Pre-exercise muscle and liver glycogen concentrations are essential substrate sources during prolonged moderate- to high-intensity exercise because they are both directly associated with performance (1,2). Athletes typically consume carbohydrates (CHO) before and/or during exercise as a means of improving performance and endurance capacity. The exogenous source of CHO is likely to maintain higher plasma glucose concentrations and a high rate of CHO oxidation, especially late in exercise when muscle and liver glycogen concentrations are becoming depleted (7). There is good evidence that actual blood glucose concentration and glucose flux into muscle to sustain energy demand during exercise is a primary determinant of capacity such that optimal rates are possible only at sufficient blood glucose concentration and adequate glycogen reserve (19). Pre-exercise strategies often include the consumption of CHO formulations that may include pure glucose or substances that are easily assimilated to glucose, within the hour before the commencement of exercise. The pre-exercise ingestion of glucose in comparison to placebo has been shown to have both negative (15,28) and positive (40,41) effects on endurance performance, as well as providing no additional benefit (3,24,43). Some of these findings may be reconciled because glucose ingestion can be associated with the occurrence of rebound hypoglycemia during subsequent exercise (23,29), which may limit the ability to enhance endurance performance.
There is evidence that not all individuals seem to be susceptible to rebound hypoglycemia (23,29) and some are even able to maintain endurance performance despite transient hypoglycemic episodes (14). However, previous studies have variably defined hypoglycemia, with thresholds of <2.5 mmol·L−1 (14,39), ≤3.0 mmol·L−1 (29,33), and ≤3.5 mmol·L−1 (15,23), making interpretation of susceptibility difficult. Defining rebound hypoglycemia as a plasma glucose concentration ≤3.0 mmol·L−1 is most appropriate for a continuous cycling context because it is consistent with definitions of symptomatic hypoglycemia (12,33).
Rebound hypoglycemia is associated with the occurrence of hyperinsulinemia, typically shown directly before exercise (6,15). As a consequence of hyperinsulinemia, hepatic glucose output (27) and fat oxidation (21) can be suppressed. These transient metabolic disturbances, at the start of exercise, and mechanisms that increase glycogen utilization (6,17) may explain why pre-exercise glucose does not always provide an additional benefit in comparison to placebo. Regardless, there now appears to be less concern about the efficacy and use of simple sugars in the hour before exercise (18,22,26) despite early reservations regarding rebound hypoglycemia (6,15). If rebound hypoglycemia is relevant to endurance performance, the use of other forms of CHO, such as galactose, with a low-glycemic index (GI: ∼20), which has no primary insulin drive (37), may overcome the issue. Galactose consumption would therefore be unlikely to inhibit hepatic output, but maintain fat oxidation, protecting the absorbed CHO for later use. Further, the consumption of galactose within the hour before exercise may have the potential to pre-load the liver with newly synthesized glycogen, for subsequent release, as galactose has to be converted by the liver through the Leloir pathway. This is of particular importance because the liver is as important in sustaining high-intensity exercise as muscle glycogen (2).
Only 3 studies have investigated the effects of galactose on endurance performance (24,31,42). Of these, only 1 (24) has specifically examined the pre-exercise ingestion (45 minutes before exercise) of galactose. This showed that there were no significant differences in time trial performance between galactose (mean, 42.04 ± 1.4 minutes) and glucose (mean, 41.05 ± 2.9 minutes). The use of a time trial protocol is physiologically valid (9) and is likely to detect small but potentially crucial differences. However, with a small sample size (n = 8), this study may have lacked adequate statistical power (calculated to be ∼0.3). Therefore, further research is required to establish whether or not galactose may be a useful alternative pre-exercise substrate.
The purpose of the study was to compare the effects of the pre-exercise ingestion (30 minutes before exercise) of galactose and glucose on endurance capacity using a high-intensity endurance cycling test, as well as the glycemic and insulinemic responses at rest and during exercise. The pre-exercise ingestion of galactose has been shown to produce greater stability in plasma insulin and glucose concentrations (24), a more progressive glucose oxidation response during exercise, as well as sparing pre-existing liver glycogen stores (34), which may be beneficial for prolonged exercise performance. Therefore, we hypothesized that an initial bolus of galactose 30 minutes before exercise would sustain high-intensity endurance cycling capacity more effectively than glucose. In addition, we hypothesized that the pre-exercise ingestion of galactose would reduce the occurrence of rebound hypoglycemia compared with glucose ingestion.
