HULSTON, CARL J.; WALLIS, GARETH A.; JEUKENDRUP, ASKER E.
Studies using stable (13C) and radioactive (14C) isotopes show that a single source of CHO ingested during exercise will be oxidized at rates up to approximately 1.1 g·min−1, even when much CHO are consumed (>2 g·min−1) (24). The oxidation of ingested CHO is potentially limited by gastric emptying, intestinal CHO absorption, hepatic glucose extraction, muscle glucose uptake, or a combination of these factors (23). However, recent evidence, albeit indirect, suggests that the limitation is primarily located at the level of intestinal CHO absorption (14,19-21,23,25).
Glucose is absorbed from the intestinal lumen via the sodium-dependent glucose transporter (SGLT1) (11), which it seems can become saturated at ingestion rates above 1.2 g·min−1 (20). In contrast, fructose is absorbed from the intestinal lumen by GLUT 5 transporters (11). Ingesting a beverage containing a combination of glucose and fructose has been shown to increase CHO and fluid absorption at rest (35,36) and increase exogenous CHO oxidation during exercise (19-21,25) when compared with an isocaloric amount of glucose alone. The reason for this finding is most likely due to reduced competition for intestinal absorption when two or more CHO using separate transport mechanisms (glucose = SGLT1, fructose = GLUT 5) are ingested.
During our previous studies (19-21,25), high ingestion rates (1.5-2.4 g·min−1 or 90-144 g·h−1) were used to saturate SGLT1. However, although such high rates of ingestion are not impossible, athletes typically ingest CHO at much lower rates. In fact, CHO intake among professional road cyclists has been reported to be as low as 25 g·h−1 during race situations (12). It remains unclear if combined ingestion of glucose plus fructose at lower (more practical) rates increases exogenous CHO oxidation compared with glucose alone. For example, Adopo et al. (3) observed that ingesting 50 g of glucose plus 50 g of fructose immediately before 2 h cycling increased exogenous CHO oxidation by 21% compared with 100 g of glucose (average ingestion rate 0.83 g·min−1). In contrast, Riddell et al. (33) reported that glucose plus fructose was oxidized at the same rate of glucose when ingested intermittently throughout 90 min cycling (average ingestion rate 0.75 g·min−1). These conflicting results may be due to differences in the timing of ingestion as well as differences in the training status and maturation of the subjects recruited. In the study by Adopo et al. (3), moderately trained male subjects ingested a single bolus of CHO at the onset of exercise, whereas 11- to 14-yr-old boys ingested CHO intermittently throughout exercise in the study by Riddell et al. (33). From these studies, it is not possible to draw conclusions or make recommendations about exogenous CHO intake during exercise in athletes.
Therefore, the purpose of this study was to determine whether, in well-trained adult males, combined ingestion of moderate amounts of glucose plus fructose (0.8 or 48 g·h−1) would result in higher rates of exogenous CHO oxidation when compared with an isocaloric amount of glucose alone. We hypothesize that at this lower rate of ingestion, when intestinal CHO transporters would not be saturated, rates of exogenous CHO oxidation would be similar between glucose and glucose plus fructose.
Seven endurance-trained male cyclists (mean ± SD: age = 26 ± 6 yr; body mass = 71.4 ± 8.5 kg; V˙O2max = 62.0 ± 5.9 mL·kg−1·min−1; maximal power output = 333 ± 30 W) volunteered to participate in this study. Subjects were informed of the potential risks involved with the experimental procedures before providing their written consent. The study was approved by the School of Sport and Exercise Sciences Safety and Ethics Committee (University of Birmingham, UK).
Each subject completed three experimental trials consisting of 150 min cycling at 55% W˙max while ingesting a 6% glucose solution (GLU), a 6% glucose plus fructose solution (GLU + FRU) (glucose-to-fructose ratio of 2:1), or plain water (WAT). Trials were performed in random order, using a single-blind cross-over design, and were separated by at least 7 d. The rate of CHO ingestion was 0.8 g·min−1 (48 g·h−1), and rates of exogenous CHO oxidation were determined from the 13C enrichment of expired breath.
One week before the start of the experiment, subjects performed an incremental test to exhaustion on an electromagnetically braked cycle ergometer (Lode Excalibur Sport, Groningen, The Netherlands) for the determination of maximal oxygen uptake (V˙O2max) and maximal power output (W˙max) as previously described (1). Briefly, subjects began cycling at 95 W, followed by 35-W increments every 3 min thereafter. Breath-by-breath measurements were performed throughout exercise using an automated online gas analysis system (Oxycon Pro; Jaeger, Wuerzburg, Germany). W˙max values were used to determine 55% W˙max, which was later used in the experimental trials.
