The ingestion of CHO improves prolonged cycling as well as running endurance capacity and performance (for a review, see Jeukendrup ). Although a few studies have not shown an ergogenic effect (3,18,30), it is generally accepted and recommended that athletes should ingest CHO during prolonged exercise (2,24). However, the appropriate advice for the dosage rate of CHO during exercise is still under debate. The commonly accepted recommendations of the American College of Sports Medicine (2) are primarily based on laboratory studies conducted on cycle ergometers using a CHO delivery rate of 30-60 g·h−1 (0.5-1 g·min−1; ∼6%-8% CHO solutions), with CHO mostly in the form of glucose solutions (10). A more recent and alternative recommendation (24) is largely based on studies investigating exogenous CHO oxidation during cycling exercise from ingested liquid CHO blends (e.g., glucose + fructose solutions [23,26,39]). On the basis of those studies, the ingestion of larger amounts of CHO blends results in 20%-50% greater oxidation rates (23,26,39) and performance improvements (15) compared with a single CHO source (e.g., glucose alone). Therefore, this contemporary recommendation advises athletes to take in CHO blends at higher rates of up to 90 g·h−1 (1.5 g·min−1) during prolonged high-intensity exercise (24). These present recommendations (2,24) are almost exclusively based on laboratory studies that used cycling as the mode of exercise, and the validity of these CHO intake recommendations for runners remains to be confirmed.
Currently, little is known about the potential differences in exogenous CHO utilization when comparing cycling versus running. To our knowledge, there is only one study in the literature that has compared both modes of exercise. In this study, Derman et al. (16) showed similar oxidation rates during running compared with cycling. However, the exercise intensity in that study was set at approximately 80% V˙O2max, and the running trial lasted only approximately 1 h. As described in the Methods section, the tracer methodology that is used to measure exogenous CHO oxidation is limited within the first hour of exercise and can be problematic at higher exercise intensities. Therefore, the examination of exogenous CHO oxidation during prolonged cycling as compared with running remains to be examined.
The movement and muscle recruitment patterns of the two modes of exercise are clearly different (5,20), and it is not surprising that differences in energy metabolism have been detected (1,29). A difference in exogenous CHO oxidation could be expected on the basis of the few studies that have investigated exercise metabolism during running compared with cycling (1,4,16,29). Studies investigating substrate oxidation in the fasted state with the use of a graded exercise protocol have detected higher total fat oxidation rates over a wide range of intensities during running as compared with cycling (1,29). It has also been proposed that CHO ingestion during running causes a higher elevation of plasma glucose and insulin concentrations compared with cycling (4,36), which would potentially lead to an increase in muscle glucose uptake and reduced glycogenolyses. Furthermore, running is associated with a higher prevalence for gastrointestinal (GI) distress compared with cycling (31,32), and it was speculated that one factor leading to GI symptoms during running could be altered absorption because of relatively high mechanical stress (19). Taken together, we hypothesized that exogenous CHO would be oxidized less effectively during running as compared with cycling. The present study was therefore designed to investigate whether exogenous CHO oxidation rates are different during prolonged (2 h) running compared with cycling at the same relative sport-specific exercise intensity of approximately 60% V˙O2max.
Eight well-trained male endurance cyclists or triathletes (mean ± SD: age = 37 ± 7 yr, weight = 75 ± 7 kg, height = 1.77 ± 0.05 m, V˙O2max CYCLE = 63 ± 3 mL·kg−1·min−1, V˙O2max RUN = 65 ± 4 mL·kg−1·min−1) volunteered to participate in this study. Subjects undertook both cycling and running training at least three times per week for more than 2 h per session. Furthermore, they had been involved in running and cycling training for a similar length of time and at least 2 yr. All subjects were healthy as assessed by a general health questionnaire and were informed of the purpose, practical details, and risks associated with the procedures before giving their written informed consent to participate. The studies were approved by the School of Sport and Exercise Sciences ethics subcommittee, University of Birmingham, Birmingham, UK.
