath 14 CO 2activity), oxidation rates of total fat, total CHO, and exogenousglucose and fructose were calculated.

Calculations. From V CO2 and V O2 (l/min), total CHO and fatoxidation rates (g/min) were calculated by using stoichiometric equa-tions of Frayn (9), with the assumption that protein oxidation duringexercise was negligible

CHO oxidation 4.55 V CO 2 3.21 V O2 (1)

Fat oxidation 1.67 V O2 1.67 V CO2 (2)

In the Med-Glu and High-Glu trials, the rate of exogenous glucoseoxidation (EGO) was calculated from the following equation

EGO VCO 214CO 2 6

SA Glu

1

k (3)

where 14 CO 2 is the radioactivity of 1 mmol of expired CO 2 (dpm/ mmol) multiplied by 6, because there are 6 carbon atoms per moleculeof [U- 14 C]glucose; SA Glu is the speci c activity of the ingestedglucose (dpm/mmol); and k is the amount of CO 2 (in liters) producedby the oxidation of 1 g of glucose ( k 0.7467 liter CO 2 /g glucose).

The total exogenous CHO oxidation in the Fruc Glu trial wasdetermined as the sum of EGO glucose and exogenous glucoseoxidation derived from ingested fructose [exogenous fructose oxida-tion (EFO)]. EGO in Fruc Glu was calculated by using Eq. 3 , andEFO was calculated from stable isotope measurements (see Eqs. 4 and5 below).

The isotopic enrichment was expressed as difference betweenthe 13 C/ 12 C of the sample and a known laboratory reference standard,

according to the formula of Craig (6)13C

13C/ 12C sample13C/ 12C standard

1 10 3 (4)

The 13 C was then related to an international standard (PDB).EFO was calculated by using the following formula (30)

EFO VCO2Exp Exp bkgIng Exp bkg

1

k (5)

where Exp is the 13 C enrichment of expired air during exercise withFruc Glu ingestion at different time points, Ing is the 13 C enrich-ment of the fructose in the Fruc Glu solution, and Exp bkg is the 13 Cenrichment of expired air in the Wat trial (background) at differenttime points.

A methodological consideration when using 13 CO 2 and/or 14 CO 2 inexpired air to calculate exogenous substrate oxidation is the trappingof 13 CO 2 and/or 14 CO 2 in the bicarbonate pool, in which an amountof CO 2 arising from decarboxylation of energy substrates is tempo-rarily trapped (34). However, during exercise, the V CO 2 increasesseveralfold so that a physiological steady-state condition will occurrelatively rapidly, and 13 CO 2 and 14 CO 2 in the expired air will beequilibrated with the 13 CO 2 /H13 CO 3 and 14 CO 2 /H14 CO 3 pool, re-spectively. Recovery of 13 CO 2 (and 14 CO 2) from oxidation willapproach 100% after 60 min of exercise when dilution in the bicar-bonate pool becomes negligible (28, 34). As a consequence of this, allcalculations on substrate oxidation were performed over the last 60min of exercise (60 120 min).

Statistical analyses. The data from the four trials were compared byusing a two-factor (time and treatment) ANOVA for repeated mea-

sures. A Tukey post hoc test was applied to locate differences whenANOVA revealed a signi cant interaction. Data evaluation was per-formed by using SPSS for Windows version 10.0 software package(Chicago, IL). All data are reported as means SE. Statisticalsigni cance was set at P 0.05.

RESULTS

Stable and radioactive isotope measurements. The 13 C en-richment of the resting breath samples in the Fruc Glu trialand the Wat trial were 26.11 0.09 and 26.01 0.22 vs. PDB, respectively (data not shown). Changes in isotopiccomposition of expired CO 2 in response to exercise withingestion of Wat or Fruc Glu are shown in Fig. 1 A. In the

1279OXIDATION OF COMBINED INGESTION OF GLUCOSE AND FRUCTOSE



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Fruc Glu trial, there was a signi cant increase ( P 0.001) inthe 13 C enrichment of expired breath, reaching an enrichmentdifference of 17 vs. PDB toward the end of the 120-minexercise (compared with corresponding resting breath sample).During the Wat trial, there was a small but signi cant increasein 13 C enrichment of the expired air ( P 0.05). The rise inbreath 13 CO 2 enrichment during the Wat trial was relativelysmall ( 4%) compared with the increase in breath 13 CO 2enrichment observed during the Fru Glu trial. However, al-though the background shift was small in the present study, a

background correction was made for the calculation of EFO inthe Fruc Glu trial by using the data from the Wat trial.