Diet and activity before testing.
Subjects were asked to record their food intake and physical activity for 2 d before the first trial and were then instructed to follow the same diet and activities before all remaining trials. Additionally, subjects followed a specific exercise/diet regime, which has been shown to reduce the background shift (change in 13C) from endogenous substrate stores (37). Briefly, 5 d before each experimental trial, subjects performed an exhaustive bout of exercise to oxidize any 13C-enriched glycogen and refrained from eating foods with naturally high 13C abundance thereafter. This included commercially available sports drinks and CHO derived from C4 plants such as maize and cane sugar. Finally, subjects were asked to refrain from strenuous exercise and to avoid alcohol and caffeine intake for 24 h before all trials.
On the morning of an experiment trial, subjects reported to the laboratory at 0800 h after a 10- to 12-h overnight fast. After sitting quietly for 10-15 min, a Teflon catheter (Venflon; Becton Dickinson, Plymouth, UK) was inserted into an antecubital vein of the arm to allow repeated blood sampling during exercise. Resting blood (10 mL) and expired breath samples were collected immediately before subjects began cycling at 55% W˙max (183 ± 6 W). Further blood (10 mL) and expired breath samples were collected every 15 min until cessation of exercise, along with measures of V˙O2 and V˙CO2, using an automated online gas analysis system (Oxycon Pro; Jaeger). HR was recorded continuously (15-s intervals) throughout exercise using a radiotelemetry HR monitor (Polar 625X, Kempele, Finland).
At the onset of exercise, subjects consumed 600 mL of one of the three experimental beverages (WAT, GLU, or GLU + FRU), followed by 150 mL every 15 min thereafter. Total fluid intake during exercise was 1.95 L, providing CHO at a rate of 0.8 g·min−1 (48 g·h−1). To quantify exogenous CHO oxidation, we prepared CHO solutions using corn-derived glucose and crystalline fructose, which have a high natural abundance of 13C (−10.8 and −10.7 δ‰ vs Vienna Pee Dee Belemnite, respectively). Additionally, the initial 600-mL bolus contained 3.00 g of deuterium (2H2O; 99%; Sigma-Aldrich, Dorset, UK). The appearance of 2H2O in the plasma was used as a qualitative marker of fluid availability.
Blood samples were collected into prechilled vacutainers containing K3EDTA (Becton Dickinson) and were stored on ice until centrifugation at 2300g for 10 min at a temperature of 4°C. After centrifugation, aliquots of the plasma were immediately frozen in liquid nitrogen and stored at −25°C until further analysis. Plasma samples were analyzed using commercially available spectrophotometric assays for glucose (Glucose HK; ABX Diagnostics, Shefford, UK) and lactate (Lactic Acid; ABX Diagnostics) concentration using a semiautomatic analyzer (Cobas Mira Plus; ABX Diagnostics).
For determination of plasma deuterium enrichment, 200 μL of plasma was added to a vacutainer (Labco, High Wycombe, England) containing a 5% platinum on alumina catalyst (Sigma-Aldrich). The sealed vacutainer was then flushed with a 2% hydrogen in helium gas mixture for 5 min. After a 40-min equilibration period, during which hydrogen isotopes in the plasma exchange with hydrogen ions in the headspace, a sample of the headspace gas was obtained, and deuterium enrichment was determined by isotope ratio mass spectrometry (IRMS) (Gas Bench II; IRMS, Delta Plus XP; both Thermo Finnigan, Herts, UK). The isotope enrichment was expressed as δ per milliliter verses the international laboratory standard Vienna Standard Mean Ocean Water.
Breath samples were analyzed for 13C/12C ratio by IRMS (GC, Trace GC Ultra; IRMS, Delta Plus XP; both Thermo Finnigan). From indirect calorimetry (V˙O2 and V˙CO2) and stable isotope measurements (breath 13C enrichment), total fat, total CHO, exogenous CHO, and endogenous CHO oxidation rates were calculated.
Rates of total CHO and fat oxidation were calculated using stoichiometric equations (26), with the assumption that protein oxidation was negligible:
The isotopic enrichment of expired breath was expressed as δ per milliliter difference between 13C/12C ratio of the sample and a known laboratory reference standard according to the formula of Craig (8):
Equation (Uncited)Image Tools
The δ 13C was then related to the international standard Vienna Pee Dee Belemnite.
