Numerous studies have demonstrated that ingested CHO during cycling exercise is oxidized at a peak rate of ~1 g·min−1 (for review, see reference (16)). We have recently summarized the most important factors that affect the oxidation rate of ingested CHO during exercise (16), including type and intensity of exercise, amount, type and timing of CHO ingestion, preexercise muscle glycogen concentration, and diet. However, it remains to be investigated which factors determine the maximum rate of exogenous CHO oxidation. It has been suggested that intestinal CHO absorption could be a potential factor limiting the rate of exogenous CHO oxidation (12,14,16,19).
Indirect evidence for this was recently obtained in studies from our laboratory where combined ingestion of glucose and sucrose (15) or glucose and fructose (14) resulted in peak oxidation rates of ~1.3 g·min−1 and ~20–55% higher exogenous CHO oxidation rates compared with the ingestion of an isocaloric amount of glucose. It is likely that this is caused by the fact that sucrose and fructose are absorbed by intestinal transport mechanisms that are, at least in part, different from intestinal glucose transport (1,4,8,9,30). Glucose absorption occurs via a sodium-dependent glucose transporter (SGLT1) (9), whereas fructose is absorbed from the intestine by a GLUT-5 transporter (4,9). It has been suggested that sucrose is hydrolyzed at the brush-border membrane to glucose and fructose and the monosaccharides are subsequently absorbed by conventional monosaccharide transport mechanisms (8,30). However, others have suggested that disaccharides like sucrose are absorbed by a specific disaccharidase-related transport system (24,28).
Ingestion of two different carbohydrates during exercise (glucose and fructose or glucose and sucrose) resulted in ~20–55% higher exogenous CHO oxidation rates compared with glucose (14,15). Ingestion of three CHO that use different transport systems for absorption might further increase the rate of CHO absorption, which could potentially lead to even higher exogenous CHO oxidation rates relative to a single CHO (glucose). The aim of present study therefore was to examine the oxidation rate of a mixture of glucose, sucrose, and fructose when ingested at a high rate (2.4 g·min−1) relative to a single CHO. We hypothesized that combined ingestion of large amounts of glucose, sucrose, and fructose would result in higher exogenous CHO oxidation rates compared with the ingestion of an isoenergetic amount of glucose.
Eight trained male cyclists or triathletes aged 28.4 ± 1.9 yr and with a body mass (BM) of 71.5 ± 2.4 kg took part in this study. Subjects trained at least 3× wk−1 for more than 2 h·d−1 and had been involved in endurance training for at least 2–4 yr. Before participation, each of the subjects was fully informed of the purpose and risks associated with the procedures, and a written informed consent was obtained. All subjects were healthy as assessed by a general health questionnaire. The study was approved by the Ethics Committee of the School of Sport and Exercise Sciences of the University of Birmingham, United Kingdom.
At least 1 wk before the start of the experimental trials, an incremental cycle exercise test to volitional exhaustion was performed in order to determine the individual maximum power output (Wmax) and maximal oxygen consumption (V̇O2max). This test was performed on an electromagnetically braked cycle ergometer (Lode Excalibur Sport, Groningen, The Netherlands), modified to the configuration of a racing bicycle with adjustable saddle height and handlebar position. After reporting to the laboratory, BM (Seca Alpha, Hamburg, Germany) and height were recorded. The subjects, then, started cycling at 95 W for 3 min, followed by incremental steps of 35 W every 3 min until exhaustion. Heart rate (HR) was recorded continuously by a radiotelemetry heart rate monitor (Polar Vantage NV, Kempele, Finland). Wmax was calculated from the last completed work rate, plus the fraction of time spent in the final noncompleted work rate multiplied by the work rate increment. The results were used to determine the work rate corresponding to 50% Wmax, which was later employed in the experimental exercise trials. Breath-by-breath measurements were performed throughout exercise using an online automated gas analysis system (Oxycon Pro, Jaeger, Hoechberg, Germany). The volume sensor was calibrated using a 3-L calibration syringe and the gas analyzers were calibrated using a 5.03% CO2: 94.97% N2 gas mixture. Oxygen uptake (V̇O2) was considered to be maximal (V̇O2max) when at least two of the three following criteria were met: 1) a leveling off of V̇O2 with increasing workload (increase of no more than 2 mL·kg−1·min−1), 2) a HR within 10 beats·min−1 of predicted maximum (HR 220 − age), and 3) a respiratory exchange ratio (RER) >1.05. V̇O2max was calculated as the average oxygen uptake over the last 60 s of the test. The V̇O2max and Wmax achieved during the incremental exercise test were 64 ± 1 mL·kg−1·min−1 and 357 ± 10 W, respectively.
