Twenty healthy men who had trained aerobically or anaerobically at least 4 times a week during the last year, participated in the study (Table 1). None of the subjects had received either pharmacological treatment or vitamin or mineral supplements during the two months before the study. The study design, purpose, and possible risks were explained to the subjects, and written consent was obtained. All the procedures employed in the study were approved by the Ethics Committee of the Reina Sofía University Hospital.
Tests and Exercise
Perceived Exertion and Heart Rate
Perceived exertion was recorded using the Borg PE scale CR-10 (5) at 3 different times: midexercise (t 15), at the end of the exercise (t 30), and 30 minutes after completion of the exercise (t 60) (Figure 2). To help the subjects refer the PE appropriately, instructions were carefully given and explained. Moreover, subjects were familiar with this scale, because this method had been regularly used as part of their training routine. Subjects were asked to score PE on a scale in which “zero,” which meant no effort (rest), and “10,” which meant maximal effort. The final record (t 60) was used to indicate the subject's overall perception of the session (12) and was performed 30 minutes after conclusion of the training bout. In addition, HR was monitored throughout the session (Polar 810; Polar, Kempele, Finland) and was analyzed at the same time points as PE was.
The 10RM load was calculated on the basis of a half squat (HS) exercise on a multipower machine (Gervasport, Madrid, Spain), using the protocol for submaximal force testing developed by Kraemer and Fry (26). The sequence employed in this exercise was 3 seconds per repetition (1.5 seconds in the eccentric phase and 1.5 seconds in the concentric phase), controlled by means of a digital metronome (MA-30, Korg, Tokyo, Japan). The mass of all weight plates used was verified with a precision scale. The actual mass of all plates was used to calculate 10RM in the HS exercise. To minimize possible errors in 10RM testing, several strategies for giving information, monitoring, and encouraging the subjects were implemented; these strategies had been used previously (10). For a repetition to be taken as valid, the typical range of motion for this exercise had to be fully carried out. For this purpose, subjects were placed in an HS position, with shoulders touching the bar; the starting knee angle for movement execution was set at 90°. During each repetition, the subjects started from the 90° flexed-knee position and performed concentric extension of the leg muscles (hip, knee, and ankle) until reaching full extension at 180°, thereafter returning to the initial 90° position, with no pauses between the 10 repetitions.
The SE performed during experimental trials consisted of a bout of 10 series of 10 HS, with the first and second series being performed at 70 and 80% of 10RM, respectively, and the remainder at 90% of 10RM. There was a recovery period of 165 seconds between each series. The total duration of each bout (including exercise and interseries recovery periods) was 30 minutes. The subjects used the same machine and sequence of exercises as in the preliminary 10RM test.
All subjects performed a progressive test until exhaustion on a cycloergometer (Ergometrics 800; Ergoline, Barcelona, Spain) under identical environmental conditions (21-24°C; 45-55% relative humidity) to determine their EE load. The test protocol commenced with 4 minutes of warm-up, at a load of 25 W during the first 2 minutes, followed by 50 W for the other 2; the load was thereafter increased by 25 W·min−1 until exhaustion. The subjects were asked to maintain a constant pedaling rate of between 60 and 70 rpm. During the tests, a breath by breath automatic system (Oxycon Delta; Jaeger, Höchberg, Germany) was used to measure the following parameters: oxygen and carbon dioxide consumption (o2 and CO2, in l minute-1 STP); ventilation (E, in l minute-1 body temperature, ambient pressure, and saturated with water vapor [BPTS]), E/o2, VE/CO2, and end-tidal partial pressure of oxygen and carbon dioxide (PETO2 and PECO2). The values given were means calculated for 15-second intervals. The workloads (W) corresponding to the ventilatory thresholds 1 and 2 (VT1 and VT2, respectively) were calculated following the method of Davis et al. (11).