Experimental Approach to the Problem
Cyclists completed 3 experimental trials of a variable high-intensity endurance cycling test to exhaustion (35); each test separated by 7 days. This exercise protocol was chosen because competitive endurance cycling is characterized by high-intensity efforts interspersed with sustained steady state exercise (36,44) rather than constant load tests. Each trial involved the ingestion (30 minutes before exercise) of either 40 g of galactose (Gal, D-galactose; Inalco, Milan, Italy), 40 g of glucose (Glu, D-glucose; Cargill, Manchester, United Kingdom), or a placebo (water), as 1 L formulations, using a randomized, double-blind experimental design. Each cyclist was randomly assigned the order they would complete the experimental trials and followed their fixed sequence. All formulations contained 26 mmol·L−1 sodium chloride, as well as sweetener and flavoring to blind the participants to each condition. None of the cyclists reported that they recognized the placebo.
Ten trained male cyclists, aged 31 ± 7 years (range: 24–44 years), with a body mass of 76.2 ± 5.0 kg, body fat percentage of 9.7 ± 4.6% (BOD POD, COSMED USA, Inc., Chicago, IL, USA), V[Combining Dot Above]O2max of 58.1 ± 5.6 ml·kg−1·min−1, and maximal power output (Wmax) of 364.3 ± 20.5 W participated in this study. The cyclists had trained for ≥15 hours per week, for at least the past 3 years, were competitive club-level road racers, and in a maintenance phase of training throughout the duration of the study. The experimental procedures were fully explained to each cyclist before the study, and all cyclists provided written informed consent. The protocol used during this investigation received institutional ethical approval and was performed in accordance with the ethical standards specified by the Declaration of Helsinki (1964).
Cyclists completed a familiarization ride to allow habituation to the laboratory equipment and procedures used (35). A week later, the cyclists completed a maximal incremental cycle test to volitional exhaustion to determine their individual Wmax (30). This preceded the experimental trials by at least 1 week. Wmax was used to determine the relative exercise intensities to be undertaken by each cyclist during the experimental trials (viz., power output [W] at a given % Wmax). All exercise testing was performed on a standardized adjustable road bicycle fitted with SRM Powermeters (SRM, Julach, Germany) mounted on an air-braked cycle ergometer (Kingcycle Ltd, High Wycombe, United Kingdom). The Kingcycle was calibrated as described by Schabort et al. (38). The SRM Powermeters, calibrated before the study, enabled high precision (manufacturers technical error <0.5%) measurements of power output (W).
Cyclists were asked to record their food intakes and activity patterns during the 72 hours before the first experimental trial. They were then instructed to repeat this diet and activity pattern for the remaining trials. Cyclists were also instructed to refrain from any strenuous activity, alcohol, or caffeine consumption in the previous 24 hours.
After an overnight fast (≥12 hours), each cyclist commenced his experimental trials at the same time of the day (between 0600 and 0900) to avoid any influence of circadian variability. All trials were performed under normal environmental conditions (temperature, 18° C; relative humidity, 60%). On arrival at the laboratory, a catheter was inserted into an antecubital vein for repeated blood sampling. Resting venous blood samples were drawn at −5 minutes and −2 minutes before fluid consumption and analyzed for plasma glucose, plasma lactate, and serum insulin concentrations.
Thirty minutes before exercise, participants consumed either the Gal, Glu, or placebo formulation. Venous blood samples were drawn at 13, 18, 23, and 28 minutes after fluid consumption. Cyclists then completed four 5 minutes of continuous progressive workload increments corresponding to 70, 75, 80, and 85% Wmax. This was followed by ten 90-second sprints at 90% Wmax, separated by 180-second recovery at 55% Wmax (35). Venous blood samples were drawn, and heart rate and ratings of perceived exertion (RPE) were recorded throughout the exercise period.
If a cyclist completed all 10 sprints, after a 180-second interval at 55% Wmax, cycling to volitional exhaustion was undertaken at 90% Wmax. Exhaustion was defined as an inability to maintain power output within 5 W of that required and an inability to restore this within 15 seconds despite verbal encouragement. The same criteria were applied constantly throughout the protocol to ensure the maintenance of the prescribed power outputs. No feedback on elapsed time or heart rate was provided to prevent potential bias from cyclists targeting previous times or heart rates.
Blood samples drawn for both plasma glucose and plasma lactate measurements were collected in fluoride oxalate containing tubes (Becton Dickinson, Oxford, United Kingdom), whereas those for serum insulin were collected in plain tubes (Becton Dickinson). Blood samples were stored on ice and centrifuged with aliquots of plasma and serum then being analyzed for selected metabolites. Plasma glucose (Glucose Oxidase kit; Siemens Healthcare Diagnostics Inc, New York, USA), plasma lactate (Lactate kit; Siemens), and serum insulin (Insulin IRI kit, Seimens) concentrations were analyzed using a semiautomatic analyser (ADVIA Centaur System; Bayer Diagnostics, Newbury, Berks, United Kingdom). The within-run precision (coefficient of variation) for plasma glucose, plasma lactate, and serum insulin was 0.5–0.6%, 1.0–1.9%, and 3.2–4.6%, respectively.