Each subject performed three exercise trials which consisted of 150 min of cycling at 50% while ingesting a glucose+sucrose+fructose drink Wmax (MIX) (the ingested glucose-to-sucrose-to-fructose ratio was 2:1:1), an isoenergetic glucose drink (GLU), or plain water (WAT). To quantify exogenous glucose oxidation, corn-derived glucose monohydrate (Cerestar, Manchester, UK) and crystalline fructose (Krystar 300, A. E. Staley Manufacturing Company, Illinois) and sugar cane-derived sucrose (Tate and Lyle Europe, London, United Kingdom) were used which have a high natural abundance of 13C (−10.8, −10.7, and −11.2% vs Pee Dee Bellemnitella (PDB), respectively). The 13C-enrichment of the ingested glucose, fructose, and sucrose was determined by elemental analyzer-isotope ratio mass spectrometry (IRMS; Europa Scientific GEO 20-20, Crewe, UK). To all drinks 20 mmol·L−1 of sodium chloride (Sigma-Aldrich, Dorset, UK) was added. The order of the experimental drinks was randomly assigned in a crossover design. Experimental trials were separated by at least 5 d.
Diet and activity before testing.
Subjects were asked to record their food intake and activity pattern 2 d before the first experimental exercise trial and were then instructed to follow the same diet and exercise activities before the other two trials. In addition, 5–7 d before each experimental testing day, they were asked to perform an intense training session (“glycogen-depleting” exercise bout) in an attempt to deplete any 13C-enriched glycogen stores. Subjects were further instructed not to consume any food products with a high natural abundance of 13C (carbohydrates derived from C4 plants: maize, sugar cane) at least 1 wk before and during the entire experimental period in order to reduce the background shift (change in 13 CO2) from endogenous substrate stores.
Subjects reported to the Human Performance Laboratory in the morning (between 7:00 and 9:00 a.m.) after an overnight fast (10–12 h) and having refrained from any strenuous activity or drinking 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 influence of circadian variance. On arrival in the laboratory, a flexible 21-gauge Teflon catheter (Quickcath, Baxter BV, Norfolk, UK) was inserted in an antecubital vein of an arm and attached to a three-way stopcock (Sims Portex, Kingsmead, UK) to allow for repeated blood sampling during exercise. The catheter was kept patent by flushing with 1.0–1.5 mL of isotonic saline (0.9% NaCl, Baxter) after each blood sample collection.
The subjects then mounted a cycle ergometer and a resting breath sample was collected in 10-mL Exetainer tubes (Labco Ltd. Brow Works, High Wycombe, UK), which were filled directly from a mixing chamber in duplicate in order to determine the 13C/12C ratio in the expired CO2.
Next, a resting blood sample (10 mL) was taken and stored on ice and later centrifuged. Subjects then started a 150-min exercise bout at a work rate equivalent to 50% Wmax (62 ± 1%V̇O2max). Additionally, blood samples weredrawn at 15-min intervals during exercise. Expiratory breath samples were collected every 15 min until the end of exercise. V̇O2, V̇CO2 (carbon dioxide production) and RER were measured every 15 min for periods of 4 min using an online automated gas analysis system as previously described.
During the first 3 min of exercise, subjects drank an initial bolus (600 mL) of one of the three experimental drinks: GLU, MIX, or WAT. Thereafter, every 15 min a beverage volume of 150 mL was provided. The total fluid provided during the 150-min exercise bout was 1.95 L. The average rate of glucose intake in the GLU and MIX trial was 2.4 and 1.2 g·min−1, respectively. Furthermore, in the MIX trial subjects ingested on average 0.6 g·min−1 of sucrose and 0.6 g·min−1 fructose which brought the total CHO intake rate in the MIX trial to 2.4 g·min−1.
Subjects were asked to rate their perceived exertion (RPE) for whole body and legs every 30 min on a scale from 6 to 20 using the Borg category scale (3). In addition, subjects were asked every 30 min to fill in a questionnaire in order to rate (possible) gastrointestinal problems (13). All exercise tests were performed under normal and standard environmental conditions (18–22°C dry bulb temperature and 55–65% relative humidity). During the exercise trials, subjects were cooled with standing floor fans in order minimize thermal stress.