At least 1 wk before the start of the experimental trials, two incremental exercise tests to volitional exhaustion were performed in randomized order, separated by at least 3 d. Each test was performed to determine the relationship between oxygen consumption and power output or speed as well as maximal oxygen consumption (V˙O2max) and lactate threshold (LT) for cycling or running on a cycle ergometer and treadmill, respectively. To determine the exercise intensity for the following experimental trials, a linear regression of V˙O2 against speed or power output was plotted, and the running speed or cycling power output at 60% of V˙O2max was calculated for running and cycling, respectively. LT was also determined for each mode of exercise according to the method of Coyle et al. (13), where LT is defined as the speed or power output at which plasma lactate concentrations rises 1 mmol·L−1 above baseline. During the first visit to the laboratory, body mass (Seca Alpha, Hamburg, Germany) and height were recorded. Before each test, a 20-gauge Teflon catheter (Venflon, BD, Plymouth, UK) was inserted into an antecubital vein of an arm of the subject and attached to a three-way stopcock (Sims Portex, Kingsmead, UK) to allow for repeated blood sampling during exercise and subsequent analyses of plasma lactate.
Preliminary cycling test protocol.
This test was performed on an electromagnetically braked cycle ergometer (Lode Excalibur Sport, Groningen, The Netherlands). Subjects started cycling for 3 min at 95 W, followed by incremental steps of 35 W every 3 min until exhaustion. A blood sample (∼2 mL) was taken at the end of each step. HR was recorded continuously by a radio telemetry HR monitor (Polar 625X, Kempele, Finland). Breath-by-breath measurements were performed throughout exercise using an automated online gas analysis system (Oxycon Pro; Jaeger, Würzburg, Germany).
Preliminary running test protocol.
This test was performed on a treadmill ergometer (h/p Cosmos Quasar, h/p/Cosmos, Traunstein, Germany) and was modified according to the protocol of Costill and Fox (11). Before commencement of the study, the protocol was tested with four subjects to ensure that V˙O2max values were reached. The subjects started to run at 6 km·h−1, followed by incremental steps of 2 km·h−1 every 3 min until a speed of 14 km·h−1 was reached. From this point, the speed was held constant, and the gradient was increased by 1.5% per step. Blood samples were taken at the end of each 3-min step. When the RER reached 1.0 (100% CHO oxidation), the incremental protocol steps were shortened to 1 min, and the test was stopped when a subject clearly indicated exhaustion.
Each subject completed four exercise trials in random order, separated by at least 5 d. The randomized trials consisted of 120 min of cycling (CYCLE) or running (RUN) at approximately 60% V˙O2max while ingesting either 1) 1.5 g·min−1 CHO (glucose and fructose in the ratio of 2:1) in the form of a 13.3% maltodextrin plus fructose drink (CHO) or 2) a control trial of plain water (WAT). The CHO intake rate was based on recent recommendations for CHO intake from multiple transportable CHO (24,28).
To quantify exogenous CHO oxidation, corn-derived maltodextrin (Glucidex 19, Roquette, France) and fructose (Krystar 300 Crystalline Fructose; Tate & Lyle, Decatur, IL) were used for preparation of the DRINK, which have a high natural abundance of 13C (−11.22 and −11.00 δ‰ vs Pee Dee Bellemnitella, respectively). The 13C enrichment of the ingested CHO was determined by elemental analyzer-isotope ratio mass spectrometry (Europa Scientific GEO 20-20, Crewe, UK).
Diet and activity before testing.
Before the first trial, advice was given to follow a diet rich in CHO. It was made sure that CHO intake was >4 g·kg−1 body weight, which in combination with light training or rest would prevent participants to start the trials with depleted muscle glycogen stores. Subjects were asked to record their food intake and activity patterns for 24 h before the first experimental trial and were then instructed to follow the same diet and activities before the next three experimental trials. Compliance was assessed with a 24-h recall the day before each of the remaining trials. In addition, subjects were instructed to refrain from strenuous exercise and drinking any alcohol in the 24 h before the experimental trials. Furthermore, 3-7 d before each experimental trial, the subjects were told to perform a long (>2 h) and hard training session in an attempt to deplete glycogen stores and to reduce any 13C-enriched glycogen stores. Subjects were instructed before the first trial about the requirements of a "glycogen depleting exercise." They were free to choose the exact protocol but had to repeat the same procedure before each trial. Subjects were also instructed not to consume products with a high natural abundance of 13C (CHO derived from C4 plants such as maize and sugar cane) at least 1 wk before each experimental trial to reduce the background shift (change in 13C) from endogenous substrate stores. Compliance with the instructions for a "glycogen depleting" training bout and with the "low 13C diet" was assessed verbally before each trial.
