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Exercise and glucose metabolism

Exercise and glucose metabolism

Diabetes Care —, b. Hashimoto, T. Thomas D, Metabo,ism EJ, Naughton GA Exercise for type 2 diabetes mellitus.

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Ahlborg, G. Article PubMed CAS Google Scholar. Allen, F. Google Scholar. American Diabetes Association, a, Position statement: Diabetes mellitus and exercise. Diabetes Care American Diabetes Association, b, Technical review: Exercise and NIDDM.

Diabetes Care —, b. Andres, R. Measurements of oxygen and glucose uptake and carbon dioxide and lactate production in the forearm. Berger, M.

Diabetologia Björkman, O. Article Google Scholar. Horton, and R. Terjung, eds. Bondy, P. Patients with diabetic ketosis, before and after the administration of insulin.

Coderre, L. PubMed CAS Google Scholar. Coggan, A. Sports Med. Cryer, P. DeFronzo, R. Devlin, J. Diabetes Eriksson, K. Galbo, H. Diabetes Metabolism Rev. Article CAS Google Scholar. Goodyear, L.

Hilstead, J. Hirsch, I. Hoelzer, D. Am J Physiol E Holloszy, J. Acta Med. Horton, E. Medical Clinics N. America CAS Google Scholar. Hübinger, A. Diabetes Res. PubMed Google Scholar. Jenkins, A. Metabolism Jorfeldt, L. Quantitative aspects of glucose uptake and lactate production during prolonged exercise.

Karamanos, B. Berger, P. Christacopoulos, and J. Wahren, eds. Kelley, D. Kemmer, F. Kjaer, M. Koivisto, V. Acta Endocrinol. Krotkiewski, M. Lawrence, R. Lyngsjoe, J. Marliss, E. Marker, J.

Minuk, H. Paternostro-Bayles, M. Rogers, M. Ruderman, N. Diabetes 28 Suppl 1 Schneider, S. Segal, K. Vranic, M. Rifkin, and D. Porte Jr, eds. Wahren, J. Wallberg-Henriksson, H. Wasserman, D. Wolfe, R. Annals Med. Zinman, B. Download references. Department of Chemistry and Biology, Victoria University of Technology, Footscray, Victoria,Australia.

Department of Clinical Physiology, Karolinska Hospital, S 01, Stockholm, Sweden. You can also search for this author in PubMed Google Scholar. Reprints and permissions.

Martin, I. Glucose Metabolism During Physical Exercise in Patients with Noninsulin-Dependent Type II Diabetes. In: Östenson, C. eds New Concepts in the Pathogenesis of NIDDM. Advances in Experimental Medicine and Biology, vol Springer, Boston, MA.

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: Exercise and glucose metabolism

Skeletal muscle energy metabolism during exercise | Nature Metabolism High intensity exercise inhibits carnitine palmitoyltransferase-I sensitivity to L-carnitine. In humans, acidosis does not appear to impair maximal isometric-force production, but it does limit the ability to maintain submaximal force output , thus suggesting an effect on energy metabolism and ATP generation The authors have no competing interests to declare that are relevant to the content of this article. Article CAS PubMed Google Scholar Lee, A. J Appl Physiol 85 4 —
Skeletal muscle energy metabolism during exercise

Goodyear, L. Hilstead, J. Hirsch, I. Hoelzer, D. Am J Physiol E Holloszy, J. Acta Med. Horton, E. Medical Clinics N. America CAS Google Scholar. Hübinger, A. Diabetes Res. PubMed Google Scholar. Jenkins, A. Metabolism Jorfeldt, L. Quantitative aspects of glucose uptake and lactate production during prolonged exercise.

Karamanos, B. Berger, P. Christacopoulos, and J. Wahren, eds. Kelley, D. Kemmer, F. Kjaer, M. Koivisto, V. Acta Endocrinol. Krotkiewski, M. Lawrence, R. Lyngsjoe, J. Marliss, E. Marker, J. Minuk, H. Paternostro-Bayles, M. Rogers, M.

Ruderman, N. Diabetes 28 Suppl 1 Schneider, S. Segal, K. Vranic, M. Rifkin, and D. Porte Jr, eds. Wahren, J. Wallberg-Henriksson, H. Wasserman, D. Wolfe, R. Annals Med. Zinman, B. Download references. Department of Chemistry and Biology, Victoria University of Technology, Footscray, Victoria, , Australia.

Department of Clinical Physiology, Karolinska Hospital, S 01, Stockholm, Sweden. You can also search for this author in PubMed Google Scholar. Reprints and permissions. Martin, I. Glucose Metabolism During Physical Exercise in Patients with Noninsulin-Dependent Type II Diabetes.