The rate of exogenous CHO oxidation was calculated using the formula:
Equation (Uncited)Image Tools
where δExp is the 13C enrichment of expired breath during exercise, δIng is the 13C enrichment of the ingested beverage, δExpbkg is the 13C enrichment of expired breath in the WAT trial (background), and k is the volume of CO2 produced by the oxidation of 1 g of glucose (k = 0.7467 L).
A methodological consideration when using 13CO2 in expired air to calculate exogenous CHO oxidation is the trapping of 13CO2 in the bicarbonate pool where a proportion of CO2 arising from the oxidation of ingested glucose is temporarily retained (34). However, during exercise, V˙CO2 increases severalfold so that a physiological steady-state condition will occur and the 13CO2 in expired air will be equilibrated with the CO2/HCO3 pool. Under exercising conditions, recovery of 13CO2 from the oxidation of ingested 13C-glucose will approach 100% after 60 min when the dilution in the bicarbonate pool becomes negligible (31). Consequently, calculations of substrate oxidation were performed over the final 90 min of exercise (60-150 min).
The oxidation efficiency was determined as the percentage of ingested CHO that was oxidized and was calculated by dividing exogenous CHO oxidation by the CHO ingestion rate and then multiplying by 100.
All data are expressed as mean ± SE unless otherwise stated. Two-way (trial × time) ANOVA for repeated measures was performed to study differences in substrate metabolism and plasma metabolite concentrations. Significant effects were followed up by post hoc comparisons (Tukey HSD). Data analysis was performed using Statistical Package for the Social Sciences for Windows version 13.0 software (SPSS Inc., Chicago, IL) or by hand. Significance was accepted at P < 0.05.
V˙O2, RER, total CHO, and fat oxidation.
Data for V˙O2, RER, total CHO, and fat oxidation rates during the 60- to 150-min exercise period are shown in Table 1. There was no significant difference in V˙O2 among the three experimental trials. RER was significantly lower in the WAT trial compared with GLU and GLU + FRU (P < 0.05) but was similar in the two CHO trials. Average CHO oxidation rates over the 60- to 150-min exercise period were 1.71 ± 0.04, 2.07 ± 0.13, and 2.13 ± 0.14 g·min−1 for WAT, GLU, and GLU + FRU, respectively. CHO oxidation was significantly higher after CHO ingestion compared with WAT (P < 0.05). No difference in CHO oxidation was found between GLU and GLU + FRU. Total fat oxidation was significantly higher in the WAT trial than that in GLU and GLU + FRU (P < 0.05). Average fat oxidation rates over the 60- to 150-min exercise period were 0.73 ± 0.03, 0.58 ± 0.07, and 0.58 ± 0.07 g·min−1 for WAT, GLU, and GLU + FRU, respectively.
Exogenous CHO oxidation, endogenous CHO oxidation, and oxidation efficiency.
Exogenous CHO oxidation rates appeared to increase during the first 60 min of exercise and were relatively stable for the remaining 90 min of exercise (Fig. 1 and Table 1). Peak exogenous CHO oxidation rates were not significantly different between GLU and GLU + FRU (0.60 ± 0.06 and 0.57 ± 0.06 g·min−1, respectively). Furthermore, average exogenous CHO oxidation rates during the 60- to 150-min exercise period were not significantly different between GLU and GLU + FRU (0.58 ± 0.05 and 0.56 ± 0.06 g·min−1, respectively). The contribution of exogenous CHO to total energy expenditure was 17 ± 1% and 16 ± 2% for GLU and GLU + FRU, respectively (Fig. 2).
Average endogenous CHO oxidation rates during the 60- to 150-min exercise period were not significantly different among the three trials (1.71 ± 0.04, 1.48 ± 0.14, and 1.58 ± 0.17 g·min−1 for WAT, GLU, and GLU + FRU, respectively). The contribution of endogenous CHO to total energy expenditure was 49 ± 2%, 43 ± 4%, and 45 ± 5% for WAT, GLU, and GLU + FRU, respectively (Fig. 2).
The total amount of CHO ingested during exercise was 120 g. During the 2.5-h bout of exercise, a minimum of 75 ± 5 g was oxidized in GLU, and a minimum of 76 ± 8 g was oxidized in GLU + FRU. This represents an oxidation efficiency of 63% for both experimental beverages.