For the EE performed during experimental trials, subjects pedaled at 25 and 50 W during the first and second minutes, respectively (warm-up phase) before completing a total of 30 minutes at an intensity equivalent to the value of W that they had reached at a point equidistant between VT1 and VT2 during the preliminary o2max test. The same cycloergometer and pedaling rate were used in the endurance trials as in the preliminary tests.
Nutritional Status and Diet
A retrospective qualitative-quantitative assessment of the frequency of food intake over the 4 weeks before preliminary evaluations was obtained from each subject by a nutritionist. Subjects were thereafter instructed to ingest an isocaloric diet, with a moderate glycemic load (GL) and glycemic index (GI). The daily ration of vegetables and fruit was set in accordance with the recommended dietary intake of ascorbic acid. This diet was followed throughout the 2 weeks before the first experimental trial and the washout periods between each trial; furthermore, caffeine, alcohol, and foods with a high sugar content were not to be consumed during the day before each test. A 24-hour diary of food consumption was maintained to confirm that the dietary recommendations were adhered to, and diet composition was calculated with the aid of food-composition tables. The GL and GI using formulae proposed by Liu et al. (29) and Jenkins et al. (20), respectively are given in Table 2.
Participants arrived at the laboratory between 08.00 and 09.00, after 10-12 hours of overnight fasting. A cannula (Vennflon, 16 G, London, United Kingdom) was inserted into the antecubital vein. Twenty milliliters of blood was drawn off 15 minutes before the beginning of the exercise tests (t −15), and immediately thereafter, the subjects ingested a solution of 50 g of G (glucose anhydride C6H12O6 99,5%) or 50 g G plus 15 g F monosaccharide (GF) in 400 ml water. The 50 g of glucose, which requires no hydrolysis for absorption, was established as the minimal amount of glycemic CHO in the 4 trials, to provide the same threshold for detecting changes in glycemic behavior when F was given simultaneously in the GF trial. For this reason, 2 nonisocaloric supplements were used, as in other studies (19,36).The G and GF solutions used had total concentrations of 12.5 and 16.5%, respectively. The amount of F in the combined supplement was determined on the basis of previous reports of its digestibility and absorption under resting and exercise conditions (17,39), and its specific concentration in solution was 3.75%, which is lower than that reported as being capable of being absorbed without causing gastrointestinal symptoms (41). During the 2 hours after the consumption of the supplement (postprandial period), which included a brief digestive rest (t −15 to t 0), the exercise phase (t 0, t 15, and t 30) and the recovery phase (t 45, t 75, and t 105), venous blood samples were drawn. The subjects were also asked to avoid performing moderate or severe exercise for 24 hours before each preliminary session and experimental trial, which was controlled by means of a self-recorded exercise questionnaire. Basal serum creatine kinase values above 200 U·L−1 were considered as an exclusion criterion for the experiment.
Blood and Urine Samples and Analytical Assays
Blood samples were collected in tubes containing 1 g ethylenediaminetetraacetic acid (EDTA); tubes were stored immediately in ice, and plasma was separated by centrifugation at 1,500 rpm for 15 minutes at 4°C. Tubes were protected from light at all times. Glucose concentrations were determined by spectrophotometric methods, using a modular analyzer (ISE-4-DDPPEEPP, Hoffmann-La Roche®, Basel, Switzerland). Plasma insulin levels were measured by chemiluminescent microparticle immunoassay (Architect i-4000, Abbott®, Chicago, IL, USA). Plasma lactic acid was measured by an enzymatic colorimetric assay using an automated analyzer (Cobas 400; Hoffman-La Roche, Basel, Switzerland).