The subjects arrived in the laboratory in the morning (between 6:00 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) was inserted into an antecubital vein of an arm and attached to a three-way stopcock (Sims Portex) 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 or treadmill, and a resting breath sample was collected into 10-mL Exetainer tube (Labco Ltd., Brow Works, High Wycombe, UK), which was 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 the 120-min exercise bout at a work rate calculated to be equivalent to 60% V˙O2max for that respective exercise mode (either CYCLE or RUN). Respiratory gas measures were taken after 10 min, and if necessary, workload or speed was adjusted to match 60% V˙O2max. Additional blood samples were drawn at 15-min intervals until the cessation of exercise, along with measures of V˙O2 and V˙CO2, using an automated online gas analysis system (Oxycon Pro; Jaeger). Within the last 60 s of each 3-min period, Exetainer tubes were filled in duplicate for breath 13C/12C ratio as described earlier.
During the first 2-3 min of exercise, subjects ingested an initial bolus of one of the two experimental treatments: 300 mL of water (WAT) or 300 mL of 13.3% CHO drink (DRINK). Thereafter, a beverage volume of 150 mL of WAT or 150 mL of 13.3% CHO DRINK was provided every 15 min. The total fluid intake during the exercise bout was 1.35 L (675 mL·h−1), whereas the total CHO intake was 180 g (90 g·h−1 or 1.5 g·min−1). All exercise tests were performed under normal and standard environmental conditions (16°C-24°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 to directly assess GI tolerance. GI symptoms were scored on a 10-point scale (0 = no problem at all, 9 = the worst it has ever been). A score >4 was registered as serious. RPE were collected using a 6- to 20-point Borg scale (6).
All blood samples were collected into prechilled test tubes containing EDTA and centrifuged at 2300g for 10 min at 4°C. Aliquots of the plasma were frozen 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 (NEFA-C Kit, Alpha Laboratories, UK) concentration on a semiautomatic analyzer (Cobas Mira S-Plus; ABX Diagnostics). Insulin was analyzed by ELISA (DRG® Ultrasensitive Insulin ELISA; DRG Instruments GmbH, Marburg, Germany). Breath samples were analyzed for 13C/12C ratio by continuous flow IRMS (GC, Trace GC Ultra and IRMS, Delta Plus XP; both Thermo Finnigan, Herts, UK). From indirect calorimetry (V˙O2 and V˙CO2) and stable isotope measurements (breath 13C enrichment), rates of total fat, total CHO, and exogenous CHO oxidation were calculated.
From V˙O2 and V˙CO2 (L·min−1), CHO and fat oxidation rates (g·min−1) were calculated using stoichiometric equations (27), 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 following formula (14):
The δ13C was then related to an international standard (Pee Dee Bellemnitella).
In the CHO trials, the rate of exogenous CHO oxidation was calculated using the following formula (33):
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 (34). 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 (34). As a consequence, all calculations on substrate oxidation were performed over the last 60 min of exercise (60-120 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 multiplying by 100.
A two-way (trial × time) ANOVA for repeated-measures was used to compare differences in substrate utilization and in blood metabolites between the trials. A Tukey post hoc test was applied, where a significant F-ratio was detected. Paired sample t-tests were applied when two mean values were compared. All values are presented as mean ± SD. Statistical significance was set at P < 0.05. All statistics were performed using the Statistical Package for the Social Sciences for Windows (Version 15; SPSS Inc., Chicago, IL).
V˙O2, EE, HR, RPE, and LT.
Oxygen uptake (V˙O2) was not significantly different between treatments within a given mode of exercise. V˙O2 over the final 2 h was higher (P = 0.002) during RUN compared with CYCLE within the WAT trial but not significantly different with CHO treatment (P = 0.1). The set workload elicited similar relative exercise intensities of 59.7% ± 2.0% and 59.2% ± 1.9% V˙O2max for RUN and CYCLE, respectively. Energy expenditure was similar between the CHO and the WAT treatments for both running (3603 ± 251 and 3581 ± 266 kJ for WAT and CHO, respectively) and cycling trials (3436 ± 204 and 3464 ± 260 kJ for WAT and CHO, respectively). However, energy expenditure was higher during RUN compared with CYCLE during the WAT trials (P = 0.003) but not significant in the CHO trials (P = 0.08). Average HR over the last hour (127 ± 12, 123 ± 10, 130 ± 13, and 127 ± 12 bpm for WAT RUN, WAT CYCLE, CHO RUN, and CHO CYCLE, respectively) was significantly higher during RUN compared with CYCLE within the WAT trial (P = 0.04) and not significantly different with CHO treatment (P = 0.06). RPE values were similar between all trails (11 ± 1, 12 ± 1, 11 ± 1, and 11 ± 1 for WAT RUN, WAT CYCLE, CHO RUN, and CHO CYCLE, respectively). Subjects exercised at significantly higher percentage of LT during RUN compared with CYCLE (79% ± 3% and 72% ± 3% LT, respectively, P = 0.02).