Data were tested for normal distribution (Kolmogorov-Smirnov test) and are presented as mean ± SD. A Friedman 2-way analysis of variance (ANOVA) by ranks was used for the analysis of differences in time to exhaustion between trials because these data were not normally distributed. Where significance was detected, post hoc analysis was performed using a Wilcoxon signed-rank test with Bonferroni adjustment (alpha level of 0.0166 per test [0.05/3]). Statistical comparisons for time to exhaustion were made using Cohen's effect size (ES) with threshold values for small (0.2), medium (0.6), large (1.2), very large (2.0), and extremely large (4.0) effects (20). A 1-way ANOVA was used to assess whether there was an order effect of the randomization of the trials for time to exhaustion, as well as the mean of the total area under the curve (AUC) for plasma glucose and serum insulin. Two-way ANOVA for repeated measures was used to compare differences in blood-related variables and heart rate over time and between conditions. Where significance was detected for both a 1-way and 2-way ANOVA, post hoc analysis was performed using a paired t-test with Bonferroni adjustment to establish differences between conditions and condition and time interactions (alpha level of 0.0166 per test [0.05/3]). A Friedman 2-way ANOVA by ranks was used to analyze differences in RPE over time and between conditions. A Wilcoxon signed-rank test, with Bonferroni adjustment (alpha level of 0.0166 per test [0.05/3]) was used to analyze the interaction between time and condition. Only the 8 participants who completed 65 minutes of the exercise protocol (period over which these variables are reported) had their blood-related variables, heart rate, and RPE evaluated using SPSS for Windows version 17 (SPSS, Inc., Chicago, IL, USA). A 0.95 level of confidence was predetermined to denote statistical significance (p ≤ 0.05).
Time to Exhaustion
The pre-exercise ingestion of Gal produced longer times to exhaustion than Glu (68.7 ± 10.2 vs. 58.5 ± 24.9 minutes, ES = 0.68, p = 0.005 [Figure 1]). In fact, when ranking individual responses to Gal and Glu, all 10 cyclists produced longer times to exhaustion on Gal, with these improvements ranging from 1.4 to 47.1 minutes. There were no differences in time to exhaustion between placebo (63.9 ± 16.2 minutes) and glucose (ES = 0.36, p = 0.0214) or placebo and galactose (ES = 0.27, p = 0.0214). There were no differences between results according to the randomized order in which the 3 trials were completed, showing that there was no order effect. Eight of 10 cyclists produced longer times to exhaustion on placebo compared with Glu, whereas only 2 cyclists performed worse than placebo on galactose. Overall, there was a range of endurance times of 18.5 minutes–85.9 minutes. After the ingestion of Gal, only 1 cyclist did not complete all ten 90% Wmax sprints fatiguing at 44 minutes. Two cyclists while taking Glu (one of which was the cyclist reported above) and 1 of these during placebo did not complete any of the sprints, fatiguing during the initial 20 minutes of progressive increases in exercise intensity. All cyclists were included in the nonparametric analysis of these data. Further, none of the cyclists reported any gastrointestinal problems before or during the exercise period.
Plasma glucose concentrations increased to 8.0 ± 1.0 mmol·L−1 over the 28 minutes before exercise after Glu ingestion (p < 0.001), which were higher than Gal (5.4 ± 0.5 mmol·L−1, p < 0.001) and placebo (4.9 ± 0.3 mmol·L−1, p < 0.001; Figure 2A). After Gal ingestion, there was a smaller increase in plasma glucose concentration (0.5 mmol·L−1). After the onset of exercise, plasma glucose concentrations fell rapidly after the ingestion of Glu to a nadir of 3.9 ± 1.2 mmol·L−1, at 15 minutes into exercise. The decrease in plasma glucose concentrations was less evident after Gal ingestion (nadir 4.4 ± 0.8 mmol·L−1) at 15 minutes into exercise. During the placebo condition, plasma glucose concentrations remained stable. Plasma glucose concentrations fell below the hypoglycemic threshold of 3.0 mmol·L−1 (12,33) during the initial 20 minutes of exercise for 3 cyclists during the Glu trial, though they did not report any symptoms and only 1 cyclist was unable to continue exercising. After the first 20 minutes of exercise, plasma glucose concentrations increased to slightly above baseline concentrations by 59 minutes (5.5 ± 1.3 mmol·L−1) for Glu, with stability thereafter. During the galactose condition, no cyclists had plasma glucose concentrations below the hypoglycemic threshold. After Gal and placebo ingestion, plasma glucose concentrations increased to a relative hyperglycemia by 59 minutes (6.7 ± 1.5 mmol·L−1 and 6.9 ± 1.2 mmol·L−1, respectively) and subsequently decreased to values comparable to the Glu condition. Even though there were different glycemic patterns of response between conditions, there were no significant differences in the mean plasma glucose AUC between conditions (placebo: 486.8 ± 113.8 mmol·L−1·min−1, Glu: 487.8 ± 119.2 mmol·L−1·min−1, Gal: 509.0 ± 62.6 mmol·L−1·min−1).
