The benefits of consuming a high-carbohydrate (CHO) diet in preparation for prolonged exercise have been extensively documented (31). Most of the studies reported in these reviews used prolonged constant-intensity cycling or running to examine the efficacy of consuming carbohydrate before and during exercise. Although prolonged cycling and running are popular forms of exercise, both as competitive sports and for recreation, there is greater participation in sports that involve intermittent exercise, such as football, soccer, rugby, and hockey, and also in multiple-sprint sports, such as basketball, tennis, and badminton. Participation in these sports involves a combination of brief periods of high-intensity exercise punctuated by periods of low-intensity exercise such as jogging and walking. The high-intensity periods last no more than 2 to 5 s but are repeated frequently, often with short rest periods of only 20-30 s (25). A number of recent studies have examined the influences of carbohydrate solutions on performance during intermittent exercise. These studies are based on a shuttle running protocol that requires participants to complete repeated periods (often 15 min) that include walking, jogging, running, and sprinting for a distance of 20 m (21), often to the point of volitional fatigue. The combination and timing of these activities are designed to closely resemble those in sports such as soccer and basketball (21,29).
A number of studies using these intermittent exercise protocols have shown that ingesting glucose-based carbohydrate solutions immediately before and during exercise improves endurance capacity (19,29). It has been suggested that the improved endurance running capacity may be a consequence of a glycogen-sparing effect. Nicholas and colleagues (20) report that ingesting a carbohydrate-electrolyte solution (CHO-E) during 90 min of intermittent high-intensity shuttle running resulted in less muscle glycogen use, particularly in the Type II fiber population, than when a placebo solution was ingested. This was a similar result to that reported for constant-pace treadmill running to exhaustion, where glycogen sparing, after the ingestion of a CHO-E solution, was evident only in Type I (28). However, those studies were performed on subjects who did not carbohydrate-load before the trials and who, therefore, had normal resting muscle glycogen stores.
It is well known that a carbohydrate-rich diet after prolonged exercise increases muscle and liver glycogen stores and improves submaximal exercise capacity compared with consuming a normal, mixed diet (2). However, there is some evidence that the performance benefits of ingesting a carbohydrate solution during exercise may be relatively minor when preexercise muscle and liver glycogen stores are high. For example, Widrick and colleagues (30) found no improvements in performance during 120 min of self-paced cycling when their carbohydrate-loaded subjects ingested a carbohydrate solution during exercise, suggesting that endogenous body glycogen stores affect the efficacy of exogenous CHO provision during exercise.
Therefore, the purpose of this study was to investigate the effects of ingesting a CHO-E solution on performance and muscle glycogen use during prolonged intermittent high-intensity running to fatigue in carbohydrate-loaded men. We hypothesized that a preexercise increase in the body's glycogen stores may reduce the benefits of ingesting a carbohydrate solution during intermittent high-intensity running on both performance and muscle glycogen use.
Six recreationally active male games players (age 22.7 ± 3.4 yr; body mass (BM) 75.0 ± 4.3 kg; height 1.8 ± 0.1 m; V˙O2max 60.2 ± 1.6 mL·kg−1·min−1) volunteered, with informed written consent, to participate in this study, which was approved by the Loughborough University ethics committee.
Subjects performed a multistage fitness test (23) to assess their V˙O2max. Subjects performed the intermittent shuttle running protocol for 45 min (described in the Experimental protocol section) to familiarize themselves with the running patterns and experimental procedures. They were first matched for V˙O2max values and then, where possible, their sprint performance. This was undertaken so that the competition between the paired subjects would increase motivation, especially during the latter stages of the protocol.
Subjects performed two experimental trials separated by 14 d, after carbohydrate loading for 2 d. To eliminate any trial order effect, treatments were assigned randomly in a crossover design. On each occasion, subjects consumed either a 6.4% maltodextrin CHO-E solution (sodium 50.4 mL·100 mL−1; potassium 10.3 mL·100 mL−1; osmolality 115 mOsm·kg−1) (GlaxoSmithKline, UK) or a taste-matched placebo (PLA) free of carbohydrate (sodium 2.0 mL·100 mL−1; potassium 11.1 mL·100 mL−1; osmolality 25 mOsm·kg−1). Solutions were administered in a double-blind fashion immediately before the trials (8 mL·kg−1 BM) and at subsequent 15-min intervals (3 mL·kg−1 BM) until cessation of the exercise. Previous unpublished studies from our laboratory have shown these fluid volumes to be well tolerated during intermittent high-intensity running. Ingestion of the preexercise bolus and the smaller volumes every 15 min provided exogenous CHO delivery of approximately 90 g·h−1 in the CHO-E trial.