The 14 CO 2 radioactivity of expired breath samples (cor-rected for background) is shown in Fig. 1 B. In all three CHOtrials, the 14 C activity of the expired CO 2 increased signi -cantly ( P 0.001) during exercise and leveled off after 90 minof exercise.

Exogenous and endogenous CHO oxidation. Peak exoge-nous CHO oxidation rates were reached at the end of exercise(120 min) and were signi cantly higher ( P 0.001) in theFruc Glu trial (1.26 0.07 g/min) compared with the Med-Glu and High-Glu trials (0.80 0.04 and 0.83 0.05 g/min,respectively) (Fig. 2). No difference was found in peak oxida-

tion rates between Med-Glu and High-Glu. The average EGOrates over the 60- to 120-min exercise period were 0.75 0.04,0.75 0.04, and 0.77 0.04 g/min for Med-Glu, High-Glu,and Fruc Glu, respectively ( P 0.05) (Table 1). There wereno signi cant differences in EGO among the three CHO trials.

In the Fruc Glu trial, the average EFO rate during the nal60 min of exercise was 0.38 0.02 g/min, and this resulted ina total exogenous CHO oxidation rate (EGO EFO) of 1.160.06 g/min. Exogenous CHO oxidation in the Fruc Glu trialwas 55% higher ( P 0.001) compared with that in theisoenergetic glucose trial (High-Glu) and the Med-Glu trial(Table 1 and Fig. 2).

Endogenous CHO oxidation was calculated by subtractingexogenous CHO oxidation from total CHO oxidation (Table 1and Fig. 3). There were no signi cant differences in endoge-nous CHO oxidation rates among trials. However, there was atrend for a lower endogenous CHO oxidation in Fruc Glucompared with Med-Glu and High-Glu ( P 0.075).

V O2 , RER, total CHO, and fat oxidation. Data for V O2 , RER,total CHO, and fat oxidation over the 60- to 120-min exercise

Fig. 1. A: change in breath 13 CO 2 enrichment during exercise (compared withresting breath sample) without ingestion of carbohydrate (CHO) [plain water(Wat)] or with ingestion of fructose and glucose (Fruc Glu). B: breath 14 CO 2radioactivity during exercise (corrected for background) with ingestion of moderate amounts of glucose (Med-Glu), with ingestion of large amounts of

glucose (High-Glu), or with ingestion of Fruc Glu. Values are means SE;n 8. PDB, Pee Dee Bellemnitella.

Fig. 2. Exogenous CHO oxidation during exercise with ingestion of Med-Glu,High-Glu, or Fruc Glu. EGO, exogenous glucose oxidation in Fruc Glu;EFO, exogenous fructose oxidation in Fruc Glu. Values are means SE; n8. aSigni cantly different from Med-Glu and High-Glu, P 0.01.

Table 1. Oxygen uptake, respiratory exchange ratio, totalcarbohydrate oxidation, total fat oxidation, endogenouscarbohydrate oxidation, and exogenous glucose and fructoseoxidation during the 60- to 120-min period of exercise

Trial

Wat Med-Glu High-Glu Fruc Glu

VO2 , l/min 3.05 0.12 3.09 0.12 3.09 0.10 3.08 0.12RER 0.84 0.01 0.90 0.01* 0.91 0.01* 0.90 0.01*CHO tot , g/min 1.85 0.23 2.67 0.18* 2.86 0.18* 2.77 0.15*Fat tot , g/min 0.82 0.05 0.54 0.07* 0.47 0.07* 0.50 0.06*Endogenous CHO,

g/min 1.85 0.23 1.92 0.18 2.11 0.19 1.61 0.13EGO, g/min 0.75 0.04 0.75 0.04 0.77 0.04EFO, g/min 0.38 0.02

Values are means SE; n 8 subjects; V O2 , oxygen uptake; RER,respiratory exchange ratio; CHO, carbohydrate; CHO tot , total CHO oxidation;Fat tot , total fat oxidation; EGO, exogenous glucose oxidation; EFO, exogenousfructose oxidation; Wat, plain water; Med-Glu, medium glucose; High-Glu,high glucose; Fruc Glu, fructose plus glucose. *Signi cantly different fromWat, P 0.05.




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period are shown in Table 1. There was no difference in V O2among the four trials. RER in the Wat trial was signi cantlylower ( P 0.01) compared with that in the three CHO trials(Table 1). CHO oxidation was signi cantly higher ( P 0.01)after CHO ingestion compared with Wat ingestion. No signif-icant differences in total CHO oxidation were found amongCHO trials. Total fat oxidation was markedly suppressed withCHO ingestion ( P 0.01). During the nal 60 min of exercise,total fat oxidation rates were 0.82 0.05, 0.54 0.07, 0.470.07, and 0.50 0.06 g/min for Wat, Med-Glu, High-Glu, andFruc Glu, respectively. The relative contribution of substratesto total energy expenditure is depicted in Fig. 3.