Figure 2B shows that after the ingestion of Glu, serum insulin concentrations significantly (p < 0.001) increased to peak values of 29.6 ± 15.2 μU·ml−1 at 28 minutes, which were higher than insulin concentration after Gal (12.5 ± 6.2 μU·ml−1, p < 0.001) and placebo (4.5 ± 1.9 μU·ml−1, p < 0.001). Concentrations after Gal were also higher than placebo (p = 0.001). Throughout the initial 20 minutes of exercise, serum insulin concentrations decreased toward basal values for Glu and Gal. Serum insulin was higher throughout this period during the Glu trial, though only significantly so at 35 minutes (19.0 ± 11.9 μU·ml−1) in comparison to Gal (6.2 ± 3.5 μU·ml−1, p = 0.003) and placebo (3.6 ± 1.5 μU·ml−1, p = 0.007). Thereafter, values then converged and remained relatively stable until the end of the exercise. The different insulinogenic responses between conditions produced differences in the mean serum insulin AUC between conditions, with Glu (897.8 ± 3.15.0 μU·ml−1·min−1) being significantly greater than placebo (339.4 ± 172.8 μU·ml−1·min−1, p < 0.001) and Gal (513.1 ± 170.4 μU·ml−1·min−1, p = 0.011) as well as Gal being significantly greater than placebo (p = 0.011).
Plasma lactate concentrations changed over time and increased from typical resting values after the initial period of exercise (p < 0.001) and then decreased for the remainder of the prescribed part of the exercise protocol (Figure 2C). Plasma lactate concentrations were higher for Gal (1.8 ± 0.7 mmol·L−1) in comparison to Glu (1.2 ± 0.4 mmol·L−1, p = 0.002) and placebo (1.1 ± 0.3 mmol·L−1, p = 0.013) at 28 minutes. Glu produced higher plasma lactate concentrations in comparison to placebo at 72.5 minutes (9.4 ± 3.7 vs. 7.7 ± 3.4 mmol·L−1, p = 0.009).
Heart Rate and Ratings of Perceived Exertion
Both heart rate (Figure 3A) and RPE (Figure 3B) showed a predictable pattern of physiological responses consistent with exercise at different intensities, with no significant main effect of condition or interactions between conditions and time.
This study demonstrates that the chance of improving performance after the ingestion of carbohydrate within the hour of exercise commencing was small in comparison to placebo. However, the pre-exercise ingestion of galactose was more effective at maintaining endurance capacity in comparison to glucose, producing greater times to exhaustion on all occasions. Galactose ingestion produced similar glycemic responses to placebo during exercise, maintaining superior plasma glucose concentrations during the initial phase of the sprints compared with glucose. In contrast, 30% of the cyclists were susceptible to rebound hypoglycemia during the initial 20 minutes of exercise after glucose ingestion; however, only 1 cyclist was sensitive to this and was unable to continue exercising.
Pre-exercise ingestion of Gal and Glu did not produce a significant endurance capacity advantage in comparison to placebo. The latter is in agreement with Refs. 22 and 43 and also in contrast with previous literature (28,41). The variation in time to exhaustion within conditions was relatively large (CV: placebo 25.4%, Glu 13.3%, Gal 14.8%), which may explain why there are no significant differences from the placebo condition for either CHO condition. Nevertheless, Gal had a mean difference of +4.7 minutes and Glu −5.5 minutes compared with placebo, which could be considered physiologically significant. Accordingly, this study supports previous concerns over the consumption of glucose as a pre-exercise formulation in comparison to a placebo (15,28) for some individuals.