Plasma glucose and lactate concentrations at rest and during exercise are shown in Figure 3A and B, respectively. Resting plasma glucose concentrations were not significantly different between trials (4.7-4.9 mmol·L−1). During exercise in the WAT trial, plasma glucose concentration remained relatively stable and above 4.0 mmol·L−1 at all time points. In the two CHO trials, plasma glucose concentrations increased to peak values (∼6.3 mmol·L−1) at 15 min, being significantly higher than WAT at this time point (P < 0.05). Thereafter, plasma glucose concentrations were not significantly different among the three trials. Resting plasma lactate concentrations were not significantly different between trials (1.0-1.1 mmol·L−1). Plasma lactate concentrations increased during the first 15 min of exercise in all three exercise trials (P < 0.05). Thereafter, plasma lactate concentrations remained relatively stable throughout the exercise period. However, at 15- and 30-min time points, plasma lactate concentrations were significantly higher in GLU + FRU than GLU (P < 0.05).
Plasma deuterium enrichment rapidly increased during the first 45 min of exercise in all three trials (Fig. 4). At 30 min, plasma deuterium enrichment was significantly higher in WAT than GLU (P < 0.05). At the same time point, there was also a trend for plasma deuterium enrichment to be higher in GLU + FRU than GLU, but this did not reach significance (P = 0.07). There was no difference in plasma deuterium enrichment between WAT and GLU + FRU.
FIGURE 4-Plasma deut...Image Tools
We have previously shown that ingesting a beverage containing glucose plus fructose results in higher (20-50%) rates of exogenous CHO oxidation during exercise when compared with an isocaloric amount of glucose alone (19-21,25). These higher oxidation rates have been associated with decreased ratings of perceived exertion and higher self-selected cadence in cyclists during very prolonged exercise (25) as well as improved exercise performance (9). During these studies, CHO was ingested at relatively high rates (1.5-2.4 g·min−1 or 90-144 g·h−1) in an attempt to saturate the intestinal sodium-dependent glucose transporter SGLT1 while at the same time providing substrate for another CHO transporter (GLUT 5). Higher exogenous CHO oxidation rates with multiple transportable CHO provide indirect evidence to support the theory that exogenous CHO oxidation is primarily limited by intestinal CHO absorption. Although such high ingestion rates are not impossible and have been recommended for very prolonged exercise (22), they are much higher than typically ingested by athletes (12). The recommended rate of CHO ingestion during endurance exercise is 30-60 g·h−1 (2). Whether a combination of CHO, using separate intestinal transporters, offers an oxidative advantage compared with a single source of CHO ingested within this range remains unknown. We hypothesized that at lower rates of ingestion, when intestinal CHO transporters would not be saturated, rates of exogenous CHO oxidation would be similar between glucose and glucose plus fructose.
The main finding of the present study was that at lower rates of ingestion (0.8 g·min−1 or 48 g·h−1) rates of exogenous CHO oxidation were similar between glucose and glucose plus fructose containing beverages. This finding is to be expected given the theory that exogenous CHO oxidation is primarily limited by intestinal CHO absorption with high CHO ingestion rates (>1.2 g·min−1) (23). At lower ingestion rates, we suggest the availability of CHO is not limited by intestinal absorption, and therefore the addition of a second CHO (fructose), which uses a separate transport mechanism (GLUT 5), may not increase the amount of CHO available for oxidation. One study has reported higher rates of exogenous CHO oxidation during exercise with moderate intake of glucose (50 g) plus fructose (50 g) compared with glucose (100 g) alone (3). This apparent discrepancy between the findings of Adopo et al. (3) and that of the present study is most likely due to differences in the timing of CHO ingestion rather than the total amount of CHO consumed (100 vs 120 g). In the study by Adopo et al. (3), 100 g of glucose was ingested in 500 mL of water immediately before 2 h cycling exercise. This 20% CHO solution is more concentrated than the 6% CHO solution used in the present study. We speculate that ingesting such a concentrated CHO solution may have saturated intestinal CHO transporters during the early stages of exercise, thereby limiting the amount of CHO available for oxidation. If this is the case, then replacing part (50 g) of the total CHO load with fructose may have increased intestinal CHO absorption, thus increasing the amount of CHO available for oxidation.
