Stable 13C and radioactive 14C isotope studies show that ingested single carbohydrates (CHO) can be oxidized at rates up to ∼1.1 g·min−1 (for review, see 12). Even when large amounts of single CHO were ingested, oxidation rates did not exceed ∼1.1 g·min−1 (10,11,14,19,23). Recently, two studies from our laboratory have reported exogenous CHO oxidation rates above 1.1 g·min−1 with combined ingestion of glucose and fructose or glucose and sucrose (10,11). Peak exogenous CHO oxidation rates of ∼1.25 g·min−1 were observed during prolonged cycling exercise when ingesting large amounts (ingestion rate: 1.8 g·min−1) of glucose and fructose or glucose and sucrose solutions, and this was ∼20–55% higher than oxidation rates observed with ingestion of isoenergetic amounts of glucose solutions.
The maximal absorption rate for glucose in the intestine has been estimated to range from 1.2 to 1.7 g·min−1 under resting conditions (5). It has been suggested that intestinal CHO absorption and subsequent entry into the systemic circulation is a major limiting factor for exogenous CHO oxidation when large amounts of single CHO are ingested during exercise (12,14). Glucose is absorbed from the intestinal lumen at the brush border of the intestinal epithelium via sodium dependent glucose transporters (SGLT1) (6). Although direct evidence is lacking, it has been speculated that glucose transport via SGLT1 becomes saturated at glucose ingestion rates greater than 1.2 g·min−1 and higher ingestion rates will not result in higher oxidation rates during exercise (10). In contrast, fructose is transported from intestinal lumen to the cytosol by GLUT 5 transporters (6). Moreover, ingestion of beverages containing glucose in combination with fructose or sucrose results in higher CHO absorption than ingestion of glucose alone under resting conditions (21,22). Therefore, the ingestion of multiple transportable CHO (e.g., glucose and fructose, glucose and sucrose) may enhance intestinal absorption and could explain the higher exogenous CHO oxidation rates when two forms of simple carbohydrates are ingested rather than only one form (10,11).
Glucose polymers (maltodextrins) are commonly included in commercial sports drinks due to their neutral taste and relatively low osmolality compared with free glucose. Maltodextrins are hydrolyzed to free glucose molecules in the upper part of the small intestine, after which they are absorbed through the same SGLT1 transporters as ingested free glucose. As the intestinal absorption pathway for ingested maltodextrins and glucose are identical, it would be expected that both substrates would result in similar rates of exogenous CHO oxidation during exercise. Studies by Massicotte et al. (16) and Rehrer et al. (19) have reported similar oxidation rates from ingestion of isoenergetic amounts of glucose or maltodextrins (ingestion rate: ∼0.8 and ∼2.8 g·min−1 for each study, respectively) during cycling exercise. Indeed, Wagenmakers et al. (23) demonstrated that increasing the ingestion rate of maltodextrins to ∼2.4 g·min−1 during exercise will not increase oxidation rates above 1.1 g·min−1, further demonstrating the similarity to ingesting free glucose.
In accordance with the similarity in oxidation rates from ingesting maltodextrins or glucose, it would be expected that ingesting combinations of maltodextrins and fructose during exercise would elicit higher oxidation rates than maltodextrins alone through the utilization of multiple intestinal CHO transporters, as discussed above. It is not unlikely that ingesting large amounts (1.8 g·min−1) of maltodextrins and fructose will result in exogenous CHO oxidation rates during exercise higher than 1.1 g·min−1 as reported by Jentjens and colleagues for glucose and fructose (10) or glucose and sucrose (11), although this has never been systematically investigated.
Therefore, the purpose of the present study was to test the hypothesis that combined ingestion of a maltodextrins (1.2 g·min−1) and fructose (0.6 g·min−1) solution during 150 min of cycling exercise would lead to exogenous CHO oxidation rates higher than 1.1 g·min−1, and this would be higher than oxidation rates observed from ingesting an isoenergetic maltodextrins only solution.