Exogenous CHO oxidation, endogenous CHO oxidation, and oxidation efficiency.
Exogenous CHO oxidation rates increased similarly over time during both modes of exercise (Fig. 1). Peak exogenous CHO oxidation rates were reached at the end of 120 min of exercise and were not significantly different between RUN and CYCLE trials (1.25 ± 0.10 vs 1.19 ± 0.08 g·min−1, respectively, P = 0.13). The average exogenous CHO oxidation rates over the final hour of exercise were also not significantly different between RUN and CYCLE trials (1.14 ± 0.10 and 1.11 ± 0.11 g·min−1, respectively, P = 0.94; Table 1). Furthermore, the oxidation efficiency was not different between trials (76% ± 6% vs 72% ± 7%, respectively, P = 0.33).
Endogenous CHO oxidation during the last 60 min of exercise was significantly lower with CHO ingestion compared with WAT trials irrespective of mode of exercise (P = 0.005 and 0.01 for RUN and CYCLE, respectively; Table 1). There was a trend for lower endogenous CHO oxidation during the RUN compared with the CYCLE trials; however, those results were not statistically significant (P = 0.09 for WAT and CHO).
RER, total CHO, and fat oxidation.
RER and total CHO and fat oxidation rates over the 60- to 120-min exercise period are shown in Table 1. Significantly lower RER were measured in both WAT trials compared with the two CHO ingestion trials (P = 0.002 and 0.003 for RUN and CYCLE, respectively) but were not significantly different between modes of exercise. Average total CHO oxidation rates over the last 60 min of exercise were not significantly different between WAT RUN and WAT CYCLE or between CHO RUN and CHO CYCLE. Both CHO trials produced significantly higher total CHO oxidation as compared with the WAT trials (P = 0.02 and 0.03 for RUN and CYCLE, respectively).
Average fat oxidation rates over the last hour were significantly lower with CHO ingestion compared with WAT trials (P = 0.003 and 0.005 for RUN and CYCLE, respectively). With the ingestion of water significantly higher, fat oxidation rates were measured in the RUN trial compared with the CYCLE trial (P = 0.02). With the ingestion of CHO, fat oxidation rates tended to be higher during RUN as compared with CYCLE (P = 0.09).
Resting concentration of plasma glucose, insulin, and lactate were not significantly different before the onset of the four trials. Within a given treatment (CHO vs WAT), there were no statistical differences found between the modes of exercise (CYCLE vs RUN) for any of the plasma measures. Plasma glucose and insulin concentrations are shown in Figures 2 and 3, respectively. During exercise in the WAT trial, plasma glucose concentrations stayed relatively stable and above approximately 4.7 mmol·L−1 over the entire exercise period. Plasma glucose concentrations increased with the ingestion of both CHO trials to peak values of approximately 6.5 mmol·L−1 at 30 min during both modes of exercise. In both the RUN and the CYCLE trials, plasma glucose concentrations were significantly higher over the whole period, except the 60-min time point with both treatments, the 120-min measure in the RUN trial, and the 105-min time point in the CYCLE trial. Plasma insulin concentrations increased with the ingestion of CHO to peak values of approximately 35 μU·mL−1 after 30 min during RUN and CYCLE trial. In both WAT ingestion trials, plasma insulin concentrations decreased to values approximately 10 μU·mL−1 over the 120-min exercise period. Plasma insulin concentrations were significantly higher with the ingestion of CHO over the whole exercise period compared with WAT for both the RUN and the CYCLE trials. No difference between modes of exercise was detected with both treatments.
Plasma lactate concentrations increased during the first 30 min of exercise in all four exercise trials (Fig. 4). Thereafter, plasma lactate concentrations remained relatively stable throughout the exercise period. Plasma lactate concentrations were not significantly different between CHO trials for RUN versus CYCLE (P = 0.1). However, higher lactate concentrations were measured during CYCLE trials compared with RUN in the WAT trial (P = 0.03).
GI symptoms and perceived fullness.