Subjects performed a glycogen-reducing trial comprising 90 min of intermittent shuttle running (21) 48 h before the experimental trials, and they refrained from strenuous exercise, caffeine, tobacco, and alcohol during the recovery period (Fig. 1). After the glycogen-reducing trial, subjects were administered a carbohydrate-rich diet for 48 h (energy intake ≈ 55 kcal·kg−1 BM·d−1; carbohydrate ≈ 10 g·kg−1 BM·d−1 (70% of energy intake); fat ≈ 1 g·kg−1 BM·d−1 (15%); protein ≈ 2 g·kg−1 BM·d−1 (15%)). Subjects reported to the laboratory for the experimental trial after an overnight fast (≥ 10 h), and they voided before the measurement of nude BM. A urine sample was collected before exercise and at fatigue and was analyzed for osmolality, using a cryoscopic osmometer (Osmomat 030). An indwelling cannula (Venflon, 16-18G, Ohmeda, Hatfield, Herts, UK) was inserted into an antecubital vein and kept patent by frequent flushing with sterile saline. A resting muscle sample was then obtained from the middle portion of m. vastus lateralis by needle biopsy. Subjects stood for 15 min before a resting blood sample was obtained. Resting heart rate was monitored during a 5-min period. Ten minutes before commencing the main trial, the subjects consumed the prescribed solution and completed a standardized warm-up and stretching protocol.
On completion of the 90 min of intermittent running, a second muscle sample was obtained after the subject had been transferred to an examination couch in the laboratory adjacent to the sports hall. After this sample, subjects ran to volitional fatigue or until they were withdrawn by the investigators, at which point a final muscle sample was obtained. Subjects were withdrawn by the investigators if they failed to maintain the desired exercise intensity (as dictated by the audio signal) or if their sprint performance declined to < 95% of the mean sprint time for the first 45 min.
The intermittent exercise protocol used in the glycogen-depleting trials and the main experimental trials was the Loughborough Intermittent Shuttle-running Test (LIST) (21). The LIST is a free-running exercise protocol designed to simulate the activity patterns of a game of soccer (Fig. 1). Subjects ran the LIST for 90 min in six blocks of 15 min separated by 3-min rest periods. After 90 min, subjects continued with this pattern of intermittent shuttle running, this time with no rest breaks, until fatigue. Fluid was administered during the rest phases for the first 90 min and then at 15-min intervals during the walking phases of the continuous protocol.
Heart rate was monitored every 15 s during exercise, using short-range telemetry (Polar Model 810, Kempele, Finland), and the mean was recorded for each 15-min exercise period and the run to fatigue. Subjective ratings of perceived exertion were recorded, using the Borg scale (4), during the walk phase of the final cycle of each block.
Blood and muscle analyses.
An 11-mL blood sample was taken at rest, after 30, 60, and 90 min of exercise, and at fatigue, with 4 mL dispensed into lithium heparinized tubes. From the venous blood samples, duplicate 20-μL aliquots were deproteinized with 200 μL of 2.5% perchloric acid, centrifuged, and frozen at −20°C for subsequent analysis of blood lactate concentration, using a method previously described (17). Hemoglobin and hematocrit concentrations were analyzed in triplicate by the cyanomethemoglobin method (Boehringer Mannheim GmbH Diagnostica, Mannheim, Germany) and microcentrifugation (Hawksley Ltd., Lancing, UK), respectively, and the results obtained were used to calculate changes in plasma volume (9). The remaining whole blood was centrifuged at 4°C, and the plasma was divided into aliquots and frozen at −20°C for later analysis of free fatty acids (FFA) and glucose, using commercially available kits (NEFA-C test, WAKO, Germany and Roche, R-Biopharm GmbH, Germany respectively), and glycerol, using a method described in our earlier study (27). Serum was obtained by centrifugation for 15 min at 4°C of coagulated whole blood; this was stored at −70°C for subsequent analysis of insulin (Coat-A-Count Insulin, Diagnostica Products Corporation (DPC), Caernarfon, UK) and cortisol (Coat-A-Count Cortisol, DPC, Caernarfon, UK), using commercially available radioimmunoassay kits and an automated gamma counter (Packard, Cobra 5000, Pangbourne, UK).
