Below is an excerpt from one of the lab reports I conducted on the effects of glucose ingestion during submaximal exercise. What are the benefits? Read the lengthy discussion to see what the literature has to offer!
Exogenous Glucose Intake during Exercise and The Effects on Substrate Utilization
Figure 1 simplistically represents the journey exogenous glucose goes through until it is oxidized by mitochondria. The maximal rate of intestinal glucose absorption is approximately 1.3-1.7g/min and has been labeled as one of the rate limiting factors for exogenous carbohydrate (CHO) oxidation, but can be surpassed through saturation of transporter proteins with different isomers of glucose (Jeukendrup, 2010). Research suggests that another rate limiting factor for exogenous CHO oxidation is hepatic glucose output (Jeukendrup & Jentjens, 2000) which is tightly regulated. When increasing amounts of glucose enter the liver (>1g/min), glycogenesis may occur in the liver (Jeukendrup et al., 1998; Juekendrup & Jentjens, 2000) resulting in suppression of hepatic glycolysis. Findings by Hawley et al. (1994) further support the notion that blood glucose concentration is tightly regulated by the liver and that the maximal rate of exogenous CHO oxidation is 1.1g/min.
When glucose is ingested during exercise, a decrease in FAT metabolism occurs. The decrease in lipid (FAT) oxidation is in response to an increased blood glucose concentration which can sufficiently supply the energy demands and the high concentration can suppress lipolysis (Horowitz et al., 1997). Additionally, the time of CHO ingestion during exercise has no effect on the rate of exogenous CHO oxidation (Jeukendrup & Jentjens, 2000). An increase in CHO oxidation rates occurs 75-90 minutes after initial CHO ingestion and then plateaus (Krzentowski et al., 1984). Furthermore, the modality of secreting glucose into the blood (either ingestion or intravenously) can affect the rate of CHO and FAT oxidation (Hawley et al., 1994). When CHO is obtained through intravenous, insulin levels do not increase similarly to oral ingestion and FAT oxidation is increased (Hawley et al., 1994).
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Figure 1 Simplified flow chart identifying the pathway of CHO from ingestion to oxidation. Adapted from Jeukendrup & Jentjens (2000). |
The ingestion of exogenous glucose and high insulin levels (Ramnanan et al., 2010) activates Protein Phosphatase 1 which inactivates the enzyme phosphorylase kinase into the B isoform (Aggen, Nairn, & Chamberlin, 2000). This mechanism inhibits glycolysis at the hepatic level, thus sparing liver glycogen. The maximal amount of glucose which can be secreted from the liver into circulation is approximately 1.1 grams per minute. Studies have shown that ingesting a solution containing different isomers of glucose (example: fructose) can increase the amount of glucose secretion from the liver by saturating the protein transporters present on epithelium of small intestine to increase absorption (Jeukendrup, 2010). Furthermore, the consumption of a solution containing fructose and glucose during exercise has been shown to increase performance (Triplett et al., 2010) and CHO oxidation (Adopo et al, 1994).
In a study conducted by Smith et al. (2010), they observed the changes in fuel utilization throughout 4 different experimental trials when the rate of carbohydrate ingestion varies (no glucose, 15g/hour, 30g/hour, and 60g/hour). As the rate of ingested CHO increased, the relative rate of energy derived from exogenous CHO increased as well. In addition, muscle glycogen depletion was constant throughout each condition, but hepatic glycogen sparing was positively related to an increased rate of CHO ingestion (Smith et al., 2010). Riddell et al. (2003) further support the findings through their study testing the substrate utilization of endurance athletes when glucose is ingested during exercise.
Many studies have concluded the same findings as presented in this report. The ingestion of exogenous glucose during exercise reduces the breakdown of glycogen at the liver level but not at the muscle (Smith et al., 2010). Even during moderate intensity shivering, the same phenomena occurs when CHO is ingested (Blondin et al., 2010). Few studies have attempted to illustrate if muscle glycogen utilization is suppressed when ingesting high amounts of CHO during exercise with mixed results due to the complicated methodologies (Jeukendrup & Jentjens, 2000). Future studies should attempt to definitively answer if muscle glycolysis is affected by CHO ingestion during exercise.
Trained individuals may have a greater capacity for blood glucose uptake due to increased muscular capillary beds, an increase in amount of mitochondria (Cox et al., 2010), and increased amount of GLUT-4 (Jeukendrup & Jentjens, 2000). Cox et al. (2010) demonstrated that a training program which implements CHO ingestion during exercise can increase exogenous CHO oxidation. Krzentowski et al. (1984) reported similar findings stating that CHO oxidation is increased by 17% in trained individuals.
The physiological advantage of the ingestion of CHO during prolonged exercise at the same intensity would be to spare hepatic glycogen stores. By sparing endogenous sources of energy, the body would be able to sustain energy during prolonged exercise. The notion of constant exogenous glucose to sustain the energy demand of working tissue, therefore increase endurance capacity, is not clear. Lacerda et al. (2009) demonstrated that carbohydrate ingestion during submaximal intensity does not delay the unset of fatigue. However, Maughan, Fenn, & Leiper (1989) observed that a combination of CHO, electrolytes and fluid served to attenuate fatigue and increase endurance capacity. One can postulate that ingestion of CHO, in combination with electrolytes and fluid, during prolonged exercise bouts can increase endurance capacity.