In: Östenson, C. eds New Concepts in the Pathogenesis of NIDDM. Advances in Experimental Medicine and Biology, vol Springer, Boston, MA. Publisher Name : Springer, Boston, MA.

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Provided by the Springer Nature SharedIt content-sharing initiative. Policies and ethics. Skip to main content. Abstract The beneficial effects of physical exercise on glucose metabolism in diabetic patients were documented already before the discovery of insulin.

Keywords Glucose Utilization Glucose Production Blood Glucose Concentration Glucose Output Moderate Exercise These keywords were added by machine and not by the authors. Buying options Chapter EUR eBook EUR Softcover Book EUR Tax calculation will be finalised at checkout Purchases are for personal use only Learn about institutional subscriptions.

Preview Unable to display preview. References Ahlborg, G. Article PubMed CAS Google Scholar Allen, F. Google Scholar American Diabetes Association, a, Position statement: Diabetes mellitus and exercise. Google Scholar American Diabetes Association, b, Technical review: Exercise and NIDDM.

Google Scholar Andres, R. Article PubMed CAS Google Scholar Berger, M. Article PubMed CAS Google Scholar Björkman, O. Article Google Scholar Björkman, O.

Google Scholar Bondy, P. Article PubMed CAS Google Scholar Coderre, L. PubMed CAS Google Scholar Coggan, A. Article PubMed CAS Google Scholar Cryer, P. PubMed CAS Google Scholar DeFronzo, R.

Article PubMed CAS Google Scholar Devlin, J. Article PubMed CAS Google Scholar Eriksson, K. Diabetes 35 5 — Kang J, Robertson RJ, Hagberg JM, Kelley DE, Goss FL, Dasilva SG, Suminski RR, Utter AC Effect of exercise intensity on glucose and insulin metabolism in obese individuals and obese NIDDM patients.

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J Appl Physiol — Download references. Australian National Phenome Centre, Health Futures Institute, Murdoch University, Perth, Australia. Discipline of Exercise Science, Murdoch University, Perth, WA, , Australia.

Soo, A. Raman, P. The Centre for Healthy Aging, Health Futures Institute, Murdoch University, Perth, Australia. Institute of Neuroscience, Université Catholique de Louvain, Louvain-la-Neuve, Belgium. School of Human Sciences Exercise and Sport Science , The University of Western Australia, Crawley, WA, Australia.

The Centre for Molecular Medicine and Innovative Therapeutics, Health Futures Institute, Murdoch University, Perth, Australia.

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Reprints and permissions. Soo, J. et al. The role of exercise and hypoxia on glucose transport and regulation. Eur J Appl Physiol , — Download citation. Received : 24 August Accepted : 06 January Published : 23 January Issue Date : June Anyone you share the following link with will be able to read this content:.

Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Download PDF. Abstract Muscle glucose transport activity increases with an acute bout of exercise, a process that is accomplished by the translocation of glucose transporters to the plasma membrane.

Exercise-stimulated glucose uptake — regulation and implications for glycaemic control Article 14 October Exercise-Regulated Skeletal Muscle Glucose Uptake Chapter © The Impact of Type 1 Diabetes on the Physiological Responses to Exercise Chapter © Use our pre-submission checklist Avoid common mistakes on your manuscript.

Introduction Maintaining blood glucose concentration within a narrow range is not trivial, with postprandial glycaemic excursions overlaying the fasting blood glucose concentrations. Glucose transport Cellular uptake of glucose occurs through facilitated diffusion using a carrier protein from the glucose transporter GLUT family.

Full size image. Insulin sensitivity and responsiveness Insulin sensitivity refers to the concentration of insulin required to achieve half of its maximal effect on glucose transport Holloszy Table 1 The acute and chronic hormonal responses during exercise with and without hypoxia Full size table.

Glucose transport measurement in humans The in vivo measurement of glucose transport in humans is challenging and relies on tracer-labelled glucose such as [ 13 C]glucose, [ 2 H]glucose Zinker et al. The role of exercise intensity on glucose regulation Increasing exercise intensity results in greater recruitment of muscle fibres as well as an increased reliance on plasma glucose and muscle glycogen Coggan ; Jeukendrup ; Sahlin ; Vollestad and Blom for energy.

Changes in systemic plasma glucose post-exercise: a balance between the rate of glucose appearance and disappearance While acute exercise may increase the uptake of glucose, it should be noted that systemic plasma glucose concentration ultimately reflects the balance between the rate of glucose appearance R a or entry, and the rate of glucose disappearance R d or exit from the circulation.