The performance advantage of Gal compared with Glu is contrary to the findings of Jentjens and Jeukendrup (24). However, that study used a different carbohydrate dose (75 vs. 40 g) and exercise protocol in comparison to this study (time trial vs. time to exhaustion). The high-intensity time to exhaustion protocol used in this study, though less ecologically valid, was deliberately designed to test differences between metabolic aspects of fatigue, which is not possible with a time trial design. Time to exhaustion protocols have the advantage of providing a controlled environment for the comparison of metabolic variables (10), such as plasma glucose concentrations, compared with time trials, which are likely to produce variability in exercise intensity. Furthermore, though time trial designs are likely to detect small and potentially crucial differences, when combined with small sample sizes may lack adequate statistical power. This study produced statistical power of 0.7, which is higher than the 0.3 reported by Jentjens and Jeukendrup (24).
The distinct peak in plasma glucose concentration after Glu ingestion, during the pre-exercise period (∼8 mmol·L−1), was higher in comparison to plasma glucose concentration attained after Gal ingestion. This is to be expected because plasma glucose concentrations should rise after ingestion and absorption of just glucose, but galactose, after absorption, can only be a precursor for plasma glucose on specific metabolism. Circulating glucose enters the muscle cell directly where it is converted to glucose-6-phosphate. This may at rest provide sufficient substrate for glycogen synthesis but also is “demand led” during exercise to support glycolytic flux for energy production. In contrast, on entering the circulation, ingested galactose is preferentially taken up by the liver (45), before conversion to glucose-1-phosphate through the Leloir pathway. Glucose-1-phosphate is then available for the formation of glycogen in the liver or is released as free glucose. This may explain the lower postprandial plasma glucose concentrations in the pre-exercise period, which is likely to be almost exclusively the controlled release of glucose, formed from galactose by the liver, into the circulation (16). This is consistent with increases in plasma glucose concentrations of no more than 1 mmol·L−1 reported within a galactose tolerance test (50 g (16)) or 75 g of galactose consumed 45 minutes before exercise (24).
The decline in plasma glucose concentrations, albeit from different absolute concentrations, after the appearance of exogenous glucose or galactose reflects a change in glucose flux into the muscle during the initial 20 minutes of exercise but the prevalence and change was different for each substrate. Hyperinsulinemia after glucose before exercise combined with an effect of increased contractile activity on exercise on muscle glucose uptake would combine to accelerate disposal of plasma glucose (13,32) at a time when glucose production from the liver would be inhibited. During exercise, such imbalance between production and disposal, if continued, would lead to low glucose concentrations that are insufficient to support muscle glucose uptake (27). There is also potential, as a consequence of hyperinsulinemia, inhibition of lipolysis (21) and also increased reliance on muscle glycogen stores (6,17). All of these likely mechanisms theoretically may explain the significantly shorter times to exhaustion after pre-exercise ingestion of Glu compared with Gal ingestion, but do not seem to influence endurance capacity in comparison to placebo. This suggests that low plasma glucose concentrations overall may not be a concern with respect to matching performance on placebo, but would be a concern in that it did not improve performance. Even though plasma glucose concentrations might be sufficient in the early stages of moderate- to high-intensity exercise, some individuals may be more sensitive than others to this situation (8). Plasma glucose concentrations after galactose ingestion were far less sensitive to reduction and in contrast the decline was also not associated with hyperinsulinemia. Therefore, the small decline was more likely a reflection of increased disposal of plasma glucose into the working muscle upon the initiation of exercise (32). Absence of hyperinsulinemia is unlikely to have suppressed lipolysis and fat oxidation. Furthermore, because plasma glucose concentrations were very similar to those produced by placebo, Gal ingestion was unlikely to have affected hepatic glucose output during this period. Thus, the flux of glucose into the muscle is unlikely to be compromised after galactose ingestion. These differences between glucose and galactose in homeostatic balance may underlie differences in exercise capacity. Yet, differences in individual sensitivity to plasma glucose concentration related to insulin concentration and receptor sensitivity may confound simple interpretation and explanation of differences between glucose and galactose conditions. However, note that serum insulin AUC was far greater during glucose, and under this condition exhaustion was likely to occur earlier than under galactose.