Exogenous CHO oxidation appeared to increase during the first 60 min of exercise (Fig. 1B). However, it should be noted that any loss of 13C within the bicarbonate pool during this period would result in underestimated rates of oxidation and thus exaggerate the increase we observed. Nonetheless, and as stated above, there was no difference in the oxidation rates between the two experimental beverages (Fig. 1B). Interestingly, fructose has been reported to be oxidized at lower rates than glucose (13,17,27-30), which may be due to slower intestinal absorption (32) and/or the necessity for its conversion to glucose by the liver before oxidation (17). However, in this study, although the amount of glucose was reduced in one of the trials and replaced by a CHO (fructose), which has previously been demonstrated to be oxidized at lower rates, the amount of exogenous CHO oxidized remained the same. Given the use of a single isotope tracer (13C), we cannot quantify the respective oxidation rates for each CHO during the GLU + FRU trial. However, our results appear similar to one recent study (7) that reported the same rates of oxidation for glucose and fructose when ingested during exercise. Taken together, these results suggest that within the low to moderate range of ingestion, there is little difference between the oxidation rates of glucose and fructose. However, when ingested in large amounts, the maximal capacity for fructose oxidation is lower than that of glucose. Furthermore, there is some evidence that fructose can be taken up and directly oxidized by the peripheral tissues without first being converted to glucose (4). The results of the present study suggest that a beverage containing GLU + FRU can be equally effective in providing exogenous CHO during exercise as one containing GLU alone when ingested at rates below the saturation of intestinal glucose transporters.
In the present study, CHO ingestion did not reduce rates of endogenous CHO oxidation compared with ingestion of water (Table 1; P = 0.49). This may have been due to lower rates of CHO ingestion compared with our previous studies. However, we also acknowledge the possibility that a relatively small sample size (n = 7) may have contributed to this overall result.
Plasma lactate concentrations during the first 30 min of exercise were significantly higher in the GLU + FRU trial compared with the GLU trial (Fig. 3B). This is consistent with several previous studies reporting elevated plasma lactate concentrations after GLU + FRU ingestion (9,18,21,25,38). In the liver, fructose is rapidly phosphorylated to fructose-1-phosphate, resulting in elevated concentrations of glycolytic intermediates (i.e., pyruvate) and thus elevated lactate formation (15). Additionally, animal studies suggest that during the process of intestinal absorption, some of the ingested fructose is converted to lactate (6,16). Most of the lactate is secreted into the portal vein and taken up by the liver; however, it is possible that some "spillover" into the systemic circulation could account for the higher plasma lactate concentrations observed with GLU + FRU ingestion. The metabolic fate of this additional lactate remains unclear. However, studies combining the use of isotope tracers and arterial-venous balance techniques demonstrate that lactate is an important substrate during exercise, with much lactate being taken up and oxidized by active skeletal muscle (5).
Fatigue during prolonged exercise can be attributed to dehydration as well as glycogen depletion. Therefore, consuming CHO containing beverages during exercise has become a common practice to meet the demand for fluid and CHO replenishment. In the present study, the accumulation of deuterium in plasma was used as a relative marker of fluid availability from the ingested beverages. Overall, plasma deuterium enrichment was similar between all three beverages (Fig. 4). This is in line with the observations of Davis et al. (10), who reported similar plasma deuterium profiles when ingesting water, 6%, 8%, and 10% CHO solutions. Davis et al. (10) suggested that ingesting a relatively dilute (i.e., < 10%) CHO solution was unlikely to reduce the rate at which fluid enters the systemic circulation when compared with water. Whether or not the slightly lower plasma deuterium enrichment in GLU compared with WAT at 30 min (Fig. 4) represents a real difference in fluid availability is unclear. Previously (21), we reported higher plasma deuterium enrichment after ingestion of deuterium-labeled water and GLU + FRU when compared with GLU. In that study, CHO was ingested at a relatively high rate (1.5 g·min−1) during exercise in a warm environment (32°C), which may reduce blood flow to the splanchnic region. These two factors may have contributed toward reduced intestinal CHO and fluid absorption during the GLU trial and suggests that GLU + FRU can increase fluid availability compared with GLU when intestinal absorption is limiting. During the present study, it appears that the low CHO ingestion rate and cool environment (∼20°C) did not reduce fluid absorption during the CHO trials when compared with WAT. Therefore, a dilute CHO solution, like the 6% solution used in the present study, can be just as effective at replacing fluid losses during exercise as plain water.
In summary, the present study demonstrates that at moderate rates of ingestion (0.8 g·min−1 or 48 g·h−1), exogenous CHO oxidation is similar between glucose and glucose plus fructose containing beverages. From a practical point of view, the results of the present study demonstrate that both CHO beverages are equally effective at providing energy within the dose range recommended by the ACSM guidelines.
This study was supported by a research grant from GlaxoSmithKline Consumer Healthcare, United Kingdom.
The results of the present study do not constitute endorsement by ACSM.
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