Total urine produced also was collected in sterile containers before CHO ingestion (t 215), at the end of the exercise period (t 30), and the end of the recovery period (t 105). The subjects were recommended to drink water ad libitum during the exercise and recovery periods to encourage urine production. Urinary concentrations of adrenaline (epinephrine), noradrenaline (norepinephrine), and creatinine were determined by high performance liquid chromatography (HPLC), using a chromatograph (Bio-Rad Laboratories, Hercules, CA, USA) with a reverse-phase column (flow rate of 1 ml·min−1) and an electrochemical detector (at 500 mV and 10 nA). Urinary concentrations of adrenaline and noradrenaline were expressed relative to urinary creatinine (nmol·mmol−1 of creatinine). In addition, 1 day before collecting the urine, the subjects were asked not to consume bananas, coffee, pineapple, or walnuts. Subjects were not permitted to take any of the following drugs: pheothiazin, paracetamol, salsinol, isoproterenol, and α-methyldopa.
Reproducibility of Measurements
The CR-10 scale and the 10RM test had been used regularly by the subjects during their last training year, which enabled good reproducibility of measurements (intraclass correlation [ICC] = 0.90 and 0.93, respectively); consequently, in the present experiment, a familiarization period was not deemed necessary. The o2max test was performed using a regularly calibrated gas analyzer; moreover, since subjects performed cycling at least once a week, they were used to the exercise they had to perform with the cyclo-ergometer. Biochemical measurements were generally made at the hospital laboratory in accordance with Standard ISO 15189. The laboratory is involved in internal and external quality control programs. External quality control is provided monthly by The Spanish Society of Clinical Biochemistry and Molecular Pathology.
Traditional statistical methods were used to calculate mean ± SEM. Sample normality was calculated using the Shapiro-Wilk test. The effect of the different interventions (G + SE, F + SE, G + EE, and F + EE; independent variables) on PE, FC, blood G, insulin, lactate, adrenaline, and noradrenaline (dependent variables) was analyzed by means of analysis of variance with repeated measures. A Sidak correction was used to adjust the p value with regard to the number of contrasts performed, and a p ≤ 0.05 criterion was used to establish statistical significance. Effect size was calculated for paired variables (7). The SPSS 11.5 package for Windows was used for all statistical tests.
Perceived exertion displayed similar behavior during both SE and EE (Figure 3). After GF supplementation, subjects PE as less intense both during SE (t 15; effect size = 0.43, p < 0.05 and t 30; effect size = 0.48, p < 0.05) and EE (t 15; effect size = 0.23, p < 0.05 and t 30; effect size = 0.29, p < 0.05). Subjective assessment of the overall session, performed 30 minutes after exercise, was also lower in SE and EE after GF supplementation (effect size = 0.78, p < 0.05 and effect size = 0.32, p < 0.05, respectively). During SE, no statistical difference in HR values (Figure 3) was found between G and GF. In EE, by contrast, HR values were lower for GF, both during exercise (t 15; effect size = 0.46, p < 0.05 and t 30; effect size = 0.47, p < 0.05, respectively), and at t 75, during recovery (effect size = 0.49, p < 0.05).
The variables analyzed in this study behaved differently in response to G vs. GF supplementation, for both SE and EE. Blood G values during SE (Table 3) were statistically lower for GF during exercise at t 15, and higher during recovery at t 45 (p < 0.05). By contrast, there was no statistically significant difference in G values between G and GF during EE.
No differences were recorded in plasma insulin levels between G and GF trials during SE (p > 0.05). During recovery, at t 45, insulin values for GF were higher than those for G (p < 0.05). For EE, insulin values were higher for GF at t 15, during exercise, and t 75 during recovery (p < 0.05). Blood lactate values at the end of SE, t 30 (Table 3), were lower in subjects taking GF than in those taking only G (p < 0.05). Conversely, during recovery, at t 45 and t 75, GF showed greater lactate values (p < 0.05). During EE, lactate values differed between trials only at t 75, during recovery (p < 0.05).
No statistical difference was noted between G and GF for urinary catecholamine values (Figure 4) measured at rest (t −15), at the end of exercise (t 30), and at the end of the recovery period (t 105), in SE. In EE, by contrast, GF displayed lower values than in G at the end of exercise (t 30), for both adrenalin and noradrenalin (effect size = 1.18, p < 0.05 and effect size = 0.91, p < 0.05, respectively).