Glucoregulatory effects of key hormones associated with exercise: epinephrine, glucagon, growth hormone and cortisol Increased hepatic glucose output is essential to sustaining prolonged exercise capacity and preventing hypoglycaemia Trefts et al.

Mediator to simulate or enhance the effects of exercise on glucose regulation While duration total training duration; acute session duration and intensity are important considerations, findings from longer-term training studies 6 months suggest that total work or energy expenditure is likely more important than either intensity or duration alone Houmard et al.

Stimulation of glucose uptake by hypoxia Although insulin and muscle contraction are the primary means to facilitate GLUT-4 translocation and increase glucose uptake, additional physiological stimuli including hypoxia can also increase glucose uptake Fig.

Hypoxia exposure under resting conditions on glucose tolerance and insulin sensitivity Although in vitro experiments have shown that hypoxia stimulates glucose transport via activation of GLUT-4 translocation in the myocytes, it remains unclear if similar mechanistic pathways regulating glucose uptake and GLUT-4 translocation will be activated in vivo by hypoxia in humans.

Insulin and glucose response following acute exercise bout in hypoxia Exercising in hypoxia compared to normoxia reduces oxygen availability and therefore induces a proportional shift in metabolic pathway flux Davison et al.

Effects of exercise training in hypoxia on insulin sensitivity Findings from studies assessing the effects of exercise training in hypoxia on insulin sensitivity have been inconsistent Haufe et al.

Hypoxic training—an integrated physiology approach The hypothesis that hypoxic training may potentiate the effect of exercise on glucose tolerance is based on the findings that hypoxia activates glucose transport via pathways similar to muscle contraction Kang et al.

Conclusion Systemic glucose regulation is intricately linked to cellular glucose transport, which is mediated by the translocation of glucose transport i.

Data availability The data generated in the current study are available from the corresponding author on reasonable request.

Change history 27 February Missing Open Access funding information has been added in the Funding Note. References Azevedo JL, Carey JO, Pories WJ, Morris PG, Dohm GL Hypoxia stimulates glucose transport in insulin-resistant human skeletal muscle.

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Glucose uptake through physical exercise

However, under special conditions such as physical exercise, alterations in the levels of intracellular molecules such as ATP and calcium actto regulate GLUT4 translocation and glucose uptake in skeletal muscle, regardless of insulinlevels.

Regular physical exercise, due to stimulating pathways related to glucose uptake, is an important non-pharmacological intervention for improving glycemic control in obese and diabetic patients. In this mini-review the main mechanisms involved in glucose uptake in skeletal muscle in response to muscle contraction will be investigated.

The knowledge that exercise plays an important role in health is widely disseminated. In ancient Greece, the philosopher Hippocrates had mentioned in his works that both exercise and a healthy diet could promote health and prevent certain diseases. Nonetheless, the author did not imagine that several molecular changes might occur in response to exercise, culminating in many physiological responses, including the glucose uptake increment.

With the advent of modern science and especially of molecular biology, the understanding of this process was significantly expanded. One pioneering study that confirmed glucose uptake with muscle contraction measured the arteriovenous difference in glucose derived from the masseter muscle in horses, demonstrating a reduction in the amount of glucose in this tissue after hay-chewing 1 1 Chauveau MA, Kaufmann M.

C R Acad Sci. Some decades later, Lawrenceshowed that physical exercise could enhance the effects of the hormone insulin, resulting in increased glucose consumption and internalization, suggesting that physical exercise could be relevant for the treatment of diabetic people 2 2 Lawrence RD.

The Effect of Exercise on Insulin Action in Diabetes. Br Med J. Insulin injection prior to exercise resulted in greater reduction in blood glucose when compared to their peers who also exercised but did not receive the hormone.

Following this evidence, it was shown that physical exercise increases the rate of glucose utilization in animals and humans 3 3 Christophe J, Mayer J. Effect of exercise on glucose uptake in rats and men.

J Appl Physiol. Human forearm muscle metabolism during exercise. Substrate utilization in prolonged fasting. Scand J Clin Lab Invest. In a complementary way, it was also observed that the magnitude of the effect depends on the duration and intensity of the exercise 6 6 Coyle EF, Hagberg JM, Hurley BF, Martin WH, Ehsani AA, Holloszy JO.

Carbohydrate feeding during prolonged strenuous exercise can delay fatigue. Therefore, insulin and exercise have agonist actions in glucose uptake by skeletal muscle tissue process. Further investigations have shown that a single exercise session can positively influence glucose uptake by muscle.