The mean plasma glucose concentrations after the pre-exercise ingestion of Glu (3.9 ± 1.2 mmol·L−1) and Gal (4.4 ± 0.8 mmol·L−1) did not fall below 3.0 mmol·L−1, which has previously been defined as hypoglycemic (12,33), during the initial 30 minutes of exercise. However, 30% of the participants were shown to be below the threshold (3.0 mmol·L−1) and thus susceptible to this rebound hypoglycemia, after the pre-exercise ingestion of Glu. This adds to the evidence that rebound hypoglycemia occurs, but not all individuals seem to be susceptible (23,29). Individual responses appear very relevant. One cyclist in this study only managed to complete 18.5 minutes, after the ingestion of Glu. In this case, premature fatigue coincided with rebound hypoglycemia. The cyclist was able to perform for 66.8 minutes after the ingestion of placebo. The other 2 cyclists were able to perform for 75.0 and 66.7 minutes despite rebound hypoglycemia, demonstrating some individuals are more sensitive to low plasma glucose concentrations than others, as previously suggested (8). Therefore, even though research unequivocally supports the consumption of CHO during endurance exercise to sustain endurance capacity (25), it may not be to some individuals advantage to consume a glucose formulation 30 minutes before exercise. Additional research is warranted to evaluate those susceptible to rebound hypoglycemia and whether this has a true effect on endurance performance, as well as gauging how many athletes are affected by this phenomenon.
A feature of this study is the difference in the recovery of plasma glucose concentrations between the 3 conditions, after the initial 20 minutes of exercise. By the third repeat sprint, plasma glucose concentrations increased to a relative hyperglycemia after the ingestion of placebo and Gal, which was associated with a small increase in plasma insulin concentrations. The maintenance of higher plasma glucose concentrations after Gal and placebo during the repeated sprints could be explained by either a reduction in plasma glucose disposal compared with the Glu condition (unlikely because of the intensity of the exercise), or a relative increase in hepatic glucose production, or an adequate hepatic production of glucose. The latter hypothesis is particularly attractive for galactose because it is known to be an excellent precursor of liver glycogen compared with glucose (11). Therefore, it is possible that the pre-exercise ingestion of galactose produces during exercise, a situation where the liver is more able to maintain plasma glucose concentration a key determinant of muscle glucose uptake, as it is not associated with the effects of hyperinsulinemia or other homeostatic imbalances. The lower plasma glucose concentrations, though not below basal concentrations, during the use of Glu are likely to be a consequence of the continued inhibition of hepatic glucose output because of the enduring effects of hyperinsulinemia (27,32). The differences in plasma glucose concentrations after galactose and glucose ingestion are unlikely to be related to intestinal absorption, as they both share the same transport mechanism. Both galactose and glucose are “actively” transported across the brush border membrane into the cell primarily by the same sodium cotransport system (46). Therefore, the greater times to exhaustion shown for Gal may in part be related to the more effective availability of plasma glucose from subsequent hepatic production, especially because plasma glucose concentrations have been shown to be important with regard to endurance capacity (4,5). The higher plasma glucose concentrations are likely to reflect more effective maintenance of glucose oxidation (19), especially because there is evidence that galactose can produce higher exogenous glucose oxidation rates during the latter stages of exercise in comparison to glucose (34). This by itself may postpone fatigue (7), alternatively it may reduce reliance on endogenous glycogen stores which could sustain endurance performance more effectively than glucose in this scenario. However, these metabolic differences between glucose and galactose do not explain why neither was able to produce greater performances to placebo, particularly galactose. Galactose was as effective as placebo at maintaining relatively high plasma glucose concentration during the initial repeated sprints. Therefore, with the accompanying rise in serum insulin concentrations similar to placebo, it might be logical to assume that the rate of glucose uptake by the exercise muscles was similar. This might explain why there were no performance differences between these 2 conditions, with galactose only able to match the normal “situation.”
In conclusion, this study showed that the pre-exercise consumption of galactose 30 minutes before exercise provided stable and higher plasma glucose concentrations throughout exercise for metabolism by the exercising muscles, as well as lower insulin responses. Further, this study has also highlighted that after pre-exercise ingestion of CHO, 30% of the trained male cyclists were susceptible to rebound hypoglycemia from Glu in comparison to Gal. The hypothesis that pre-exercise galactose ingestion would reduce the occurrence of rebound hypoglycemia compared with glucose ingestion can then be accepted. Additionally, the hypothesis that pre-exercise galactose ingestion would produce significantly longer times to exhaustion during a high-intensity endurance capacity test in comparison to glucose can also be accepted. However, neither CHO treatment enhanced performance in comparison to placebo, which remains to be explained.
The results of this study show that the ingestion of CHO within the hour before exercise alone does not provide a performance capacity benefit. Therefore, if glycogen reserves are optimal, then the consumption of CHO within the hour before exercise may not be required for such an endurance performance scenario.
The authors thank Cadbury Schweppes for supporting this research and Mr. Ran Kurvits for his technical assistance. The authors declare that there is no conflict of interest. The results of this study do not constitute endorsement of the product by the authors or the National Strength and Conditioning Association.
