The ratio of the two hormones insulin and glucagon determines the metabolic processes during physical exertion in terms of energy supply. Both are produced by the pancreas and are antagonists. Insulin lowers the blood sugar level and glucagon leads to an increase in blood sugar via the formation of new glucose (gluconeogenesis). The production of both hormones is in turn regulated by other hormones. In addition to the catecholamines dopamine, noradrenaline and adrenaline (see Part 1), glucocorticoids and in particular the stress hormone cortisol play an important role in sport. Cortisol is a steroid hormone that regulates important defense mechanisms of the body during stress and helps to regulate blood sugar levels. Although cortisol is known to inhibit glucose uptake in the muscle, cortisol is an important hormone, especially during high physical exertion. Cortisol is released during exercise and leads to an increase in glucagon.
Glucagon stimulates the formation of new glucose in the liver through gluconeogenesis. How much glucose is produced depends on the intensity and condition of the training. At low intensities and especially when training on an empty stomach, blood sugar remains constant and fat utilization is promoted. If a carbohydrate-rich meal was eaten before exercise, which caused the blood sugar to rise, the blood sugar drops again during light physical activity. During low to moderate intensity exercise (<60% VO(2max)), there is a gradual, sometimes slight to moderate increase in blood sugar due to glucose production in the liver. During intensive physical activity (>80% VO(2max)), glucose is the muscle fuel of choice.

In order to cover the muscles’ need for glucose for energy production, carbohydrate stores in the muscles and liver must be accessed. This also applies when carbohydrates are supplied through food. The regulation of glucose production and glucose utilization must therefore take place differently than during low-intensity exercise. In contrast to low to moderate physical exertion, glucose utilization increases three to fourfold and glucose production seven to eightfold during intensive training. As a result, blood sugar also rises sharply. This increase is triggered by stress hormones and especially at the beginning by cortisol and can also be observed in a fasted state without energy intake. During low-intensity training sessions, the release of stress hormones is relatively low. The intake of glucose causes an increase in blood sugar levels, which is accompanied by a corresponding release of insulin, which in turn reduces fat breakdown and fat burning. Glucose immediately before exercise increases blood sugar and insulin levels and leads to increased carbohydrate oxidation during exercise. The meal before training therefore has an influence on energy metabolism. According to a study, ingesting 75 grams of glucose 45 minutes before training increased glycogen utilization in the muscles by 17 percent. The level of stress hormones rises with increasing physical exertion. Adrenaline and noradrenaline increasingly inhibit the release of insulin in the pancreas, so that rising blood sugar does not automatically lead to a significant release of insulin when new glucose is produced through gluconeogenesis. The rise in blood sugar associated with gluconeogenesis occurs even if a lot of insulin has been released by glucose-rich food before training and is already circulating in the bloodstream, as the sharp rise in cortisol restricts the absorption of sugar in the muscles and fatty tissue. However, the blockade of insulin secretion by adrenaline can be softened or overridden by very high blood sugar concentrations, such as those caused by increased carbohydrate intake. In a study with well-trained athletes who completed a 3-hour training session at medium intensity, it was shown that the insulin concentration initially increased with the onset of exertion within the first hour and then decreased as the training progressed. The levels of noradrenaline and adrenaline in the blood showed a steady increase until the end of a similarly structured 3-hour test. At the end of an intensive training session or competition, there is an immediate rise in blood glucose before a rapid drop occurs. The levels of noradrenaline and adrenaline in the blood show a steady increase until the end of a similarly structured 3-hour test. At the end of intensive training or competition, there is an immediate increase in blood glucose before a rapid drop occurs. During short-term exercise, the cortisol level in the blood rises in proportion to the intensity of the exercise as soon as the exercise exceeds a critical threshold (50-60% VO2max). At very low levels of exertion, the cortisol level sometimes does not rise above the resting level or even falls. Therefore, short rides for regeneration at low intensity do not necessarily mean additional unhealthy stress for the body. Only if the low-intensity activity lasts longer can cortisol levels gradually rise above resting levels over time. If the load is above the critical threshold intensity, the cortisol level initially rises and then reaches a plateau, provided that it is a steady-state load and the intensity is not increased further. The height of the plateau is proportional to the intensity of the exercise performed.