Subjects were asked to fill out a questionnaire every 30 min during the exercise trials. The questionnaire contained questions regarding the presence of gastrointestinal (GI) problems at that moment and addressed the following complaints: stomach problems, gastrointestinal cramping, bloated feeling, diarrhea, nausea, dizziness, headache, belching, vomiting, or urge to urinate/defecate. While subjects were on the bike and continued their exercise, each question was answered by simply ticking a box on the questionnaire that corresponded to the severity of the GI problem addressed. The items were scored on a 10-point scale (1 = not at all, 10 = very, very much). The severity of the GI symptoms was divided into two categories; severe and nonsevere symptoms, as was previously described by Jeukendrup et al. (18). Severe complaints included nausea, stomach problems, bloated feeling, diarrhea, urge to vomit, stomach, and intestinal cramps because these are symptoms that commonly impair performance and may bring with them health risks. The above symptoms were only registered as severe symptoms when a score of 5 or higher of 10 was reported. When a score below 5 was given, they were registered as nonsevere. All other symptoms were registered as nonsevere regardless of the score reported.
Blood samples were collected into prechilled EDTA containing tubes (Becton Dickinson, Plymouth, UK) and centrifuged at 2300 × g and 4°C for 10 min. Aliquots of plasma were immediately frozen in liquid nitrogen and stored at −25°C until analyses for glucose and lactate. Plasma glucose (Glucose HK kit, Sigma-Aldrich, Dorset, UK) and lactate (Lactate kit, Sigma-Aldrich) were analyzed on a COBAS BIO semiautomatic analyzer (La Roche, Basel, Switzerland).
Breath samples were analyzed for 13C/12C ratio by gas chromatography continuous flow isotope ratio mass spectrometry (GC-IRMS)(Europa Scientific, Crewe, United Kingdom). From indirect calorimetry (V̇O2 and V̇CO2) and stable isotope measurements (breath 13CO2/CO212 ratio), oxidation rates of total fat, total CHO, and exogenous glucose were calculated.
From V̇CO2 andV̇O2 (L·min−1), total CHO and fat oxidation rates (g·min−1) were calculated using stoichiometric equations of Frayn (10) with the assumption that protein oxidation during exercise was negligible:
The isotopic enrichment was expressed as δ per mil difference between the 13C/12C ratio of the sample and a known laboratory reference standard according to the formula of Craig (7):
The δ 13C was then related to an international standard (PDB-1).
In the GLU and MIX trials, the rate of exogenous glucose oxidation (EGO) was calculated using the following formula (27): in which δ Exp is the 13C enrichment of expired air during exercise at different time points, δ Ing is the 13C enrichment of the ingested CHO solution, δ Expbkg is the 13C enrichment of expired air in the WAT trial (background) at different time points, and k is the amount of CO2(in L) produced by the oxidation of 1 g of glucose (k = 0.7467 L of CO2·g−1 of glucose).
A methodological consideration when using 13CO2in expired air to calculate exogenous substrate oxidation is the trapping of 13 CO2 in the bicarbonate pool, in which an amount of CO2 arising from decarboxylation of energy substrates is temporarily trapped (29). However, during exercise the CO2 production increases several-fold so that a physiological steady state condition will occur relatively rapidly, and 13CO2 in the expired air will be equilibrated with the 13CO2/H13CO3− pool, respectively. Recovery of 13CO2 from oxidation will approach 100% after 60 min of exercise when dilution in the bicarbonate pool becomes negligible (26,29). As a consequence of this, calculations on substrate oxidation were performed over the last 90 min of exercise (60–150 min).
Two-way ANOVA for repeated measures was used to compare differences in substrate utilization and in blood-related parameters over time between the trials. A Tukey post hoc was applied in the event of a significant F-ratio. Where appropriate, comparison of variables between two conditions was conducted by using a Student’s t-test for paired samples. Data evaluation was performed using SPSS for Windows version 10.0 software package (Chicago, IL). All data are reported as means ± SE. Statistical significance was set at P < 0.05.