1. Bergstrom J, Hermansen L, Hultman E, Saltin B. Diet, muscle glycogen and physical performance. Acta Physiol Scand 71: 140–150, 1967.
2. Casey A, Mann R, Banister K, Fox J, Morris PG, Macdonald IA, Greenhaff PL. Effect of carbohydrate
ingestion on glycogen resynthesis in human liver and skeletal muscle, measured by (13)C MRS. Am J Physiol Endocrinol Metab 278: E65–E75, 2000.
3. Chryssanthopoulos C, Hennessy LC, Williams C. The influence of pre-exercise glucose ingestion on endurance running capacity. Br J Sports Med 28: 105–109, 1994.
4. Coggan AR. Plasma glucose metabolism during exercise in humans. Sports Med 11: 102–124, 1991.
5. Coggan AR, Coyle EF. Reversal of fatigue during prolonged exercise by carbohydrate
infusion or ingestion. J Appl Physiol (1985) 63: 2388–2395, 1987.
6. Costill DL, Coyle E, Dalsky G, Evans W, Fink W, Hoopes D. Effects of elevated plasma FFA and insulin on muscle glycogen usage during exercise. J Appl Physiol Respir Environ Exerc Physiol 43: 695–699, 1977.
7. Coyle EF, Coggan AR, Hemmert MK, Ivy JL. Muscle glycogen utilization during prolonged strenuous exercise when fed carbohydrate
. J Appl Physiol (1985) 61: 165–172, 1986.
8. Coyle EF, Hagberg JM, Hurley BF, Martin WH, Ehsani AA, Holloszy JO. Carbohydrate
feeding during prolonged strenuous exercise can delay fatigue. J Appl Physiol Respir Environ Exerc Physiol 55: 230–235, 1983.
9. Currell K, Jentjens RL, Jeukendrup AE. Reliability of a cycling time trial in a glycogen-depleted state. Eur J Appl Physiol 98: 583–589, 2006.
10. Currell K, Jeukendrup AE. Validity, reliability and sensitivity of measures of sporting performance. Sports Med 38: 297–316, 2008.
11. Decombaz J, Jentjens R, Ith M, Scheurer E, Buehler T, Jeukendrup A, Boesch C. Fructose and galactose enhance postexercise human liver glycogen synthesis. Med Sci Sports Exerc 43: 1964–1971, 2011.
12. Fanelli CG, Pampanelli S, Porcellati F, Bolli GB. Shift of glycaemic thresholds for cognitive function in hypoglycaemia unawareness in humans. Diabetologia 41: 720–723, 1998.
13. Febbraio MA, Keenan J, Angus DJ, Campbell SE, Garnham AP. Preexercise carbohydrate
ingestion, glucose kinetics, and muscle glycogen use: Effect of the glycemic index. J Appl Physiol 89: 1845–1851, 2000.
14. Felig P, Cherif A, Minagawa A, Wahren J. Hypoglycemia during prolonged exercise in normal men. N Engl J Med 306: 895–900, 1982.
15. Foster C, Costill DL, Fink WJ. Effects of preexercise feedings on endurance performance. Med Sci Sports 11: 1–5, 1979.
16. Gannon MC, Khan MA, Nuttall FQ. Glucose appearance rate after the ingestion of galactose. Metabolism 50: 93–98, 2001.
17. Hargreaves M, Costill DL, Katz A, Fink WJ. Effect of fructose ingestion on muscle glycogen usage during exercise. Med Sci Sports Exerc 17: 360–363, 1985.
18. Hargreaves M, Hawley JA, Jeukendrup A. Pre-exercise carbohydrate
and fat ingestion: Effects on metabolism and performance. J Sports Sci 22: 31–38, 2004.
19. Hawley JA, Bosch AN, Weltan SM, Dennis SC, Noakes TD. Glucose kinetics during prolonged exercise in euglycaemic and hyperglycaemic subjects. Pflugers Arch 426: 378–386, 1994.
20. Hopkins WG, Marshall SW, Batterham AM, Hanin J. Progressive statistics for studies in sports medicine and exercise science. Med Sci Sports Exerc 41: 3–13, 2009.
21. Horowitz JF, Mora-Rodriguez R, Byerley LO, Coyle EF. Lipolytic suppression following carbohydrate
ingestion limits fat oxidation during exercise. Am J Physiol 273: E768–E775, 1997.
22. Jentjens RL, Cale C, Gutch C, Jeukendrup AE. Effects of pre-exercise ingestion
of differing amounts of carbohydrate
on subsequent metabolism and cycling performance. Eur J Appl Physiol 88: 444–452, 2003.