Muscle samples were obtained through separate incisions from the lateral portion of the vastus lateralis muscle, using the needle biopsy procedure with suction applied (10). All incisions were made through the skin and muscle fascia under local anesthetic (2-3 mL of 1% lignocaine) before the start of exercise while the subjects lay supine on an examination couch. Each muscle sample was snap-frozen in liquid nitrogen, and, at a later date, a 15- to 20-mg fragment of muscle was placed in a freeze-dryer (Pirani 10, Edwards, UK) for 24 h at −50°C and between −10−1 and −10−2 mbar. The freeze-dried muscle fragments were then washed with 1 mL of petroleum ether to remove any excess lipid before each sample was reduced to a fine powder using an agate pestle and mortar. The precise quantity of powder obtained from each fragment was determined using an electronic balance scale (Mettler AE240, Switzerland), and these powdered samples of dry matter (DM) were then stored at −80°C, pending later acid extraction and metabolite analysis.
The mixed muscle extracts were assayed for proglycogen, macroglycogen, phosphocreatine (PCr), free glucose, glucose-6-phosphate (G-6-P), and lactate, using methods described in our earlier studies (27,28). Muscle samples were also analyzed for the purine nucleotides ATP, ADP, and IMP, using a method previously described (12).
Statistical comparisons of the physiological, biochemical, and metabolic parameters were analyzed using a two-way (treatment × time) analysis of variance for repeated measures (SPSS 11). Mauchly's test for sphericity was used; where asphericity was assumed, the Greenhouse-Geisser correction was used for epsilon < 0.75; if not, then the Huyn-Feldt correction was used. Where significant F values were found, a Holm-Bonferroni stepwise method was used to determine the location of the variance (1). When there were only single comparisons, a Student's t-test for correlated data was used to determine whether any differences between treatments existed. Furthermore, a Shapiro-Wilks test for normality was used to test whether differences in data were normally distributed; if this was found to be significant, then a nonparametric Wilcoxon signed ranks test was used instead of the Student's t-test. Relationships between variables were determined by Pearson product-moment correlation coefficients. Null hypotheses were rejected at an alpha level of P < 0.05. All data are reported as means ± standard deviation (SD).
Running capacity and sprint performance.
All subjects ran longer during the CHO-E trial compared with the PLA trial. They ran for 158.0 ± 28.4 min during the CHO-E trial and 131.0 ± 19.7 min during the PLA trial (P = 0.028), representing a 21% increase in intermittent running capacity. The mean 15-m sprint times were similar between trials (CHO-E 2.61 ± 0.08 s vs PLA 2.58 ± 0.08 s) and increased over time, irrespective of treatment (F6,30 = 4.1; P = 0.004).
There were no differences in preexercise muscle glycogen concentrations between trials. Neither were there differences between trials for muscle concentrations of proglycogen and macroglycogen (Fig. 2). There was a similar rate of muscle glycogen use between trials from before exercise to 90 min (~2 mmol glucosyl units per kilogram DM per minute) and a trend (P = 0.1) for a higher rate of muscle glycogen use from 90 min to fatigue in the PLA trial (4.2 ± 2.8 mmol glucosyl units per kilogram DM per minute) compared with the CHO-E trial (2.5 ± 0.7 mmol glucosyl units per kilogram DM per minute). It was not possible to attribute these changes in muscle glycogen use to the individual components, because there were no differences in the use of proglycogen and macroglycogen (Fig. 2). There were modest correlations between muscle glycogen content and muscle glycogen use for the first 90 min (r = 0.658; P < 0.05) and from 90 min to fatigue (r = 0.656; P < 0.05). Interestingly, fatigue occurred at similar muscle glycogen concentrations in both trials (~200 mmol glucosyl units per kilogram DM).
There were no differences between trials in muscle concentrations of PCr, G-6-P, and lactate. Similarly, there were no differences between trials in the concentrations of adenine nucleotides ATP and ADP or for IMP, the product of total adenine nucleotide deamination (Table 1). It should be noted, however, that there was a short time delay of 38 s (± 7) and 52 s (± 13) between the end of the exercise and the time of muscle sampling for the 90 min and fatigue biopsy samples, respectively. Despite the expedient and efficient sampling procedures, this slight delay was attributable to the time required for the subject to return to the laboratory, at the end of the run, from the adjacent gymnasium. This delay may compound interpretation of some muscle metabolite data; however, earlier studies from our laboratory have shown that muscle glycogen concentrations (both soluble and insoluble fractions) are unaffected by recovery periods of up to 6 min (3).