The main finding of this study was that subjects receiving a GF supplement 15 minutes before exercising perceived effort as less intense than when ingesting only a G supplement, during both SE and EE (Figure 3). In SE, GF supplementation reduced the postprandial glycemic peak by 8% compared to G and prompted a second glycemia and insulinemia peak during recovery. In EE, G and GF (GI 100 vs. 84, respectively) prompted a similar glycemic response. The insulin response during EE and during recovery from EE was 37.2 and 25.8% higher, respectively, for GF compared to G alone. The GF also kept the HR lower during EE and during recovery from EE; this was not found for SE. To the best of our knowledge, this is the first study to use an experimental design in which the effects of addition of F to a G supplement in SE and EE are assessed.
Physical exertion comprises a number of factors involving the central nervous system (CNS) and peripheral nervous system, mostly linked to muscular metabolism. With regard to CNS-related factors, it has been suggested that hypoglycemia is the main factor limiting the endothelial transport of G to the brain, affecting the oxidative metabolism and thus PE (6). Here, for all experimental situations (i.e., G + SE, GF + SE, G + EE, and GF + EE), blood G levels during exercise were higher than baseline values (Table 3); consequently, G levels did not represent a limiting factor that might prompt differences in the activation of central fatigue mechanisms. It would therefore appear that differences in PE between G and GF were specifically because of peripheral factors linked to CHO availability and thus to energy flow in metabolically active tissues.
In both SE and EE, the GF supplement prompted a glycemic response equal to or lower than that prompted by G alone, suggesting greater tolerance to the increased CHO ingestion (and consequently greater energy availability) after the addition of F. This varying response may also signify that part of the combined CHO supplement was oxidated to produce energy or converted into neoglycogenic substrate. Two earlier studies (21,22) have reported a marked increase in exogenous CHO oxidation after joint ingestion of G and F. In the first of these, 8 trained cyclists exercised for 120 minutes at 60% of o2max; during exercise, they ingested nonisocaloric supplements containing 1.2 g·min−1 G or 1.2 g·min−1 G plus 0.6 g·min−1 F. In the second study, the same subjects exercised for 150 minutes at the same intensity while consuming 1.2 g·min−1 G or 1.2 g·min−1 G plus 1.2 g·min−1 F. Interestingly, in both studies, the addition of F prompted an increase of around 50% in exogenous CHO oxidation, with no difference in RG as a function of the supplement ingested. A number of other studies (9,25) have confirmed the favorable effect of increased exogenous CHO oxidation on sporting performance, resulting from reduced PE and increased working capacity (pedaling power and time to exhaustion).
In the SE, the reduction in PE may additionally have been because supplement-related differences in lactate production. Lower-blood lactate levels after ingestion of GF suggest a lower internal muscle pH, which could be a decisive factor in PE reduction (as local input for exercising muscle). Reduced immediate G availability for the glycolytic pathway, mediated by the lower glycemic peak in GF, may have contributed to lower lactate production compared to the G supplement. At the same time, a second glycemic peak and higher residual lactate concentrations were observed during acute recovery from SE in subjects receiving GF. Both these findings have been reported as the result of hepatic F metabolism (33) and might reflect greater availability of direct or indirect substrates for energy production at the muscular level. Improved availability of energy-producing substrates during recovery may also have had an indirect influence on the lower overall PE observed in GF.
Another important finding was that, in EE, HR was significantly lower in subjects receiving GF; insulin values were also higher (Table 3), whereas adrenalin and noradrenalin values were lower (Figure 4). Other authors have demonstrated that an increase in insulin levels, because of CHO supplementation, reduces adrenergic activation by means of the antagonistic action of insulin on catecholamine levels during exercise (3). Given that, during exercise, HR is modulated by parasympathetic inhibition and sympathetic activation (30,35) and that catecholamines play a major role in this process, it may be assumed that GF supplementation modulates the response of the HR by means of a cascade effect. Here, reduced adrenergic activation was consistent with the increase in blood insulin levels associated with F supplementation and with a decrease in PE in GF. These findings are in agreement with other evidence that peripheral inputs, such as HR, are key modulators of PE during EE (13).