No severe GI problems (>4) were recorded in any of the trials. Mean scores for upper abdominal problems were not significantly different between trials (0.0 ± 0.0, 0.0 ± 0.0, 0.0 ± 0.1, and 0.0 ± 0.0 during WAT RUN, WAT CYCLE, CHO RUN, and CHO CYCLE, respectively). Accordingly, mean scores for lower abdominal problems were not significantly different between all trials (0.0 ± 0.0, 0.0 ± 0.0, 0.1 ± 0.2, and 0.0 ± 0.0 during WAT RUN, WAT CYCLE, CHO RUN, and CHO CYCLE, respectively). Furthermore, no difference in perceived stomach fullness was detected.
In the present study, we investigated exogenous CHO oxidation during running compared with cycling at the same relative intensity (∼60% V˙O2max). The main finding was that peak and average exogenous CHO oxidation rates were similar between the two modes of exercise. Previous research investigating exogenous CHO oxidation rates has predominantly been conducted on cycle ergometers, and these findings have been used to base general CHO intake recommendations during prolonged endurance activities, including running. The similar exogenous CHO oxidation rates in the current study provide evidence that the previous exogenous CHO oxidation findings in cycling studies can also be extrapolated to running.
In contrast to our hypothesis, we found no difference in exogenous CHO oxidation rates between both modes of exercise. With the present CHO intake rate of 1.5 g·min−1 of a 2:1 GLU/FRU ratio, we anticipated intestinal glucose transporters (SGLT-1) to become saturated and exogenous CHO oxidation rates to peak at approximately 1.2 g·min−1 (26) during cycling. Indeed, the observed oxidation rates in the CYCLE trial matched these expectations. During the RUN trial, similarly high exogenous CHO oxidation rates were detected. This finding is supported by a study of Derman et al. (16), which also reported similar oxidation rates during running compared with cycling. However, these results have to be regarded with caution because of limitations in their methodology to measure exogenous CHO oxidation. When the applied 14C tracer is metabolized, some of the arising 14CO2 will be temporarily trapped in the bicarbonate pool, even more so during high-intensity exercise. Over time, the turnover of this pool increases severalfold so that a physiological steady-state condition will occur relatively rapidly and 14CO2 in the expired air will equilibrate with the 14CO2/H14CO2 pool, respectively. However, complete recovery of 14CO2 will approach only after approximately 60 min of exercise (34). As the exercise protocol was only approximately 1 h and was set at relatively high intensities, the interpretation of results from tracer measurements is limited in that study.
One reason why we hypothesized that exogenous CHO oxidation would be different between running and cycling is associated with increased GI distress during running (31,32). Altered mechanical stress because of the bouncing nature of running has been linked to a higher prevalence of GI distress (8). One factor leading to GI symptoms during running could be altered absorption because of relatively high mechanical stress (19). In contrast to previous research (31,32), we did not find differences in ratings of GI symptoms between modes of exercise. However, we have to acknowledge that the used exercise intensities were moderate in the present study, whereas previous research has investigated GI distress during competition (31) or in a laboratory study at higher exercise intensities (75% V˙O2max) over a prolonged period (3 h) (31,32). GI distress is reported to increase with exercise intensity as well as with increasing exercise duration (for a review, see Brouns and Beckers ), and therefore differences might occur during competition. However, the finding that exogenous CHO oxidation rates were similar between running and cycling suggests that absorption at moderate-intensity exercise is not impaired during running.
Cycling and running elicit very different movement and muscle recruitment patterns (5,20); hence, it is not surprising that differences in energy metabolism have been detected between both modes of exercise (1,4,9,16,29). Our investigation revealed approximately 10% higher fat oxidation rates during running compared with cycling at approximately 60% V˙O2max, which were significant in the WAT trial but failed to reach statistical significance in the CHO trial (P = 0.09; Table 1). This finding contradicts a study of Arkinstall et al. (4), who did not detect differences in fat oxidation rates during 60 min of continuous cycling and running. In contrast to our investigation, the study by Arkinstall et al. (4) normalized exercise intensities at LT, which elicited a higher percentage of V˙O2max during running compared with cycling (78% and 69% V˙O2max, respectively). However, the most complete picture can be derived from studies comparing both modes of exercise with the use of graded exercise protocols (1,4,16,29). For example, a study by Achten et al. (1) measured substrate oxidation during running and cycling over a wide range of intensities. In support of our data, it was shown that total fat oxidation rates were higher during running compared with cycling between 50% and 80% V˙O2max. Accordingly, it has been suggested that a larger muscle mass is involved in the running movement compared with cycling (22). Consequently, it could be speculated that the work rate of a single muscle fiber is greater during cycling, and thus because of the higher exercise intensity that each muscle fiber is working at, a higher reliance on CHO could be expected (1).