Adopo, E., Peronnet, F., Massicotte, D., Brisson, G.R., & Hillaire-Marcel, C. (1994). Respective oxidation of exogenous glucose and fructose given in the same drink during exercise. The Journal of Applied Physiology, 76(3), 1014-1019.
Aggen, J. B., Nairn, A. C., & Chamberlin, R. (2000). Regulation of protein phosphatase-1. Chemistry & Biology, 7(1), R13-R23.
Blondin, D., Dépault, I., Imbeault, P., Péronnet, F., Imbeault, M., & Haman, F.. (2010). Effects of two glucose ingestion rates on substrate utilization during moderate-intensity shivering. European Journal of Applied Physiology, 108(2), 289-300.
Cox, G.R., Clark, S.A., Cox, A.J., Halson, S.L., Hargreaves, M., Hawley, J.A., Jeacocke, N., Snow, R.J., Kian Yeo, W., & Burke, L.M. (2010). Daily training with high carbohydrate availability increase exogenous carbohydrate oxidation during endurance cycling. The Journal of Applied Physiology, 109(1), 129-134.
Hawley, J. A., Bosch, A. N., Weltan, S. M., Dennis, S. C., & Noakes, T. D. (1994). Effects of glucose ingestion or glucose infusion on fuel substrate kinetics during prolonged exercise. European Journal of Applied Physiology & Occupational Physiology, 68(5), 381-389.
Horowitz, J.F, Mora-Rodriguez, R., Byerley, L.O., & Coyle, E.F. (1997). Lipolytic suppression following carbohydrate ingestion limits fat oxidation during exercise. American Journal of Physiology – Endocrinology and Metabolism, 273(4), E768-E775.
Jeukendrup, A.E. (2010). Carbohydrate and exercise performance: the role of multiple transportable carbohydrates. Current Opinion in Clinical Nutrition & Metabolic Care. 13(4), 452-457.
Jeukendrup, A.E. & Jentjens, R. (2000). Oxidation of carbohydrate feedings during prolonged exercise: current thoughts, guidelines and directions for future research. Sports Medicine, 29(6), 407-424.
Jeukendrup, A. E., Mensink, M., Saris, W. H. M., & Wagenmakers, A. J. M. (1997). Exogenous glucose oxidation during exercise in endurance-trained and untrained subjects. Journal of Applied Physiology, 82(3), 835-840.
Jeukendrup, A.E., Wagenmakers, A.J.M., Stegen, J.C.H., Gijsen, A.P., Brouns, F., & Saris, W.H.M. (1999). Carbohydrate ingestion can completely suppress endogenous glucose production during exercise. American Journal of Physiology – Endocrinology and Metabolism, 276(4), E672-E683.
Krzentowski, G., Jandrain, B., Pirnay, F., Mosora, F., Lacroix, M., Luyckx, A. S., & Lefebvre, P. J. (1984). Availability of glucose given orally during exercise.Journal of Applied Physiology, 56(2), 315-320.
Lacerda, A.C., Alecrim, P., Damasceno, W.C., Gripp, F., Pinto, K.M., & Silami-Garcia, E. (2009). Carbohydrate ingestion during exercise does not delay the onset of fatigue during submaximal cycle exercise. Journal of Strength and Conditioning Research, 23(4), 1276-1281.
Maughan, R. J., Fenn, C. E., & Leiper, J. B. (1989). Effects of fluid, electrolyte and substrate ingestion on endurance capacity. European Journal of Applied Physiology & Occupational Physiology, 58(5), 481-486.
Riddell, M. C., Partington, S. L., Stupka, N., Armstrong, D., Rennie, C., & Tarnopolsky, M. A. (2003). Substrate utilization during exercise performed with and without glucose ingestion in female and male endurance-trained athletes. International Journal of Sport Nutrition & Exercise Metabolism, 13(4), 407-421.
Smith, J.E., Zachwieja, J.J., Péronnet, F., Passe, D.H., Massicotte, D., Lavoie, C., & Pascoe, D.D., (2010). Fuel selection and cycling endurance performance with ingestion of [13C]glucose: Evidence for a carbohydrate dose response. Journal of Applied Physiology, 108(6), 1520-1529.
Triplett, D., Doyle, J. A., Rupp, J. C., & Benardot, D. (2010). An isocaloric glucose-fructose beverage's effect on simulated 100-km cycling performance compared with a glucose-only beverage. International Journal of Sport Nutrition & Exercise Metabolism, 20(2), 122-131.
Welsh, R.S., Davis, J.M., Burke, J.R., & Williams, H.G. (2002). Carbohydrates and physical/mental performance during intermittent exercise to fatigue. Medicine & Science in Sports & Exercise, 34(4), 723-731
Yaspelkis, B.B., & Ivy J.L. (1991). Effect of carbohydrate supplements and water on exercise metabolism in the heat. The Journal of Applied Physiology, 71(2), 680-687.
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