Eight endurance trained male cyclists/triathletes aged 28.5 ± 2.0 yr and with a body mass of 78.8 ± 9.4 kg volunteered to participate in this study. This number of subjects exceeded the minimum sample size (calculated as N = 6, based on data from (10)) needed to detect differences in the primary dependent measure (exogenous CHO oxidation) with a power of 0.80 and a two-tailed alpha level of 0.05 (24). The subjects' maximal oxygen uptake (V̇O2max) and maximum power output (Wmax) achieved during the incremental test (see below) were 64.1 ± 3.1 mL·kg·min−1 and 359 ± 16 W, respectively. On average, subjects had been training for 11.3 ± 2.7 yr, and in the 3-month period before the study had been training 4.1 ± 0.5 d·wk−1 and 9.3 ± 1.6 h·wk−1. All subjects were informed of the purpose, practical details, and risks associated with the procedures before giving their written informed consent to participate. All subjects were healthy as assessed by a general health questionnaire. The study was approved by the School of Sport and Exercise Sciences ethics committee (Birmingham, UK).
At least 1 wk before the start of the experimental trials, an incremental cycle test to volitional exhaustion was performed in order to determine Wmax and V̇O2max. This test was performed on an electromagnetically braked cycle ergometer (Lode Excalibur Sport, Groningen, The Netherlands). Upon arrival at the laboratory, body mass (Seca Alpha, Hamburg, Germany) and height were recorded. Subjects then started cycling, with a 3-min warm-up at 95 W, followed by incremental steps of 35 W every 3 min until exhaustion. Wmax was determined by the following formula: Wmax = Wout + [(t/180)·35], where Wout is the power output (W) during the last completed stage, and t is the time (s) in the final stage. Heart rate (HR) was recorded continuously by a radio telemetry HR monitor (Polar Vantage, Kempele, Finland). Wmax values were used to determine the 55% Wmax, which was later employed in the experimental trials. Breath-by-breath measurements were performed throughout exercise by using an online automated gas-analysis system (Oxycon Pro, Jaeger, Würzberg, Germany). The volume sensor was calibrated by using a 3-L calibration syringe, and the gas analyzers were calibrated using a 5.03% CO2: 94.97% N2 gas mixture. Oxygen consumption (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 body weight per minute), 2) HR within 10 beats·min−1 of predicted maximum (HR of 220 beats·min−1 − age), and 3) a respiratory exchange ration (RER) >1.05. V̇O2max was calculated as the average V̇O2 over the last 60 s of the test.
Each subject completed three exercise trials that consisted of 150 min cycling at 55% Wmax while ingesting an 11.25% maltodextrin drink (MD), an isoenergetic maltodextrin plus fructose drink (MD+F) (the ingested MD to F-ratio was 2:1), or plain water (WAT). To quantify exogenous CHO oxidation, corn-derived MD (Glucidex 19, Roquette, France) and F (Krystar 300, A. E. Stanley Manufacturing Company, Illinois) were used, which have a high natural abundance of 13C (−11.01 and −10.87 Δ‰ vs Pee Dee Bellemnitella (PDB), respectively). The 13C enrichment of the ingested maltodextrin and fructose was determined by elemental analyzer-isotope ratio mass spectrometry (EA-IRMS; Europa Scientific GEO 20-20, Crewe, UK). The order of the trials was randomly assigned and 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 exercise trial and were then instructed to follow the same diet and activities before the next two trials. In addition, subjects were instructed to refrain from strenuous exercise and drinking any alcohol in the 24 h before the exercise trials. Furthermore, 4–7 d before each experimental trial, subjects were asked to perform an intense training session (“glycogen-depleting exercise bout”) in an attempt to empty any 13C-enriched glycogen stores. Subjects were further instructed not to consume products with a high natural abundance of 13C (carbohydrates derived from C4 plants such as maize and sugar cane) at least 1 wk before and during the entire experimental period to reduce the background shift (change in 13C) from endogenous substrate stores. These procedures have been previously shown to reduce the background (change in 13C) from endogenous substrate stores (23).
The subjects arrived at the laboratory in the morning (between 7:00 and 9:00 a.m.) after an overnight fast (10–12 h). All experimental trials were performed at the same time of day to avoid circadian variance. On arrival, subjects were weighed before a 20-gauge Teflon catheter (Venflon, BD, Plymouth, UK) was inserted into 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 cannula was kept patent by flushing with 1.0–1.5 mL of isotonic saline (0.9%, BD) after each blood sample collection.