Changes in isotopic composition of expired CO2 in response to exercise with ingestion of water (WAT), glucose (GLU), or the mixture of glucose, sucrose and fructose (MIX) are shown in Figure 1A. In the GLU and MIX trials, the 13CO2 enrichment of expired breath increased from −26.1 ± 0.2 and ±26.4 ± 0.4% versus PDB at rest to −20.2 ± 0.2 and −18.5 ± 0.3% versus PDB by the end of the 150-min exercise, respectively. From the 45-min point onward, breath 13CO2 enrichment in the MIX trial was significantly (P < 0.01) higher compared with the GLU trial. During the WAT trial, there was a small but significant increase in 13CO2 enrichment of the expired breath (P < 0.01). Therefore, a background correction was made for the calculation of exogenous glucose oxidation in the GLU and MIX trials by using the data from the WAT trial.
V̇O2, RER, total CHO, and fat oxidation.
Data for V̇O2, RER, total CHO, and fat oxidation over the 60- to 150-min exercise period are shown in Table 1. There was no significant difference in V̇O2 between the three experimental trials. RER in the WAT trial was significantly lower (P < 0.01) compared with the GLU and MIX trials (Table 1). CHO oxidation during the last 90 min of exercise decreased in WAT and remained stable in GLU and MIX. The average CHO oxidation rates over 60- to 150-min exercise period were 1.46 ± 0.05, 2.07 ± 0.06, and 2.25 ± 0.14 g·min−1 for WAT, GLU, and MIX, respectively. CHO oxidation was significantly higher (P < 0.01) after CHO ingestion compared with WAT ingestion. No difference in total CHO oxidation was found between the GLU and MIX trials. Total fat oxidation was higher in the WAT trial than in the CHO trials (P < 0.01). The average fat oxidation rates over the 60- to 150-min exercise period were 0.87 ± 0.04, 0.66 ± 0.04, and 0.59 ± 0.07 g·min−1 for WAT, GLU, and MIX, respectively. The relative contribution of substrates to total energy expenditure during the 60- to 150-min period of exercise is depicted in Figure 2.
Exogenous and endogenous CHO oxidation.
Exogenous CHO oxidation showed a gradual increase over time and leveled off after approximately 105–120 min of exercise (Fig. 1B). Peak exogenous CHO oxidation rates were reached at the end of exercise (150 min) and were significantly higher (P < 0.01) in the MIX trial (1.70 ± 0.07 g·min−1) compared with the GLU trial (1.18 ± 0.04 g·min−1) (Fig. 1B). Exogenous CHO oxidation was ~50% higher (P < 0.01) in the MIX trial compared with the GLU trial (Table 1 and Fig. 1B and 2).
The high exogenous CHO oxidation rates during the 60-to 150-min exercise period in MIX resulted in significantly lower (P < 0.05) endogenous CHO oxidation rates compared with GLU (Table 1 and Fig. 2). It should be noted that during the last 30 min of exercise there was a trend toward a lower endogenous CHO oxidation in MIX compared with GLU, but this failed to reach statistical significance (P = 0.096). Endogenous CHO oxidation was lower (P < 0.01) in the MIX and GLU trials compared with the WAT trial. The average endogenous CHO oxidation rates over the 60-to 150-min exercise period were 1.46 ± 0.5, 1.06 ± 0.05, and 0.72 ± 0.11 g·min−1 for WAT, GLU, and MIX, respectively. Endogenous CHO oxidation represented 40 ± 2, 28 ± 2, and 19 ± 3% of total energy expenditure in WAT, GLU, and MIX, respectively (WAT>GLU>MIX; P < 0.05) (Fig. 2).
Plasma glucose and lactate concentrations at rest and during exercise are shown in Figure 3, A and B. No differences were observed in fasting plasma glucose concentrations between trials (on average 5.0 ± 0.1 mmol·L−1. Plasma glucose concentrations during exercise with WAT decreased gradually, reaching a nadir of 4.0 ± 0.2 mmol·L−1 at the end of exercise (t = 150 min). With ingestion of large amounts of CHO at the start of exercise, plasma glucose concentrations in the GLU and MIX trials peaked within the first 15 min of exercise at values ranging from 6.5 to 6.8 mmol·L−1. Thereafter, plasma glucose concentrations declined to fasting levels and remained at this concentration for the duration of exercise. Plasma glucose concentrations were higher throughout exercise in the CHO trials compared with the WAT trial, although MIX failed to reach statistical significance at t = 60 (P = 0.05). No differences in plasma glucose concentrations were found between the GLU and MIX trials.