Previous research also suggested that CHO ingestion during running results in a more marked elevation in blood glucose and insulin concentrations compared with cycling (4,36). This difference, however, was not evident in the present study. Similar to the study by Arkinstall et al. (4), plasma glucose concentrations were significantly elevated to values approximately 6.5 mmol·L−1 in the first half hour during both CHO trials. However, plasma glucose concentrations remained elevated throughout exercise in both CHO trials of the present study, whereas plasma glucose concentration gradually declined to levels around baseline (∼4.7 mmol·L−1) in the CHO cycling trial of the study by Arkinstall et al. (4). Corresponding to similarly elevated plasma glucose concentrations in the present study, plasma insulin levels were similar between CHO trials. In contrast, the study by Arkinstall et al. (4) reported significantly higher insulin concentrations during the running CHO trial after 20 min. The discrepancies between the findings of the two studies could be caused by differences in exercise intensities or by 50% greater CHO ingestion rates in the present study, which potentially maximized the insulin response in both modes of exercise.
A further difference in CHO metabolism that was suggested between running and cycling is a different effect of CHO feeding on muscle glycogen utilization (36). During cycling, the majority of studies failed to measure a significant muscle glycogen sparing effect with the ingestion of CHO (7,12,17,18), and only a small number of studies detected a significant attenuation in glycogen usage with CHO intake (21,35). Because of the fact that studies in runners by Tsintzas et al. (37,38) have reported an approximately 25% reduction in muscle glycogen utilization, the assumption was made that a glycogen sparing effect with CHO ingestion is greater during running (4,36). However, caution needs to be taken with this interpretation as the mode of exercise, exercise duration, and intensity, the CHO feeding protocol, and the methods of glycogen measurement were all different between studies. Arkinstall et al. (4) directly compared mixed muscle glycogen use during running and cycling at the individual LT and failed to detect a glycogen sparing effect with the ingestion of CHO during both modes of exercise. However, it has to be noted that although they were unable to detect a statistically significant difference, muscle glycogen utilization during running was approximately 20% reduced with CHO feeding. It therefore remains to be established whether muscle glycogen utilization during endurance running is different from cycling. In agreement with previous tracer studies (for a review, see Jeukendrup ), our study detected lower endogenous CHO oxidation rates with CHO ingestion compared with water intake, most probably because of considerably reduced liver glycogen utilization. As a result of higher fat oxidation rates during running, the sparing in endogenous CHO tended to be higher during running compared with cycling.
An important aspect that needs to be reviewed critically when two modes of exercise are compared is the influence of variation in exercise intensities. As mentioned before, exercise intensity is one of the most important regulators of substrate oxidation, which can explain equivocal findings when different modes of exercise are compared. In the present study, much care was taken to ensure that subjects exercised at the same relative intensity (∼60% V˙O2max) during both trials. This moderate exercise intensity has been chosen because it was demonstrated that exogenous CHO oxidation rates peak at exercise intensities between 51% and 65% V˙O2max (33). Hence, the influence of exercise intensity on exogenous CHO oxidation rates becomes minimal at intensities of approximately 60% V˙O2max. Furthermore, we had to choose an exercise intensity to ensure subjects could complete 2 h of treadmill running exercise because due to methodological considerations of carbon retention, we wanted to compare CHO oxidation between modes of exercise in the second hour of exercise. It can therefore be concluded that it is very unlikely that the observed similar exogenous CHO oxidation rates are confounded by differences in exercise intensities and exogenous CHO oxidation rates are indeed similar during running and cycling.
In summary, the present study demonstrates that a GLU + FRC drink was oxidized at similarly high rates of approximately 1.2 g·min−1 during both modes of exercise. Because of similar exogenous CHO oxidation rates and higher fat oxidation rates during running, utilization of endogenous CHO (muscle and liver glycogen) tended to be lower during running compared with cycling. The current study therefore suggests that recommendations for CHO intake, which were previously on the basis of measures of exogenous CHO oxidation during cycling, are indeed transferable to running. However, it has to be considered that high-intensity exercise, especially running, has been linked to increased GI distress, and it should therefore be advised that athletes test their tolerance of CHO in hard training sessions.
This study was supported by a research grant from the Nestec Ltd., Vevey, Switzerland.
The authors thank all the athletes who participated in the trials for their enthusiasm and for the time they dedicated to the study.
Results from the present study do not constitute endorsement by the American College of Sports and Medicine.
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