The subjects then mounted a cycle ergometer and a resting breath sample was collected into 10-mL Exetainer tubes (Labco Ltd., Brow Works, High Wycombe, UK), which were filled directly from a mixing chamber to determine the 13C/12C ratio in the expired air. A resting blood sample (10 mL) was collected and stored on ice until centrifugation. Subjects then started a 150-min exercise bout at a work rate equivalent to 55% Wmax (64.2 ± 3.5% V̇O2max). Additional blood samples were drawn at 15-min intervals until the cessation of exercise. Expiratory breath samples were collected every 15 min until the end of exercise for 5-min periods. During the first 4 min, V̇O2, carbon dioxide production (V̇CO2), and respiratory exchange ratio (RER) were measured using an online automated gas analysis system as previously described, while duplicate Vacutainers were filled for breath 13C/12C ratio as described above during the final 60 s of each 5-min period.
During the first 2–3 min of exercise, subjects ingested an initial bolus (600 mL) of one of the three experimental drinks: MD, MD+F, or WAT. Thereafter a beverage volume of 200 mL was provided every 15 min. The total fluid intake during the exercise bout was 2.4 L. The rate of maltodextrin intake in the MD and MD+F trials was 1.8 and 1.2 g·min−1, respectively. In addition, fructose was ingested at a rate of 0.6 g·min−1 in the MD+F trial, which brought the total CHO intake rate in each CHO condition to 1.8 g·min−1 (11.25% solutions). The osmolality of the drinks was 260 and 108 mOsm·kg−1 for MD+F and MD, respectively. All exercise tests were performed under normal and standard environmental conditions (16–26°C dry bulb temperature and 50–60% relative humidity). During the exercise trials, subjects were cooled with standing floor fans to minimize thermal stress.
Every 30 min during the exercise bout, subjects were requested to verbally answer a short questionnaire containing questions regarding the presence of gastrointestinal (GI) problems at that moment (13). GI symptoms were scored on a 10-point scale (1 = not at all and 10 = very, very much) and divided into two categories: severe and less severe symptoms. Severe complaints included nausea, stomach problems, intestinal cramps, and urge to vomit, and were only registered as severe when a score of 5 or above out 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.
All blood samples were collected into prechilled test tubes containing EDTA and centrifuged at 2300 × g for 10 min at 4°C. Aliquots of the plasma were frozen in liquid nitrogen and stored at −25°C until further analysis. Plasma samples were analyzed enzymatically for glucose (Glucose HK, ABX Diagnostics, UK), lactate (Lactic Acid, ABX Diagnostics), and free fatty acid (FFA) (NEFA-C Kit, Alpha Laboratories, UK) concentration on a semiautomatic analyzer (Cobas Mira S-Plus, ABX). Due to problems with blood sampling in one subject, data for blood parameters are for N = 7.
Breath samples were analyzed for 13C/12C ratio by gas chromatography continuous flow isotope ratio mass spectrometry (GC-IRMS; Europa Scientific, Crewe, UK). From indirect calorimetry (V̇O2 and V̇CO2) and stable isotope measurements (breath 13C/12C ratio), rates of total fat, total CHO, and exogenous CHO oxidation were calculated.
From V̇O2 and V̇CO2 (L·min−1), carbohydrate and fat oxidation rates (g·min−1) were calculated using stoichiometric equations (7), with the assumption that protein oxidation during exercise was negligible.
It should be noted, however, that protein catabolism (and oxidation) may occur during exercise (2), and this may have influenced our calculations of the proportion of energy derived from CHO and fat oxidation during exercise.
The isotopic enrichment was expressed as Δ per milliliter difference between the 13C/12C ratio of the sample and a known laboratory reference standard according to the formula of Craig (4):
The Δ13C was then related to an international standard (PDB).
In the carbohydrate trials, the rate of exogenous CHO oxidation was calculated using the following formula (18):
in which ΔExp is the 13C enrichment of expired air during exercise at different time points, ΔIng is the 13C enrichment of the ingested CHO solution, ΔExpbkg is the 13C enrichment of expired air in the WAT trial (background) at different time points, and k is the amount of CO2 (in liters) produced by the oxidation of 1 g of glucose (k = 0.7467 L of CO2 per gram of glucose).