23. Jentjens RL, Jeukendrup AE. Prevalence of hypoglycemia following pre-exercise carbohydrate
ingestion is not accompanied by higher insulin sensitivity. Int J Sport Nutr Exerc Metab 12: 398–413, 2002.
24. Jentjens RL, Jeukendrup AE. Effects of pre-exercise ingestion
of trehalose, galactose and glucose on subsequent metabolism and cycling performance. Eur J Appl Physiol 88: 459–465, 2003.
25. Jeukendrup AE. Carbohydrate
intake during exercise and performance. Nutrition 20: 669–677, 2004.
26. Jeukendrup AE, Killer SC. The myths surrounding pre-exercise carbohydrate
feeding. Ann Nutr Metab 57(Suppl.2): 18–25, 2010.
27. Jeukendrup AE, Wagenmakers AJ, Stegen JH, Gijsen AP, Brouns F, Saris WH. Carbohydrate
ingestion can completely suppress endogenous glucose production during exercise. Am J Physiol 276: E672–E683, 1999.
28. Keller K, Schwarzkopf R. Preexercise snacks may decrease exercise performance. Phys SptsMed 12: 89–91, 1984.
29. Kuipers H, Fransen EJ, Keizer HA. Pre-exercise ingestion
and transient hypoglycemia during exercise. Int J Sports Med 20: 227–231, 1999.
30. Kuipers H, Keizer HA, Brouns F, Saris WH. Carbohydrate
feeding and glycogen synthesis during exercise in man. Pflugers Arch 410: 652–656, 1987.
31. Macdermid PW, Stannard S, Rankin D, Shillington D. A comparative analysis between the effects of galactose and glucose supplementation on endurance performance. Int J Sport Nutr Exerc Metab 22: 24–30, 2012.
32. Marmy-Conus N, Fabris S, Proietto J, Hargreaves M. Preexercise glucose ingestion and glucose kinetics during exercise. J Appl Physiol (1985) 81: 853–857, 1996.
33. Mitrakou A, Ryan C, Veneman T, Mokan M, Jenssen T, Kiss I, Durrant J, Cryer P, Gerich J. Hierarchy of glycemic thresholds for counterregulatory hormone secretion, symptoms, and cerebral dysfunction. Am J Physiol 260: E67–E74, 1991.
34. O'Hara JP, Carroll S, Cooke CB, Morrison DJ, Preston T, King RF. Preexercise galactose and glucose ingestion on fuel use during exercise. Med Sci Sports Exerc 44: 1958–1967, 2012.
35. O'Hara JP, Thomas A, Seims A, Cooke CB, King RF. Reliability of a high-intensity endurance cycling test. Int J Sports Med 33: 18–25, 2012.
36. Palmer GS, Hawley JA, Dennis SC, Noakes TD. Heart rate responses during a 4-d cycle stage race. Med Sci Sports Exerc 26: 1278–1283, 1994.
37. Samols E, Dormandy TL. Insulin response to fructose and galactose. Lancet 1: 478–479, 1963.
38. Schabort EJ, Hawley JA, Hopkins WG, Mujika I, Noakes TD. A new reliable laboratory test of endurance performance for road cyclists. Med Sci Sports Exerc 30: 1744–1750, 1998.
39. Seifert JG, Paul GL, Eddy DE, Murray R. Glycemic and insulinemic response to preexercise carbohydrate
feedings. Int J Sport Nutr 4: 46–53, 1994.
40. Sherman WM, Peden MC, Wright DA. Carbohydrate
feedings 1 h before exercise improves cycling performance. Am J Clin Nutr 54: 866–870, 1991.
41. Speedy D, Kelly M, O'Brien M. The effect of pre-exercise feeding on endurance exercise performance. New Zeal J Sports Med 26: 34–37, 1998.
42. Stannard SR, Hawke EJ, Schnell N. The effect of galactose supplementation on endurance cycling performance. Eur J Clin Nutr 63: 209–214, 2007.
43. Tokmakidis SP, Volaklis KA. Pre-exercise glucose ingestion at different time periods and blood glucose concentration during exercise. Int J Sports Med 21: 453–457, 2000.
44. Vogt S, Heinrich L, Schumacher YO, Blum A, Roecker K, Dickhuth HH, Schmid A. Power output during stage racing in professional road cycling. Med Sci Sports Exerc 38: 147–151, 2006.
45. Williams CA. Metabolism of lactose and galactose in man. Prog Biochem Pharmacol 21: 219–247, 1986.
46. Wright EM, Martin MG, Turk E. Intestinal absorption in health and disease–sugars. Best Pract Res Clin Gastroenterol 17: 943–956, 2003.