Plasma glucose and serum insulin.
Plasma glucose concentration was maintained within the normal physiological range in both trials, although it was significantly higher at fatigue in the CHO-E trial compared with the PLA trial (F4,20 = 9.1; P < 0.001; Fig. 3). Although plasma glucose concentrations also seemed higher in the CHO-E trial at 30 min, this failed to reach statistical significance. Serum insulin concentrations were significantly higher throughout exercise in the CHO-E trial compared with PLA (F1,5 = 29.1; P = 0.003; Fig. 4).
Plasma FFA and glycerol.
There were main effects of the treatments on plasma FFA concentrations (F1,5 = 10.3; P = 0.024; Fig. 4) and glycerol concentrations (F1,5 = 13.8; P = 0.014; Fig. 4) during exercise, with lower values occurring in the CHO-E trial. There were also main effects of time, with concentrations of both of these substrates increasing with exercise duration (F1.2,6.1 = 26.1; F1.6,7.8 = 35.1; P < 0.001; for FFA and glycerol, respectively).
Serum cortisol was analyzed as an indicator of physical stress during the trials. There was a main effect of time on serum cortisol concentrations, with values higher in both trials at fatigue (719 ± 133 nM) than at 30 min (437 ± 103 nM), 60 min (396 ± 122 nM), and 90 min (407 ± 115 nM) of exercise (F1.4,7 = 12.5; P = 0.007); however, there was no main trial effect on this marker of physical stress.
Blood lactate, heart rate, and rate of perceived exertion.
Blood lactate concentrations increased significantly with the onset of exercise (F4,20 = 40.5; P < 0.001) from a baseline of about 1 mM to a zenith of about 4 mM; however, there were no differences between treatments. There were no differences in heart rates between trials, with mean exercise HR of 167 ± 9 and 162 ± 7 bpm for the CHO-E and PLA trials, respectively. There was a main effect of time, with HR values increasing with exercise duration and peaking at fatigue (F7,35 = 485; P < 0.001). Similarly there were no differences between trials for ratings of perceived exertion (RPE), with mean exercise values of 13 ± 1 arbitrary units for both trials. Again, there was a main effect of time, with RPE values increasing significantly with exercise duration towards peak values at fatigue (F5,25 = 10.8; P < 0.001).
Changes in urine osmolality and BM.
There were no differences in urine osmolality before and after trials in either condition. Subjects arrived at the laboratory with urine osmolalities within the range 500-600 mOsm·kg−1, and these were maintained by the end of the main trials. There were no reported incidences of gastrointestinal distress after the fluid ingestion during exercise. Furthermore, there were no net BM losses within or between trials.
The findings from this study show, for the first time, that after consumption of a carbohydrate-rich diet, carbohydrate supplementation (90 g·h−1) in the form of a 6.4% CHO-E solution during exercise led to an improvement in high-intensity intermittent running capacity, but it did not affect muscle glycogen use. Although fatigue occurred at similar muscle glycogen concentrations in both trials, the subjects were able to run for approximately 21% longer in the CHO-E trial (158.0 ± 28.4 min) compared with the PLA trial (131.0 ± 19.7 min). This enhanced endurance capacity was achieved in all subjects and was associated with higher serum insulin concentrations throughout the CHO-E trial and higher plasma glucose concentrations during the latter stages of exercise. These results show clearly that ingesting a CHO-E solution improves endurance capacity during intermittent high-intensity shuttle running, even when participants have high preexercise muscle glycogen concentrations. Therefore, this does not support our hypothesis that an antecedent CHO-rich diet may negate the ergogenic efficacy of CHO-E solutions ingested during this type of exercise.
The dietary and exercise CHO-loading protocol used in the present study was effective in increasing muscle glycogen concentrations to similar values before each trial (CHO-E, 533 ± 77 mmol glucosyl units per kilogram DM vs PLA, 512 ± 102 mmol glucosyl units per kilogram DM). These resting values are higher than those obtained in an earlier study using the same sampling and exercise (LIST) procedures (350-400 mmol glucosyl units per kilogram DM) and a similar group of subjects as used in the present study (20). Interestingly the muscle glycogen concentrations at the end of 90 min of exercise in the present study are similar to the preexercise values reported for subjects in the study by Nicholas and colleagues (20). In that study, all the subjects managed to complete the 90 min of the LIST, both in the CHO-E and PLA trials (20). Therefore, if endurance capacity during intermittent high-intensity shuttle running was dictated solely by preexercise muscle glycogen concentrations, it would be reasonable to expect the subjects in the present study to have completed an additional 90 min of exercise. However, this was clearly not the case, because in the PLA trial the subjects ran for only 41 min beyond the 90 min, and in the CHO-E trial they only achieved an additional 68 min. This, coupled with the observation that a substantial amount of muscle glycogen was still present at fatigue, suggests that factors additional to muscle glycogen concentrations may contribute to fatigue during this type of exercise.