Finally, in the SE, no significant supplement-related differences were observed in the HR. This may be because HR is not a good indicator of metabolic and physical status in discontinuous exercises such as the SE used here (1,31) and also because there were no significant differences in catecholamine levels as a function of G vs. GF supplementation in the SE.
In summary, the findings of this study suggest that PE is positively affected by GF supplementation in both SE and EE. The peripheral inputs to the nervous system appear to share similar origins in the 2 types of exercise. As suggested earlier, increased exogenous CHO oxidation might account for improved maintenance of the balance between the production and degradation of adenosine triphosphate (ATP) molecules, thus avoiding a negative ATP balance during muscular exertion (32). Additionally, and particularly in SE, the reduction in PE may be associated with inputs from muscle metabolism, such as the production and metabolic fate of lactate derived from F. In EE, the inputs reaching the CNS to configure PE may also come from the cardiovascular system and from adrenergic signaling modulated by the neuroendocrine effect of insulin. Moreover, differences in blood G and insulin values after GF vs. G ingestion may reflect to differences in the metabolic demand for G and energy depending on the type of exercise involved; this would modulate postprandial metabolic response.
The findings of this study show that GF supplementation had a positive effect on PE in both strength and EEs. In practice, in trained men, F addition to a G supplement might prove an efficient dietary strategy for ensuring compliance with a specific training protocol, in that it helps to lower fatigue perception when >1 training session is to be performed in the course of a day. Moreover, F ingestion before a SE is likely to have an anticatabolic effect (higher blood G and insulin levels) after exercise. This, together with lowered PE, could enable the coach to introduce higher-intensity training sessions. With regard to EEs, further research is required, since recent studies have shown that F may prompt major metabolic dysregulation during exercise (16).
Supported by grants from the “Andalusian Council for Tourism, Commerce and Sports,” “Reina Sofía Hospital CajaSur Fundation” and “CIBER Physiopathology of Obesity and Nutrition” an initiative of the Carlos III Health Institute (ISCIII). The first two authors contributed equally to this manuscript.
1. Achten, J and Jeukendrup, AE. Heart rate
monitoring: Applications and limitations. Sports Med
33: 517-538, 2003.
2. Bantle, JP. Is fructose the optimal low glycemic index sweetener? In: Nestle Nutrition. Clinical Performance Programme
. Bantle, JP and Slama, G, eds. Vevey, Switzerland: Karger, 2006. pp. 32-34.
3. Borer, KT. Exercise Endocrinology
. Champaign, IL: Human Kinetics, 2003.
4. Borg, GV. Perceived exertion as indicator of somatic stress. Scand J Rehab Med
2: 92-98, 1970.
5. Borg, GV. The Borg CR10 Scale: Borg's Perceived Exertion and Pain Scales
.Champaign, IL: Human Kinetics, 1998.
6. Boyle, PJ, Nagy, RJ, O'Connor, AM, Kempers, SF, Yeo, RA, and Qualls, C. Adaptations in brain glucose uptake following recurrent hypoglycemia. Proc Natl Acad Sci
91: 9352-9356, 1994.
7. Cohen, J. Statistical Power Analysis for the Behavioral Sciences
(2nd ed.). Hillsdale, NJ: L. Erlbaum Associates, 1998.
8. Crewe, H, Tucker, R, and Noakes, TD. The rate of increase in rating of perceived exertion predicts the duration of exercise to fatigue at a fixed power output in different environmental conditions. Eur J Appl Physiol
103: 569-577, 2008.
9. Currell, K and Jeukendrup, AE. Superior endurance performance with ingestion of multiple transportable carbohydrates. Med Sci Sports Exerc
40: 275-281, 2008.