Endogenous CHO oxidation was calculated by subtracting exogenous CHO oxidation from total CHO oxidation. A methodological consideration when using 13CO2 in expired air to calculate exogenous substrate oxidation is the temporary fixing of 13CO2 in the bicarbonate pool, in which an amount of CO2 arising from CHO and fat oxidation is retained (20). However, during exercise, the turnover of this pool increases severalfold so that a physiological steady state condition will occur relatively rapidly and 13CO2 in the expired air will be equilibrated with the 13CO2/H13CO2 pool, respectively. Recovery of 13CO2 from oxidation will approach 100% after 60 min of exercise when the dilution in the bicarbonate pool becomes negligible (17,20). As a consequence of this, all calculations on substrate oxidation were performed over the last 90 min of exercise (60–150 min).
The oxidation efficiency was determined as the percentage of the ingested CHO that was oxidized and was calculated by dividing exogenous CHO oxidation rate by the CHO ingestion rate and then multiplied by 100.
A two-way analysis of variance for repeated measures was used to compare differences in substrate utilization and in blood metabolites between the three trials. A Tukey post hoc test was applied where a significant F-ratio was detected. A paired samples Student's t-test was used to identify differences between the MD and MD+F trials in exogenous CHO oxidation rates averaged in 30-min blocks for the 60–90, 90–120, and 120–150 min time periods, and also averaged over the last 90 min of exercise. All values are presented as mean ± SE. Statistical significance was set at P < 0.05.
Stable isotope measurements.
Resting breath 13C enrichment was similar at the beginning of all three exercise trials, averaging −26.69 ± 0.30, −26.72 ± 0.20, and −26.52 ± 0.28 Δ‰ versus PDB for WAT, MD, and MD+F, respectively. Expired breath 13C enrichment during each trial is shown in Figure 1. In the MD and MD+F trials, expired breath 13C enrichment increased to −21.51 ± 0.23 and −19.63 ± 0.12 Δ‰ versus PDB, respectively, at 150 min of exercise (significantly different from their respective resting values, P < 0.05). In addition, the increase in breath 13C enrichment in the MD+F trial was greater than that in the MD trial from 45 min onward (P < 0.05). During the WAT trial, expired breath 13C enrichment increased slightly but significantly from resting values to a maximum of −25.88 ± 0.26 Δ‰ versus PDB at 150 min of exercise (P < 0.05). However, for the calculation of exogenous CHO oxidation, the increase in breath 13C enrichment at specific time points during WAT was subtracted from the increase in the tests with CHO ingestion to correct for the change in background enrichment.
V̇O2, RER, total CHO, and fat oxidation.
V̇O2, RER, and total CHO and fat oxidation rates for the last 90 min of the exercise period are shown in Table 1. No differences in V̇O2 were found either between trials or among time points. RER was significantly lower in the WAT trial compared with the two CHO ingestion trials but was not different between CHO trials (WAT compared with MD and MD+F, P < 0.05). Total CHO oxidation during the last 90 min of exercise was significantly higher after CHO ingestion than in the WAT trial (WAT, 1.94 ± 0.10 vs MD, 2.34 ± 0.17 g·min−1; WAT, 1.94 ± 0.10 vs MD+F, 2.60 ± 0.13 g·min−1, P < 0.05). No significant differences in total CHO oxidation were found between CHO trials. Fat oxidation was significantly higher in the WAT trial than after CHO ingestion (P < 0.05) except during the 90- to 120-min period for the MD trial. Average fat oxidation rates over the last 90 min of exercise were 0.88 ± 0.06, 0.70 ± 0.06, and 0.60 ± 0.04 g·min−1 for WAT, MD, and MD+F, respectively. Fat oxidation did not differ significantly between the two CHO trials. The relative contribution of substrates to total energy expenditure during the last 90 min of exercise is shown in Figure 2.
Exogenous CHO oxidation, endogenous CHO oxidation, and oxidation efficiency.
In line with the increase in breath 13C enrichment (Fig. 1), exogenous CHO oxidation rates gradually increased during the first 120 min of exercise and leveled off in the last 30 min of exercise. The average oxidation rates over the final 30-min exercise period were 1.06 ± 0.08 and 1.50 ± 0.07 g·min−1 for MD and MD+F, respectively (Table 1). Peak oxidation rates were reached at the end of exercise (150 min) and were significantly higher in the MD+F trial than the MD trial (1.53 ± 0.07 and 1.10 ± 0.09 g·min−1, respectively, P < 0.05; range, 1.23–1.77 and 0.78–1.40 g·min−1 for MD+F and MD, respectively). The contribution of exogenous CHO oxidation to total energy expenditure during the last 90 min of exercise was significantly higher in the MD+F trial than the MD trial (P < 0.05, Fig. 2).