Plasma metabolites. Plasma glucose and lactate concentra-tions at rest and during exercise are shown in Fig. 4, A and B,respectively. Fasting plasma glucose concentrations were sim-ilar in the four trials (on average, 4.7 0.1 mmol/l). With theingestion of large amounts of CHO at the start of exercise,plasma glucose concentrations in the three CHO trials peakedwithin the rst 15 min of exercise ( P 0.01) at values around6.0 6.4 mmol/l. Plasma glucose concentrations then droppedand were maintained at values of 4.9 5.4 mmol/l for the entireduration of exercise. Plasma glucose concentrations duringWat decreased from 4.6 0.1 mmol/l at the start of exerciseto 4.0 0.1 mmol/l by the end of exercise ( P 0.01). Plasmaglucose concentrations were higher throughout exercise in theCHO trials compared with the Wat trial, although Med-Glu

failed to reach statistical signi cance between time 30 and60 min ( P 0.05).

In addition, during the second hour of exercise, plasmaglucose concentrations were signi cantly lower in Med-Glucompared with High-Glu ( P 0.05). No other differences inplasma glucose concentrations were found among the threeCHO trials.

Resting concentrations of plasma lactate were not differentamong trials (on average, 0.8 0.1 mmol/l) (Fig. 4 B). Plasmalactate levels increased ( P 0.05) during the rst 15 min of exercise in all four trials. Thereafter, plasma lactate concentra-tions gradually declined until the end of exercise. At all timepoints during exercise, plasma lactate concentrations were

signi cantly higher ( P 0.05) compared with lactate concen-trations at rest. During the rst 75 min of exercise, plasmalactate concentrations were signi cantly higher ( P 0.05) inFruc Glu compared with Med-Glu and Wat.

GI discomfort. GI and related complaints were registered bya questionnaire. The results of the questionnaires obtainedduring the four experimental trials are presented in Table 2.The most frequently reported complaints were bloated feeling,nausea, belching, atulence, and urge to urinate and vomit.More subjects reported severe GI discomfort (bloated feeling,urge to vomit) in the High-Glu trial compared with the Med-Glu and the Fruc Glu trial. None of the subjects vomited orsuffered from diarrhea during the exercise trails.

Body mass loss. Body mass losses during exercise were notdifferent among the four experimental trials (on average, 2.00.1 kg).

DISCUSSION

To our knowledge, this study is the rst to report exogenousCHO oxidation rates during cycling exercise 1.1 g/min

(1.26 0.07 g/min). Previous studies that have investigatedexogenous CHO oxidation during cycling exercise have re-

Fig. 4. Plasma glucose ( A) and lactate ( B) during exercise with ingestion of Wat, Med-Glu, High-Glu, or Fruc Glu. Values are means SE; n 8.Signi cant differences: cWat vs. High-Glu and Fruc Glu, d Wat vs. Med-Glu,eMed-Glu vs. High-Glu, f Fruc Glu vs. Wat and Med-Glu, g Fruc Glu vs.Wat: P 0.05.

Fig. 3. Relative contributions of substrates to total energy expenditure calcu-lated for the 60- to 120-min period of exercise with ingestion of Wat, Med-Glu,High-Glu, or Fruc Glu. Values are means SE; n 8. bSigni cantlydifferent from Wat, P 0.01.




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ported peak oxidation rates of 1.0 g/min (3, 11, 21, 36, 40)for exercise durations up to 180 min. Another interestingnding was that a mixture of glucose and fructose wheningested at a high rate resulted in 55% higher exogenousCHO oxidation rates compared with ingestion of an iosoener-getic amount of glucose only.

In the present study, exogenous CHO oxidation rates did notincrease when the rate of glucose ingestion was increased from1.2 to 1.8 g/min (Table 1 and Fig. 2). Peak oxidation rates were0.80 0.04 and 0.83 0.05 g/min for Med-Glu and High-Glu, respectively. These results are in close agreement with thendings of a study by Wagenmakers et al. (40), who investi-gated the effect of four different doses of maltodextrin inges-tion on exogenous CHO oxidation. Calculated average CHOingestion rates during 120 min of cycling exercise were 0.6,1.2, 1.8, and 2.4 g/min. Exogenous CHO oxidation was higherwhen maltodextrin was ingested at a rate of 1.2 g/min com-pared with 0.6 g/min (0.87 0.13 vs. 0.53 0.17 g/min).