10. Da Silva Grigoletto, ME, Fernández, JM, Castillo, E, Nuñez, VM, Vaamond, DM, Poblador, MS, and Lancho, JL. Influence of vibration training on energy expenditure in active men. J Strength Cond Res
21: 470-475, 2007.
11. Davis, JA. Anaerobic threshold: A review of the concept and directions for future research. Med Sci Sports Exerc
17: 6-18, 1985.
12. Day, ML, McGuigan, MR, Brice, G, and Foster, C. Monitoring exercise intensity during resistance training using the session RPE
scale. J Strength Cond Res
18: 353-358, 2004.
13. Delp, MD, Armstrong, RB, Godfrey, DA, Laughlin, MH, Ross, CD, and Wilkerson, MK. Exercise increases blood flow to locomotor, vestibular, cardiorespiratory and visual regions of the brain in miniature swine. J Physiol
533: 849-859, 2001.
14. DeMarco, HM, Sucher, KP, Cisar, JC, and Butterfield, GE. Pre-exercise carbohydrate meals: Applications of glycemic index. Med Sci Sports Exerc
31: 164-170, 1999.
15. Fernandez, JM, Da Silva-Grigoletto, ME, Gomez-Puerto, JR, Viana-Montaner, BH, Tasset-Cuevas, I, Tunez, I, Lopez-Miranda, J, and Perez-Jimenez, F. A dose of fructose induces oxidative stress during endurance and strength exercise. J Sports Sci
17: 1-12, 2009.
16. Fernández, JM, Da Silva-Grigoletto, ME, Ruano-Ruíz, JA, Caballero-Villarraso, J, Moreno-Luna, R, Túnez-Fiñana, I, Tasset-Cuevas, I, Pérez-Martínez, P, López-Miranda, J, and Pérez-Jiménez F. Fructose modifies the hormonal response and modulates lipid metabolism during aerobic exercise after glucose supplementation. Clin Sci (Lond)
116: 137-145, 2009.
17. Fujisawa, T, Mulligan, K, Wada, L, Schumacher, L, Riby, J, and Kretchmer, N. The effect of exercise on fructose absorption. Am J Clin Nutr
58: 5-9, 1993.
18. Gearhart, RE, Goss, FL, Lagally, KM, Jakicic, JM, Gallagher, J, and Robertson, RJ, Standardized scaling procedures for rating perceived exertion during resistance exercise. J Strength Cond Res
15: 320-325, 2001.
19. Heacock, PM, Hertzler, SR, and Wolf, BW. Fructose prefeeding reduces the glycemic response to a high-glycemic index, starchy food in humans. J Nutr
132: 2601-2604, 2002.
20. Jenkins, DJ, Wolever, TM, Taylor, RH, Barker, H, Fielden, H, Baldwin, JM, Bowling, AC, Newman, HC, Jenkins, AL, and Goff, DV. Glycemic index of foods: A physiological basis for carbohydrate exchange. Am J Clin Nutr
34: 362-366, 1981.
21. Jentjens, RL and Jeukendrup, AE. High rates of exogenous carbohydrate oxidation from a mixture of glucose and fructose ingested during prolonged cycling exercise. Br J Nutr
93: 485-492, 2005.
22. Jentjens, RLPG, Moseley, L, Waring, RH, Harding, LK, and Jeukendrup, AE. Oxidation of combined ingestion of glucose and fructose during exercise. J Appl Physiol
96: 1277-1284, 2004.
23. Jentjens, RLPG, Underwood, K, Achten, J, Currel, K, Mann, CH, and Jeukendrup, AE. Exogenous carbohydrate oxidation rates are elevated after combined ingestion of glucose and fructose during exercise in heat. J Appl Physiol
100: 807-816, 2006.
24. Jeukendrup, AE. Carbohydrate intake during exercise and performance. Nutrition
20: 669-677, 2004.