Corstisol has fallen into disrepute in the sports scene. Studies from the 1980s, which used the testosterone/cortisol ratio as an indicator of too much stress due to excessive training in athletes, contributed to its negative image. Researchers suggested that a drop of more than 30 percent in the ratio of free testosterone to cortisol would represent a critical change in hormone status. The changes were projected to reflect an extreme imbalance between the body’s anabolic status (hormonally represented by testosterone levels) and catabolic status (represented by cortisol levels) due to excessive stress levels triggered by hard physical training. To this day, researchers, doctors and even trainers use the testosterone/cortisol ratio as an indicator of overtraining. Firstly, however, this ignores the fact that the original study was not about overtraining, but merely about “too hard” training in which a positive training stimulus can fail to materialize due to catabolic metabolic changes. Secondly, the original study did not look at total testosterone in relation to cortisol, but at free testosterone. In regular blood tests, however, total testosterone is usually measured and free testosterone in the blood is not determined.

Diet has an influence on cortisol levels. Eating a low-carbohydrate diet for several days can increase the subsequent cortisol response to submaximal exercise. In addition, ambient temperatures during exercise can drastically affect the cortisol response. Extremely hot or cold temperatures can amplify the cortisol response to a training session or competition. The more trained a person is, the lower the cortisol response to almost any submaximal training condition tends to be. Insulin and cortisol levels decrease over time after often initially rising significantly with sustained exercise. During exercise, the effects of insulin on fuel storage are suppressed. This occurs primarily through the inhibition of insulin secretion during exercise (see above), but also through the activation of local and systemic processes to mobilize fuel. In contrast, after training, the fuel depots mobilized during training must be replenished, especially the glycogen stores in the muscle. This process is facilitated by an increased insulin sensitivity of muscles that were previously physically active and channel glucose for glycogen resynthesis. In physically trained people, insulin sensitivity is also higher than in untrained people due to adaptations in the vascular system, skeletal muscles and fatty tissue. After physical exertion, adrenaline is rapidly broken down, which reduces the blockage of insulin release in the pancreas and allows growth hormones to be released to a greater extent. In addition, the increased insulin sensitivity of the muscles facilitates the replenishment of glycogen stores and the associated regeneration. The interaction between the various hormones during physical exertion is an example of how complex the processes in the body are. It shows that the effects of opposing metabolic regulatory forces can be balanced and modified under different conditions. While insulin is released especially after food intake and is the primary hormone that increases glucose uptake into cells as well as glucose storage in the form of glycogen and fatty acid storage in the form of triglycerides, exercise is a condition in which fuel stores must be mobilized and oxidized. In type 1 diabetics, the effect of insulin during exercise can be studied well, as the pancreas is unable to secrete insulin. In the absence of insulin, there is a greater depletion of the carbohydrate stores in the muscles, as the increased uptake of blood glucose through the insulin effect is absent. The carbohydrate stores in the muscles are an important source of energy during sport. If insulin-dependent and insulin-driven glucose uptake work together, glycogen storage can be maximized. There is also a positive, insulin-independent effect of fructose on glycogen formation in the muscle. In addition, different tissues – such as in the liver and muscles – have their own specific insulin sensitivity, which makes metabolism and the reaction to exogenous carbohydrates very individual, especially during sport. However, research in this area is still in its infancy.
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Literature:
Gonzalez JT, Fuchs CJ, Smith FE, Thelwall PE, Taylor R, Stevenson EJ, Trenell MI, Cermak NM, van Loon LJ. Ingestion of glucose or sucrose prevents liver but not muscle glycogen depletion during prolonged endurance-type exercise in trained cyclists. Am J Physiol Endocrinol Metab. 2015 Dec 15;309(12):E1032-9. doi: 10.1152/ajpendo.00376.2015. Epub 2015 Oct 20. PMID: 26487008.
Stellingwerff T, Boon H, Gijsen AP, Stegen JH, Kuipers H, van Loon LJ. Carbohydrate supplementation during prolonged cycling exercise spares muscle glycogen but does not affect intramyocellular lipid use. Pflugers Arch. 2007 Jul;454(4):635-47. doi: 10.1007/s00424-007-0236-0. Epub 2007 Feb 27. PMID: 17333244; PMCID: PMC1915642.