However, a further increase in the rate of maltodextrin inges-tion did not lead to a signi cant increase in exogenous CHOoxidation, and oxidation rates leveled off at 1.0 1.1 g/min.Interestingly, in the present study, combined ingestion of fructose and glucose resulted in peak oxidation rates of 1.260.07 g/min (Fig. 3), and average oxidation rates during the nal60 min of exercise were 1.16 0.06 g/min (Table 1). Further-more, ingestion of fructose in combination with glucose re-sulted in 55% higher exogenous CHO oxidation rates com-pared with the ingestion of glucose only (Med-Glu and High-Glu) (Table 1 and Fig. 2). EGO in the Fruc Glu trial wassimilar compared with EGO in the Med-Glu and High-Glutrial, and hence the higher exogenous CHO oxidation rate in

Fruc Glu could be fully attributed to the oxidation of ingestedfructose (Table 1, Figs. 2 and 3).

When large amounts of glucose or glucose polymer areingested ( 1.0 g/min) during exercise, intestinal absorptionand/or disposal by the liver may be limiting factors for exog-enous CHO oxidation (18, 21). Glucose is absorbed from theintestine by SGLT1 (8), and suggestions have been made thatthe upper limit for glucose absorption (at rest) is 1.0 g/min(31). However, others have suggested slightly higher values(1.3 1.7 g/min) (7). Although speculative, SGLT1 transportersmay become saturated at a glucose ingestion rate of 1.0 1.2g/min, and, therefore, no increase in EGO is observed whenglucose intake is further increased (Ref. 40 and present results).Fructose is absorbed from the intestine by GLUT-5 transport-ers (4, 8), and this differs from intestinal glucose transport(SGLT1). Interestingly, a study by Shi et al. (38) showed thatbeverages containing two or three transportable CHOs (fruc-tose, glucose, and/or sucrose) may increase CHO and waterabsorption. A solution that contained glucose and fructoseespecially was found to result in almost 65% higher CHOabsorption rates compared with an isoenergetic glucose solu-tion. This effect was attributed to the fact that glucose andfructose are absorbed by separate intestinal transport mecha-nisms. Furthermore, it has been shown that fructose absorptionis stimulated by the presence of glucose (13, 35), and hencethis may further contribute to a faster intestinal CHO absorp-tion rate when glucose and fructose are ingested simulta-neously. A faster intestinal CHO absorption might increase theavailability of exogenous CHO in the bloodstream, and thismight have caused the higher exogenous CHO oxidation ratesin Fruc Glu. Adopo et al. (1) also reported higher oxidationrates when a mixture of glucose and fructose was ingestedcompared with the ingestion of an isoenergetic amount of glucose. However, the rate of CHO intake in the study of

Adopo et al. was relatively low ( 0.8 g/min), and intestinalCHO transporters were probably not saturated. As a result of this exogenous CHO oxidation, rates did not exceed 1 g/min.The present data show that, when fructose and glucose areingested simultaneously at high rates during cycling exercise,exogenous CHO oxidation rates can reach peak values of 1.3g/min.

It should be noted that, over the 2-h exercise period, thepercentage of ingested CHO that was not oxidized was muchlarger in High-Glu (68 2%) compared with Fruc Glu (493%) and Med-Glu (51 3%) (data not shown). This suggeststhat, in the High-Glu trial, more CHO was accumulating in thebody, most likely in the stomach or gut. Malabsorption of CHOduring exercise may increase the risk of GI complications (32).

The higher prevalence of severe GI discomfort in the High-Glutrial compared with the Fruc Glu trial may indicate that lessCHO is leaving the GI tract and further supports the hypothesisthat exogenous CHO oxidation in High-Glu was limited at thelevel of intestinal absorption.