During the last 90 min of exercise, endogenous CHO oxidation was significantly lower in the CHO trials compared with the WAT trial (P < 0.05, Table 1). Moreover, the contribution of endogenous CHO oxidation to total energy expenditure was lower in the CHO trials compared with WAT (Fig. 2). No statistically significant differences were found in endogenous CHO oxidation rates (1.38 ± 0.11 and 1.22 ± 0.10 g·min−1) or the contribution of endogenous CHO oxidation to total energy expenditure (33.5 ± 2.4% and 29.6 ± 2.3%) over the last 90 min of exercise in the MD and MD+F trials.
The total amount of the ingested CHO that was oxidized during the entire 150 min exercise bout was significantly higher in the MD+F trial than the MD trial (170 ± 8 vs 116 ± 9 g, respectively, P < 0.05). Furthermore, the oxidation efficiency in the MD+F trial was higher (63 ± 3%) than in the MD trial (43 ± 3%, P < 0.05).
Plasma glucose, lactate, and free fatty acid concentrations at rest and during exercise are shown in Figure 3 A, B, and C, respectively. The plasma glucose concentration before exercise was similar in all trials (∼4.4–4.5 mmol·L−1). During exercise in the WAT trial, plasma glucose concentrations gradually declined from 4.4 ± 0.1 to 3.5 ± 0.2 mmol·L−1 at the end of exercise (P < 0.05). Plasma glucose concentrations were higher in the CHO trials than the WAT trial, and this reached statistical significance at 60 min (P < 0.05) and from 90 min until the cessation of exercise (P < 0.05). No differences in plasma glucose concentrations were found between the two CHO trials.
Resting plasma lactate concentrations were similar in all trials (∼0.8–0.9 mmol·L−1). Plasma lactate concentrations increased (P < 0.05) in the first 15 min of all three exercise trials. Thereafter, plasma lactate remained relatively stable throughout the entire exercise period. No differences in plasma lactate concentrations were observed between the trials, with the exception of the 60 and 90 min time points where lactate was significantly higher in the MD+F trial than the WAT (P < 0.05).
Plasma FFA concentrations were similar in all trials at rest (∼292–324 μmol·L−1). In the WAT trial, FFA concentrations were reduced to 274 ± 23 μmol·L−1 after the first 15 min of exercise (although this did not reach statistical significance) and then gradually increased throughout the duration of exercise to reach peak values of 796 ± 63 μmol·L−1. This increase became significantly different from resting values after 60 min and remained so until the cessation of exercise (P < 0.05). In both the CHO trials, plasma FFA decreased at the onset of exercise and remained lower than resting concentrations for 90–105 min but were no different to baseline by the end of exercise. Plasma FFA concentrations were higher in the WAT trial than the MD+F trial from 30 min until the end of exercise (P < 0.05), and higher than the MD trial from 75 min until the end of exercise (P < 0.05). There were no significant differences between the two CHO trials in plasma FFA concentrations.
Gastrointestinal and related complaints were registered by a questionnaire. There were four reports of severe gastrointestinal complaints in the MD, compared with one report in the MD+F trial.
The purpose of this study was to determine the rate of exogenous CHO oxidation while ingesting a solution containing a combination of MD+F during prolonged exercise. The main finding of the present study was that a mixture of MD+F when ingested at a high rate (1.8 g·min−1) during exercise resulted in peak exogenous CHO oxidation rates of ∼1.5 g·min−1, and this was ∼40% higher than oxidation rates observed with the ingestion of an isoenergetic amount of MD (Table 1).
In the present study, peak exogenous CHO oxidation rates while ingesting large amounts of MD during exercise were ∼1.1 g·min−1. These oxidation rates are in agreement with previous studies and confirm that oxidation rates will not rise above 1.1 g·min−1 when single transportable CHO are ingested during exercise (10,11,14,19,23). Combined ingestion of MD+F in the present study resulted in average peak exogenous CHO oxidation rates of ∼1.5 g·min−1. This finding is consistent with previous reports from our laboratory demonstrating exogenous CHO oxidation rates higher than 1.1 g·min−1 with combined ingestion of large amounts of glucose and fructose or sucrose during prolonged cycling exercise (10,11).