Howlett K, Galbo H, Lorentsen J, Bergeron R, Zimmerman-Belsing T, Bülow J, Feldt-Rasmussen U, Kjaer M. Effect of adrenaline on glucose kinetics during exercise in adrenalectomised humans. J Physiol. 1999 Sep 15;519 Pt 3(Pt 3):911-21. doi: 10.1111/j.1469-7793.1999.0911n.x. PMID: 10457100; PMCID: PMC2269528.
R.W. Hanson, O.E. Owen, Gluconeogenesis, Editor(s): William J. Lennarz, M. Daniel Lane, Encyclopedia of Biological Chemistry (Second Edition), Academic Press, 2013, Pages 381-386, ISBN 9780123786319, https://doi.org/10.1016/B978-0-12-378630-2.00040-2.
Melkonian EA, Asuka E, Schury MP. Physiology, Gluconeogenesis. 2023 Nov 13. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan–. PMID: 31082163.
Marliss EB, Vranic M. Intense exercise has unique effects on both insulin release and its roles in glucoregulation: implications for diabetes. Diabetes. 2002 Feb;51 Suppl 1:S271-83. doi: 10.2337/diabetes.51.2007.s271. PMID: 11815492.
Derave W, Mertens A, Muls E, Pardaens K, Hespel P. Effects of post-absorptive and postprandial exercise on glucoregulation in metabolic syndrome. Obesity (Silver Spring). 2007 Mar;15(3):704-11. doi: 10.1038/oby.2007.548. PMID: 17372321.
Coggan AR, Coyle EF. Carbohydrate ingestion during prolonged exercise: effects on metabolism and performance. Exerc Sport Sci Rev. 1991;19:1-40. PMID: 1936083.
Adams OP. The impact of brief high-intensity exercise on blood glucose levels. Diabetes Metab Syndr Obes. 2013;6:113-22. doi: 10.2147/DMSO.S29222. Epub 2013 Feb 27. PMID: 23467903; PMCID: PMC3587394.
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 43: 695–699, 1977.
Purdon C, Brousson M, Nyveen SL, Miles PD, Halter JB, Vranic M, Marliss EB. The roles of insulin and catecholamines in the glucoregulatory response during intense exercise and early recovery in insulin-dependent diabetic and control subjects. J Clin Endocrinol Metab. 1993 Mar;76(3):566-73. doi: 10.1210/jcem.76.3.8445012. PMID: 8445012.
Sluga N, Križančić Bombek L, Kerčmar J, Sarikas S, Postić S, Pfabe J, Skelin Klemen M, Korošak D, Stožer A, Slak Rupnik M. Physiological levels of adrenaline fail to stop pancreatic beta cell activity at unphysiologically high glucose levels. Front Endocrinol (Lausanne). 2022 Oct 25;13:1013697. doi: 10.3389/fendo.2022.1013697. PMID: 36387857; PMCID: PMC9640998.
Hackney AC, Walz EA. Hormonal adaptation and the stress of exercise training: the role of glucocorticoids. Trends Sport Sci. 2013;20(4):165-171. PMID: 29882537; PMCID: PMC5988244.
Adlercreutz H, Härkönen M, Kuoppasalmi K, Näveri H, Huhtaniemi I, Tikkanen H, Remes K, Dessypris A, Karvonen J. Effect of training on plasma anabolic and catabolic steroid hormones and their response during physical exercise. Int J Sports Med. 1986 Jun;7 Suppl 1:27-8. doi: 10.1055/s-2008-1025798. PMID: 3744643.
Shea JL, Wong PY, Chen Y. Free testosterone: clinical utility and important analytical aspects of measurement. Adv Clin Chem. 2014;63:59-84. doi: 10.1016/b978-0-12-800094-6.00002-9. PMID: 24783351.
Jensen TE, Richter EA. Regulation of glucose and glycogen metabolism during and after exercise. J Physiol. 2012 Mar 1;590(5):1069-76. doi: 10.1113/jphysiol.2011.224972. Epub 2011 Dec 23. PMID: 22199166; PMCID: PMC3381815.
Bally L, Kempf P, Zueger T, Speck C, Pasi N, Ciller C, Feller K, Loher H, Rosset R, Wilhelm M, Boesch C, Buehler T, Dokumaci AS, Tappy L, Stettler C. Metabolic Effects of Glucose-Fructose Co-Ingestion Compared to Glucose Alone during Exercise in Type 1 Diabetes. Nutrients. 2017 Feb 21;9(2):164. doi: 10.3390/nu9020164. PMID: 28230765; PMCID: PMC5331595.
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