Exercise induces rapid increases in GLUT4 expression, glucose transport capacity, and insulin-stimulated glycogen storage in muscle. J Biol Chem.

The justification lies in the fact that the transport of glucose stimulated by insulin or muscle contraction is increased in proportion to the increase of GLUT-4, as well as their translocation rate to the cell membrane 8 8 Host HH, Hansen PA, Nolte LA, Chen MM, Holloszy JO.

Rapid reversal of adaptive increases in muscle GLUT-4 and glucose transport capacity after training cessation. This effect may remain for up to 48 hours after physical activity, suggesting the need of practice in a chronic manner to obtain its benefits continuously.

The identification of GLUT-4, abundantly expressed in adipose and muscle tissue, favored further studies about the mechanisms by which exercise can influence glucose uptake by skeletal muscle tissue 9 9 Charron MJ, Brosius FC, Alper SL, Lodish HF.

A glucose transport protein expressed predominately in insulin-responsive tissues. Proc Natl Acad Sci U S A. Studies in animal models 10 10 Luciano E, Carneiro EM, Carvalho CRO, Carvalheira JBC, Peres SB, Reis MAB, et al.

Eur J Endocrinol. Effects of Physical Exercise in the Ampkα Expression and Activity in High-fat Diet Induced Obese Rats. Rev Bras Med do Esporte. as well asin humans 12 12 Christ-Roberts CY, Pratipanawatr T, Pratipanawatr W, Berria R, Belfort R, Kashyap S, et al.

Exercise training increases glycogen synthase activity and GLUT4 expression but not insulin signaling in overweight nondiabetic and type 2 diabetic subjects. Exercise training increases insulin-stimulated glucose disposal and GLUT4 SLC2A4 protein content in patients with type 2 diabetes.

Effects of endurance exercise training on insulin signaling in human skeletal muscle: interactions at the level of phosphatidylinositol 3-kinase, Akt, and AS have shown that physical training increases the expression of GLUT-4, promoting glucose uptake in skeletal muscle.

Although the identification of the GLUT-4 has been very important, the following findings allowed to understand that exercise exerts actions on other molecules involved in glucose uptake. Glucose uptake utilizes insulin-dependent and insulin-independent cell signalingpathways.

The finding and understanding about the mechanisms of action of some proteins that act independently of insulin on glucose uptake allow to definitely recognize the benefits of using exercise as a non-pharmacological tool in the control of glucose homeostasis and in preventing and treating diabetes.

Therefore, this mini-review aims to describe the different mechanisms involved in glucose uptake at rest and in response to physical exercise. Glucose uptake by insulin stimulation occurs after the hormone binds to its specific membrane receptor called insulin receptor IR 16 16 Leney SE, Tavaré JM.

The molecular basis of insulin-stimulated glucose uptake: signalling, trafficking and potential drug targets. J Endocrinol. The IR is a heterotetrameric protein with intrinsic tyrosine kinase activity. After this binding, the receptor undergoes a conformational alteration, triggering its autophosphorylation on tyrosine residues.

Once activated, IR promotes the tyrosine phosphorylation of different substrates, including insulin receptor substrates 1 and 2 IRS-1 and IRS The tyrosine phosphorylation of IRS-1 and IRS-2 allows them to associate and activate the phosphatidylinositol-3 kinase enzyme PI3K.

PI3K catalyzes the phosphorylation of membrane phosphoinositides at the position3 of the inositol ring to produce phosphatidylinositol 3-phosphate, phosphatidylinositol 3,4-phosphate and phosphatidylinositol-3,4,5-phosphate.

The latter product regulates the activity of phosphoinositide-dependent kinase-1 PDK When active, the Akt is responsible for the activation of AS Akt substrate of kDa 16 16 Leney SE, Tavaré JM.

The AS can act in two significant ways on GLUT4 translocation to the periphery: 1 by reducing the "tethering" of the vesicle, by proteins called TUG, and thus releasing it to the periphery; 2 byincreasing the activity of Rab proteins which will stimulate the translocation of these vesicles containing GLUT4 to the periphery.

Therefore, these activation mechanisms and the release of vesicles containing GLUT4 are essential for glucose homeostasis at baseline. The increase of GLUT4 and its translocation to the sarcoplasm are extremely important for performance and health 16 16 Leney SE, Tavaré JM.

Several studies have indicated that compromise at some point in this pathway can decrease glucose uptake, triggering important physiological changes that can lead to the development of various metabolic diseases, such as diabetes 17 17 Hotamisligil GS.