In contrast to the results from the present study, we previously have reported a greater net muscle glycogen use with placebo when compared with the ingestion of a glucose-based CHO-E solution during 90 min of the LIST, using subjects who were not CHO loaded before the trials (20). This muscle glycogen sparing was suggested as one possible mechanism to explain our earlier finding that the ingestion of a CHO-E throughout exercise increased endurance capacity during the LIST (19). Similar improvements in endurance capacity have been reported by other authors (8,29), who also have suggested that the ingestion of a mixture of glucose-fructose and sucrose-based solutions throughout prolonged, intermittent, high-intensity shuttle running was a consequence of glycogen sparing. However, the results from the present study do not show glycogen sparing during the first 90 min of the LIST. Indeed, there were no differences in muscle glycogen concentrations between trials at 90 min, nor were there any differences in the rates of muscle glycogen use during this period (~2 mmol glucosyl units per kilogram DM per minute). Furthermore, there were no differences in the concentrations of G-6-P and other muscle metabolites at 90 min of exercise. Therefore, an antecedent, CHO-rich diet preserves the ergogenic effect of glucose-based CHO solutions ingested during high-intensity intermittent running, without affecting muscle glycogen use.
These results seem similar to those of Coyle and colleagues (7), who also used subjects with high preexercise muscle glycogen stores. They reported no differences in muscle glycogen use during prolonged continuous exercise to exhaustion with or without carbohydrate feeding, in the form of a glucose polymer, but significant differences in cycling times (3 h 2 min vs 4 h 2 min for their placebo trial and CHO trial, respectively). However, in their study, the rate of glycogen degradation decreased towards the end of exercise, whereas in the present study there seemed to be an increased rate of glycogenolysis in the PLA trial. The rates of glycogen degradation during the first 90 min of the LIST were the same in both trials, but between 90 min and fatigue, the values were 4.2 ± 2.8 and 2.5 ± 0.7 mmol glucosyl units per kilogram DM per minute (P = 0.1) for the PLA and CHO-E trials, respectively. The apparent trend for a faster rate of glycogenolysis in the PLA trial may be simply a consequence of the significantly shorter run time compared with the CHO-E trial and similar glycogen concentrations at fatigue. The double-blind, randomized crossover design of this study precluded a comparison of muscle glycogen concentrations at the point of fatigue in the PLA trial with those at the same sampling time in the CHO-E trial. Nevertheless, the fact remains that the glycogen concentrations at fatigue were similar (~200 mmol glucosyl units per kilogram DM) in both trials, and yet the time to fatigue in the CHO-E trial was 21% greater than in the PLA trial. One possible explanation was that there may have been different amounts of pro- and macroglycogen used in the two trials. However, analysis of the two pools of muscle glycogen revealed no differences between trials in their concentrations before, during, and after exercise (Fig. 2). There was a greater rate of degradation of proglycogen than macroglycogen in both trials, which is consistent with the earlier studies of Graham and colleagues (11).
Another possible explanation for the results in the present study is a differential use of muscle glycogen between fiber types. It should be noted that in the study of Nicholas and colleagues (20), although glycogen sparing was apparent in both Type I and Type II muscle fibers after ingestion of a CHO-E solution, reduction of glycogen in the Type II muscle fibers towards a previously described critical level (14) ultimately seemed to determine the point of fatigue. Although no single muscle fiber analysis was performed in the present study, because of the similarities in exercise protocol and subject characteristics, it would be pertinent to suggest that there may have been a glycogen-sparing effect in the Type II fibers in the CHO-E trial in the present study. The elevated plasma glucose and serum insulin concentrations in the CHO-E trial (especially late in exercise) in the present study could have contributed to enhanced glycogen synthesis in these fibers during the low-intensity (walking, jogging, and resting) components of the exercise protocol, as has been previously reported (15), and this may explain the tendency for reduced net muscle glycogen use in this trial late in exercise.