Fasting plasma lactate concentrations were not different between trials (on average 0.8 ± 0.1 mmol·L−1)(Fig. 3B). Plasma lactate concentrations during exercise were higher (from t = 30 to t = 120 min; P < 0.05) in the MIX trial compared with the WAT and GLU trials. Furthermore, the plasma lactate concentration in MIX was significantly higher (P < 0.01) compared with GLU at t = 150 min. No differences in plasma lactate concentrations were found between the GLU and WAT trials.
Gastrointestinal discomfort and ratings of perceived exertion.
The results of the questionnaires obtained during the CHO trials are presented in Table 2. The most frequently reported complaints were stomach problems, nausea, flatulence, urge to urinate, belching, and bloated feeling. More subjects reported severe GI discomfort (nausea, bloated feeling, and urge to vomit and vomiting) in the GLU compared with the MIX trial. In the GLU trial one subject vomited after 120 min of exercise. Furthermore, two subjects were not able to completely finish the last GLU drink as they felt that this would make them sick.
No significant differences in RPE overall or RPE legs were observed between the three experimental trials. The mean values for RPE overall and RPE legs during 150-min of exercise were 11.5 ± 0.2 and 11.6 ± 0.3, respectively.
Ingestion of CHO during prolonged moderate-to-high intensity exercise can postpone fatigue and improves exercise performance by preventing hypoglycemia and maintaining high rates of CHO oxidation late in exercise, when endogenous CHO stores are nearly depleted (5,6,20). Therefore, high exogenous CHO oxidation rates may have the potential to enhance prolonged exercise performance. Studies that have investigated oxidation of a single CHO during exercise have reported oxidation rates of up 1 g·min−1 (for review, see reference (16)). However, when multiple transportable CHO (glucose+fructose or glucose+sucrose) are ingested at rates of 1.8 g·min−1 during cycling exercise, exogenous CHO oxidation rates can reach peak values of ~1.3 g·min−1 (14,15). A novel finding of the present study was that combined ingestion of glucose, fructose and sucrose resulted in peak exogenous CHO oxidation rates of 1.70 ± 0.07 g·min−1. To date, this is the highest exogenous CHO oxidation rate ever reported in the literature. The present data support the results of a study by Hawley et al. (11), who bypassed both intestinal absorption and liver glucose uptake by employing intravenous glucose infusion. The glucose infusion resulted in hyperglycemia and hyper-insulinemia which completely suppressed hepatic glucose production. More importantly the rate of glucose uptake and plasma glucose oxidation during the last 30 min of exercise increased to 1.8 g·min−1. The present data and those of Hawley et al. (11) suggest that the muscle can oxidize exogenous CHO at a high rates providing that sufficient amounts of exogenous CHO is delivered into the blood stream.
Intestinal absorption of glucose occurs via a sodium-dependent glucose transporter (SGLT1), which is located in the brush-border membrane (9). It has been postulated that intestinal glucose transporters (SGLT1) may become saturated when large amounts of glucose or glucose polymers are ingested (>1.2 g·min−1) and hence intestinal CHO absorption may be a limiting factor for exogenous CHO oxidation (14). Interestingly, there have been suggestions that a beverage containing two or three transportable CHO (glucose, fructose, and sucrose) results in higher CHO and/or water absorption rates compared with an isoenergetic glucose solution (31). Of note, fructose is absorbed from the intestine by GLUT-5, a sodium-independent facilitative fructose transporter (4,9). Sucrose is hydrolyzed at the brush-border of the intestinal epithelium to glucose and fructose. The absorption of glucose and fructose released from sucrose seems to occur via the same intestinal CHO transporters as free glucose (SLGT1) and free fructose (GLUT-5) (8,30). However, others have suggested that sucrose (and other disaccharides) is absorbed by a disaccharidase-related transport mechanism which provides a direct transfer of glucose and fructose (released from sucrose) across the brush border membrane (24,28). The fact that glucose, sucrose and fructose are absorbed (partly) by different intestinal transporters could explain the high rates of intestinal CHO absorption and the high rates of exogenous CHO oxidation observed when mixtures of these CHO are consumed. In the present study, combined ingestion of large amounts of glucose (144 g), fructose (72 g), and sucrose (72 g) during 2.5 h of cycling exercise resulted in peak exogenous CHO oxidation rates of ~1.70 g·min−1 (Fig. 1B) and resulted in ~50% higher exogenous CHO oxidation rates compared with the ingestion of an isocaloric amount of glucose (288 g). These findings further support the hypothesis that when large amounts of glucose are ingested (>1.2 g·min−1) exogenous CHO oxidation is limited at the level of intestinal absorption (14).