Evidence suggests that the most important rate-limiting factor in the bioavailability of ingested CHO is the rate of absorption of CHO from the small intestine into the systemic circulation. Studies using the triple-lumen technique have measured glucose absorption and estimated whole-body intestinal absorption rates of a 6% glucose-electrolyte solution (5). It was estimated that the maximal absorption rate of the intestine ranged from 1.2 to 1.7 g·min−1. Such measurements are usually made over 40 cm of the small intestine and extrapolations to whole-body absorption rates are problematic, especially because various sections of the gut have different absorptive capacities. Because of limitations of the techniques that measure absorption directly, there is only indirect evidence for limitations at the level of absorption. Probably the strongest evidence is from studies using CHO types that use different transport proteins for absorption across the intestinal epithelial membrane.
Studies by the group of Gisolfi (21,22) demonstrated that CHO absorption was greater with beverages containing two or three transportable substrates (glucose and fructose or sucrose) than isoenergetic beverages containing single transportable CHO (glucose or maltodextrins). The authors suggested that adding a second transportable substrate to a solution (e.g., fructose) stimulates additional transport mechanisms. The monosaccharide glucose is transported across the luminal membrane by SGLT1, whereas fructose is transported by GLUT5 (6). It was hypothesized that a mixture of these CHO may reduce competition for transport and increase total CHO absorption (21,22). Although intestinal CHO absorption rates were not determined in the present study, the fact that free glucose or glucose derived from the hydrolysis of maltodextrins and fructose are absorbed by different intestinal transporters could explain the high rates of exogenous CHO oxidation observed in the present study (and others (1,10,11)) when mixtures of these CHO are consumed.
Interestingly, in the present study, higher oxidation rates were observed from ingestion of MD+F compared with those previously reported by Jentjens and colleagues for glucose and fructose (11) or glucose and sucrose (12) [∼1.5 g·min−1 in the present study vs ∼1.25 g·min−1 in (10,11)]. The present study was similar to the previous study by Jentjens et al. (10) in that the rate of CHO ingestion was 1.8 g·min−1. However, the solution osmolality of the MD+F beverage in the present study was markedly lower (260 mOsm·kg−1) than the osmolality of the glucose and fructose beverage used by Jentjens et al. (10) (866 mOsm·kg−1). Most studies (9,16,19) report similar rates of exogenous CHO oxidation with ingestion of MD compared with glucose, suggesting that solution osmolality is not important when large amounts of single carbohydrates are ingested during exercise. However, comparing data from the present study with that of previous reports (10,11) indicates that solution osmolality may become an important factor in determining exogenous CHO oxidation rates when large amounts of multiple transportable CHO are ingested during exercise, although this remains to be systematically investigated.
CHO feeding in the present study resulted in a marked suppression of endogenous CHO oxidation (Table 1), which is in line with previous reports (14,15). There was, however, no significant difference in endogenous CHO sparing between the MD and MD+F trial (Fig. 2). In the present study, total CHO oxidation and plasma glucose concentration was higher in the CHO trials than the water trial (Table 1, Fig. 3A). The higher total CHO oxidation with CHO ingestion is most likely explained by an increase in plasma glucose oxidation (15). The benefit of CHO feedings on exercise performance is largely attributed to the maintenance of euglycemia and high rates of CHO oxidation late in exercise (3). In contrast to CHO oxidation, fat oxidation was suppressed during exercise with CHO ingestion (Table 1), although there was no significant difference in the suppression of fat oxidation between the MD and MD+F trial. Although plasma insulin concentrations were not measured in the present study, the reduction in fat oxidation observed may be explained by an elevation in circulating insulin concentrations with carbohydrate ingestion, as insulin has been shown to be a potent inhibitor of whole body lipolysis and fat oxidation during exercise (8). Indeed, the blunting of the rise in free fatty acids with CHO ingestion in the present study is in line with this notion (8) (Fig. 3C).
In summary, this study demonstrated that ingestion of large amounts MD and F during prolonged cycling exercise can result in exogenous CHO oxidation rates greater than 1.1 g·min−1, and this is ∼40% higher than oxidation rates from ingesting an isoenergetic amount of MD. In addition, the oxidation rates observed in the present study were higher than those previously reported for combined glucose and fructose/sucrose ingestion during exercise. These data suggest that if high exogenous CHO oxidation rates are required during exercise (i.e., >1.2–1.3 g·min−1), ingestion of a solution containing multiple transportable CHO in the form of maltodextrins and fructose is recommended.
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