25. Jeukendrup, AE, Moseley, L, Mainwaring, GI, Samuels, S, Perry, S, and Mann, CH. Exogenous carbohydrate oxidation during ultraendurance exercise. J Appl Physiol
100: 1134-1141, 2006.
26. Kraemer, WJ and Fry, AC. Physiological assessment of human fitness. In: Strength Testing: Development and Evaluation Methodology
. Maud, P and Foster, C, eds. Champaign, IL: Human Kinetics, 1995. pp. 115-137.
27. Lambert, GP, Chang, RT, Xia, T, Summers, RW, and Gisolfi, CV. Absorption from different intestinal segments during exercise. J Appl Physiol
83: 204-212, 1997.
28. Le, KA and Tappy, L. Metabolic effects of fructose. Curr Opin Clin Nutr Metab Care
9: 469-475, 2006.
29. Liu, S, Manson, JE, Stampfer, MJ, Holmes, MD, Hu, FB, Hankinson, SE, and Willett, WC. Dietary glycemic load assessed by food-frequency questionnaire in relation to plasma high-density-lipoprotein cholesterol and fasting plasma triacylglycerols in postmenopausal women. Am J Clin Nutr
73: 560-566, 2001.
30. Longhurst, J and Zelis, R. Cardiovascular responses to local handlimb hypoxemia: Relation to the exercise reflex. Am J Physiol
237: H359-H365, 1979.
31. Madden, KM, Levy, WC, and Stratton, JK. Exercise training and heart rate
variability in older adult female subjects. Clin Invest Med
29: 20-28, 2006.
32. McConell, G, Snow, RJ, Proietto, J, and Hargreaves, M. Muscle metabolism during prolonged exercise in humans: Influence of carbohydrate availability. J Appl Physiol
87: 1083-1086, 1999.
33. McGuinness, OP and Cherrington, AD. Effects of fructose on hepatic glucose metabolism. Curr Opin Clin Nutr Metab Care
6: 444-448, 2003.
34. Mielke, M, Housh, TJ, Malek, MH, Beck, TW, Schmidt, RJ, and Johnson, GO. The development of rating of perceived exertion-based tests of physical working capacity. J Strength Cond Res
22: 293-302, 2008.
35. Millhorn, DE, Eldrige, FL, and Waldrop, TG. Diencephalic regulation of respiration and arterial pressure during actual and fictive locomotion in cat. Circ Res
61: 53-59, 1978.
36. Moore, MC, Cherrington, AD, Mann, SL, and Davis, SN. Acute fructose administration decreases the glycemic response to an oral glucose tolerance test in normal adults. J Clin Endocrinol Metab
85: 4515-4519, 2000.
37. Noble, BJ and Robertson, RJ. Perceived Exertion
. Champaign, IL: Human Kinetics, 1996.
38. Nybo, L. CNS fatigue and prolonged exercise: Effect of glucose supplementation. Med Sci Sports Exerc
35: 589-594, 2002.
39. Riby, JE, Fujisawa, T, and Kretchmer, N. Fructose absorption. Am J Clin Nutr
58: S748-S753, 1993.
40. Shi, X, Summers, RW, Schedl, HP, Flanagan, SW, Chang, R, and Gisolfi, CV. Effects of carbohydrate type and concentration and solution osmolality on water absorption. Med Sci Sports Exerc
27: 1607-1615, 1995.
41. Skoog, SM and Bharucha, AE. Dietary fructose and gastrointestinal symptoms: A review. Am J Gastroenterol
99: 2046-2050, 2004.
42. Wallis, AG, Rowlands, DS, Shaw, C. Jentjens, RLPG, and Jeukendrup, AE. Oxidation of combined ingestion of maltodextrins and fructose during exercise. Med Sci Exerc
3: 426-432, 2005.
Keywords:© 2010 National Strength and Conditioning Association
RPE; fructose metabolism; heart rate; catecholamine