A second important finding of the present study is the lower endogenous CHO oxidation rates in MIX compared with GLU. The high exogenous CHO oxidation rates in MIX resulted in almost 30% lower endogenous CHO oxidation rates compared with GLU (Table 1 and Fig. 2). Endogenous CHO oxidation during exercise represents the sum of muscle glycogen and liver-derived (and kidney) glucose oxidation. Unfortunately, in the present study we did not measure plasma glucose enrichments and hence it is not possible to distinguish between liver-derived glucose oxidation and muscle glycogen oxidation. In a study by Jeukendrup et al. (17), however, it was shown that when large amounts of CHO are ingested during prolonged cycling exercise (average ingestion rate of 3.0 g·min−1), hepatic glucose output was completely blocked. Although the average CHO ingestion rate in the present study was slightly less (2.4 g·min−1), it is likely that hepatic glucose production was (almost) completely suppressed in both the GLU and MIX trials. If it is assumed that hepatic glucose production was completely blocked in GLU and MIX (or at least suppressed to the same extent), then the lower endogenous CHO oxidation in MIX suggests a reduced muscle glycogen oxidation. A reduced rate of muscle glycogen utilization would delay the depletion of muscle glycogen stores and possibly the onset of fatigue. More research is required to determine whether combined ingestion of different types of CHO, leading to high exogenous CHO oxidation rates (>1.5 g·min−1), would reduce muscle glycogen oxidation.
Another observation in the present study was that one subject in the GLU trial vomited after 120 min of exercise and two subjects were not able to completely finish the last GLU drink (at t = 135 min) as they felt that this would make them sick. Furthermore, more subjects reported severe GI discomfort (nausea, bloated feeling, and urge to vomit and vomiting) in the GLU compared with the MIX trial. The stomach related problems during GLU might have been caused by a gradual increase in gastric volume over the 2.5-h exercise period. An increase in stomach volume occurs when the rate of intake (fluid and carbohydrate) exceeds the rate of gastric emptying. The rate of gastric emptying is regulated by a number of factors, including nutrient state (liquid or solid), volume, concentration, and osmolality (for review, see reference (23)). When a hyperosmolar (glucose) solution is consumed, gastric emptying is, at least in part, inhibited by the stimulation of duodenal osmoreceptors which feedback on the stomach (2,25). In addition, data from studies by Lin et al. (21,22) in dogs suggest that there are chemospecific sensors to glucose located in the small intestine which trigger inhibition of gastric emptying by directly acting on the stomach. It has been postulated that the inhibition of gastric emptying by a hyperosmolar glucose solution depends more on chemospecific than on duodenal osmoreceptor feedback (22). Interestingly, the inhibition of gastric emptying by glucose seems to be related to the length of the small intestine exposed to glucose (21). Although speculative, a larger part of the small intestine might have been exposed to unabsorbed glucose in GLU compared with MIX and this may have resulted in a more potent inhibition of gastric emptying. As a result of this, more fluid and CHO might have accumulated in the stomach during GLU, and this could explain why more subjects reported gastrointestinal problems after GLU ingestion. In addition, incomplete absorption of CHO as a result of a lower intestinal CHO transport capacity may also have contributed to the higher prevalence of (severe) GI complications in the GLU trial.
In summary, combined ingestion of large amounts of glucose, fructose, and sucrose during cycling exercise resulted in peak exogenous CHO oxidation of 1.70 ± 0.07 g·min−1 and resulted in almost 50% higher exogenous CHO oxidation rates compared with the ingestion of an isocaloric amount of glucose. As a consequence, endogenous CHO oxidation rates were ~30% lower when a mixture of glucose, fructose, and sucrose was ingested compared with glucose ingestion only.
This study was supported by a grant of GlaxoSmithKline Consumer Healthcare, United Kingdom. The authors would also like to thank Cerestar (Manchester, United Kingdom) for donating glucose monohydrate, Tate and Lyle Europe (London, United Kingdom) for donating Sucrose, and A. E. Staley Manufacturing Company (U.S.) for donating fructose.
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