The plasma glucose concentrations were within the normal range throughout exercise in both trials. However, in the CHO-E trial, plasma glucose concentrations were higher at the point of fatigue, as were serum insulin concentrations, suggesting a greater availability of glucose than in the PLA trial. The results from studies on cycling to fatigue, in which subjects had high preexercise muscle glycogen concentrations, suggest that the provision of exogenous carbohydrate improves endurance capacity by preventing decreases in plasma glucose concentrations and carbohydrate oxidation (5,7). However, even in that exercise modality, it has been shown that once fatigue is impending, the delivery of exogenous glucose, either orally or by infusion, cannot sustain exercise at a high intensity (>75% V˙O2max) (6). This suggests that when muscle glycogen concentrations are reduced to critically low values, the uptake of glucose from the systemic circulation cannot occur fast enough to maintain contractile activity at the required rate (13). Therefore, the metabolic and performance consequences of a reduction in plasma glucose concentration during prolonged exercise may be closely associated with the availability of hepatic and muscle glycogen stores. For example, a modest reduction in plasma glucose concentration early in exercise, when carbohydrate stores are adequate or well stocked, may have little impact, whereas when these stores are running low, the same reduction in plasma glucose may become a significant determinant of the onset of fatigue, operating through changes in cerebral metabolism (22).
It has been postulated by Rauch and colleagues (24) that chemoreceptors constantly monitor the carbohydrate status of the muscle during exercise, by what the authors have termed a glycostat, which continually updates the brain. When carbohydrate stores are severely reduced during the latter stages of prolonged exercise, the threat to cerebral metabolism may be prevented by discontinuing exercise, by central rather than an entirely peripheral mechanism (22). This teleoanticipatory approach to the complexities of fatigue is further expanded by Lambert and colleagues (16), and it is likely that during exhaustive, high-intensity, intermittent exercise, volitional fatigue is a multifaceted consequence of peripheral as well as central mechanisms. However, the extent to which this mechanism operates during the performance of the LIST protocol, in which the subjects are not able to self-pace, remains to be determined.
Another possible contribution to the onset of fatigue may have been the "energy balance" within the working muscles towards the end of exercise. McConell and colleagues (18) exercised participants to volitional exhaustion at 69% V˙O2 max and found that CHO supplementation improved exercise capacity by 30% compared with a placebo. Although muscle glycogen concentrations were similar between trials at the point of fatigue, the authors note that muscle IMP accumulation (a marker of adenine nucleotide loss) was significantly lower in their CHO trial; they conclude that CHO ingestion attenuated muscle IMP accumulation and increased exercise capacity through an improved muscle energy balance. This is consistent with a study from our laboratory that provided evidence that CHO ingestion during prolonged, submaximal running offsets the development of fatigue by reducing the decline in oxidative ATP production (as reflected by sparing PCr and glycogen degradation) (26). In the present study, however, there was no evidence of a reduction in IMP accumulation after CHO-E supplementation. Furthermore, there were no differences in muscle PCr, ATP, and ADP concentrations, suggesting that an energy imbalance is probably not the reason for cessation of exercise, although consideration needs to be given to the timing of the muscle biopsy samples, as detailed earlier.
Because there were no differences in muscle PCr and lactate concentrations, it is reasonable to rule out the possibility of fatigue being caused by insufficient PCr resynthesis or acid imbalances within the muscle between the two trials. Some support for this speculation is derived from results of the sprint performances. Although there were decreases in sprint performance over time, there were no differences in sprint performance between trials at the point of fatigue, nor at the time point in the CHO-E trial that coincided with the point of fatigue in the PLA trial.
In summary, the results from the present study demonstrate that in subjects with high preexercise muscle glycogen concentrations as a result of dietary CHO loading, the provision of a 6.4% CHO-E solution immediately before and during exercise can significantly increase endurance capacity during prolonged, intermittent, high-intensity shuttle running. This ergogenic effect cannot be explained solely by differences in muscle glycogen and muscle metabolite concentrations at the point of fatigue. However, plasma glucose concentrations were higher towards the end of exercise in the CHO-E trial, and they would have provided a sustained source of CHO for the central nervous system in addition to an increased contribution of CHO to muscle metabolism.
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Keywords:© 2008 American College of Sports Medicine
INTERMITTENT EXERCISE; FATIGUE; CARBOHYDRATE-ELECTROLYTE SOLUTION; CARBOHYDRATE LOADING