In the present study, CHO ingestion suppressed fat oxidation(Table 1) compared with fasting (Wat). The contribution of fatoxidation to total energy expenditure was 54 4% duringWat, and this value decreased to 34 4, 29 4, and 31 3%during Med-Glu, High-Glu, and Fruc-Glu, respectively ( P0.01) (Fig. 3). A decreased fat oxidation with CHO ingestionduring exercise has been found in several other studies (1, 19,21, 24, 40). When CHO is ingested during prolonged low- to

Table 2. Gastrointestinal and related complaints during120 min of exercise

Complaint Wat Med-Glu High-Glu Fruc Glu

Nonsevere

Stomach problems 1 2 2 1Nausea 0 3 2 1Dizziness 0 0 0 0Headache 0 1 0 0Flatulence 0 2 2 2Urge to urinate 0 3 1 4Urge to defecate 0 1 2 1Urge to vomit 0 3 2 1Belching 1 5 3 2Stomach burn 0 0 1 1Bloated feeling 0 2 2 2Stomach cramps 0 0 1 0Intestinal cramps 0 0 1 0Side aches left 0 0 1 0Side aches right 0 0 0 0Reux 0 1 1 1

Severe

Stomach problems 0 0 1 0Nausea 0 0 1 0Urge to vomit 0 0 2 0Bloated feeling 0 1 4 1Stomach cramps 0 0 0 1

n 8 Subjects. Stomach cramps, urge to vomit, nausea, bloated feeling, andstomach problems were registered as severe when a score of 5 or higher (outof 10) was given.




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moderate-intensity exercise, plasma insulin concentrationsmay increase (19, 21). Insulin has been shown to be a potentinhibitor of lipolysis and the rate of appearance of free fattyacids (FFA) (14). Although plasma insulin and FFA concen-trations were not measured in the present study, it is likely thathigher plasma insulin concentrations and a decreased FFAavailability have contributed to lower fat oxidation rates in theCHO trials compared with the Wat trial. CHO ingestion alsoresulted in higher plasma glucose concentrations (Fig. 4 A) andhigher rates of CHO oxidation (Table 1) compared with Wat.In a study by Jeukendrup et al. (19), it was shown that, whenlarge amounts of CHO are ingested during exercise, plasmaglucose oxidation can contribute to 40% of total energyexpenditure and fully accounts for the increase in total CHOoxidation. In the present study, we did not measure plasmaglucose oxidation, liver-derived glucose, and muscle glycogenoxidation, and hence we can only speculate what might havecaused the higher CHO oxidations rates. It is, however, morethan likely that an increased plasma glucose oxidation hascontributed to the higher CHO oxidation rates in the CHO trials(19). Of note, endogenous CHO oxidation tended to be lowerin the Fruc Glu trial compared with the two glucose trials(P 0.075), and this might be due to lower muscle and/or liverglycogen oxidation. More studies are required to assess theeffect of combined glucose and fructose ingestion on liver andmuscle glycogen oxidation.

In the present study, plasma lactate concentrations duringthe rst 75 min of exercise were signi cantly higher in theFruc Glu trial compared with the Med-Glu and Wat trial. Thisis in agreement with the ndings of a study by Koivisto et al.(22) who found 20 25% higher lactate concentrations duringexercise when fructose was ingested in the hour before exer-cise. Fructose is rapidly phosphorylated in the liver to fructose-

1-phosphate, a reaction catalyzed by the enzyme fructokinase(12). It has been suggested that the activity of fructokinase ishigher than the activity of hexokinase and glucokinase,which phosphorylate glucose. Therefore, after ingestion of fructose, there is a large increase in the fructose-1-phos-phate concentration, which will enhance the activation of pyruvate kinase, and hence this will stimulate the formationof pyruvate and lactate (12, 39). In addition, fructolysis canalso occur without passing through the main rate-controllingstep in glycolysis catalyzed by phosphofructokinase. There-fore, fructose is rapidly phosphorylated, resulting in in-creased concentrations of glycolytic intermediates, whichwill lead to an increased glycolytic ux, evidenced by

elevated plasma lactate concentrations.In summary, this is the rst study to show that exogenousCHO oxidation rates during cycling exercise can reach values

1.1 g/min when a mixture of glucose and fructose is ingested.Furthermore, combined ingestion of glucose and fructose re-sulted in 55% higher exogenous CHO oxidation rates com-pared with the ingestion of an isocaloric amount of glucose.The present data suggest that, when high exogenous CHOoxidation rates ( 1.1 g/min) are required during exercise,ingestion of multiple-transportable CHOs is preferred abovethat of large amounts of a single CHO. More studies are neededto determine the combination of CHOs that would lead tomaximal exogenous CHO oxidation rates.

ACKNOWLEDGMENTS

The authors thank Amylum UK, London (UK) for donating glucosemonohydrate and A. E. Staley Manufacturing (US) for donating fructose. Wealso thank Dr. Bob Harris for technical assistance during the 14 CO 2 measure-ments and Dr. Guz Zabierck for valuable comments and suggestions through-out the study.

GRANTS

This study was supported by a grant from Glaxo SmithKline ConsumerHealthcare, UK.

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glucose e frutose durante exercicio fisico

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