Inflammation and metabolic disorders 1. However, it is worth mentioning that there are alternative pathways in addition to insulin that are responsiblefor regulating glucose uptake, acting jointly in the regulation of glucose homeostasis. For example, studies using MIRKO animals mice without insulin receptor in skeletal muscles - muscle insulin receptor knockout show that there is reduced insulin signaling but no effect on the IGF-1 pathway insulin-like growth factor, a growth factor similar to insulin , indicating that different pathways can act in a compensatory fashion to maintain signaling 18 18 He Z, Opland DM, Way KJ, Ueki K, Bodyak N, Kang PM, et al.

Arterioscler Thromb Vasc Biol. As there is homology between the molecules in the absence of insulin, IGF receptor receives the insulin signal and propagates intracellularly, partially compensating its absence. Thus, it is necessary to address some of the main mechanisms to promote glucose uptake, even in conditions of low levels of circulating insulin.

In skeletal muscle, glucose uptake depends on the presence of GLUT-4 on the cell membrane, so that it exerts its function of allowing the entry of glucose by facilitated diffusion.

At baseline conditions, the great majority of GLUT4 molecules is stored in vesicles within the cell, keeping it in a quiescent, waiting for the recruitment signal.

Therefore, under resting conditions, insulin is essential for glucose uptake in muscle tissue 19 19 Bradley H, Shaw CS, Bendtsen C, Worthington PL, Wilson OJ, Strauss JA, et al.

Visualization and quantitation of GLUT4 translocation in human skeletal muscle following glucose ingestion and exercise. Physiol Rep. During exercise, there is an increase in blood flow to the active muscles, creating an incentive for the dilation of blood vessels responsible for irrigation of active muscles, thereby aiming to increase the surface area available for transport of glucose 20 20 Andersen P, Saltin B.

Maximal perfusion of skeletal muscle in man. J Physiol. During muscle contraction, circulating insulin levels suffer no significant change, and in some cases even suffer a decrease. Thus, the muscle contractions and blood flow circulating levels of insulin act in synergism generating signals for translocation of GLUT4 to the membrane of the sarcolemma and t-tubules, thereby increasing glucose uptake by the cell 21 21 Richter EA, Hargreaves M.

Exercise, GLUT4, and Skeletal Muscle Glucose Uptake. Physiol Rev. The amount of GLUT4 present in the sarcolemma and in the t-tubules is influenced by the efficiency of endocytosis and exocytosis processes of vesicles containing the protein in its inactive form. Insulin increases the amount of GLUT4 in muscle membrane primarily by increasing the stimulation of exocytosis 22 22 Stöckli J, Fazakerley DJ, James DE.

GLUT4 exocytosis. J Cell Sci. The GLUT4 glucose transporter. Cell Metab. This phenomenon may explain the additive effect of exercise on insulin in muscle glucose uptake 24 24 Ploug T, Galbo H, Vinten J, Jørgensen M, Richter EA.

Kinetics of glucose transport in rat muscle: effects of insulin and contractions. Am J Physiol. The understanding that exercise cooperates in glucose uptake has led many researchers to investigate which mechanisms could be linked to muscle contraction and independently to the hormone insulin.

Increases of both glucose uptake and metabolism in response to exercise are often associated with the effects of a single session of exercise in the levels of mRNA and in the absolute levels of GLUT-4 25 25 Kraniou Y, Cameron-Smith D, Misso M, Collier G, Hargreaves M.

Effects of exercise on GLUT-4 and glycogenin gene expression in human skeletal muscle. In addition to increased levels of GLUT-4, exercise is able to increase GLUT-4 translocation to myocellular membrane related to increased exocytosis rate and lower endocytosis rate, as previously discussed , increasing the glucose uptake capacity in muscle cells 19 19 Bradley H, Shaw CS, Bendtsen C, Worthington PL, Wilson OJ, Strauss JA, et al.

The effects of exercise in increasing GLUT4 content and translocation involve some molecules that will be presented below. A few years before the description of AMPK activation by physical exercise and related experimental evidence in humans, animal researches identified a drug compound known to act as a potent activator of this molecule, AICAR 5-aminoimidazole ribonucleotidecarboxamide.

This compound, that mimics the intracellular increase in AMP, is capable of phosphorylatingAMPK promoting glucose uptake and lipid oxidation in skeletal muscle 26 26 Merrill GF, Kurth EJ, Hardie DG, Winder WW.

AICA riboside increases AMP-activated protein kinase, fatty acid oxidation, and glucose uptake in rat muscle.

Animal experiments also suggest that AMPK activation in skeletal muscle is capable of enhancinglipid oxidation and the glycogen resynthesisrate in response to exercise having a protective effect on muscle glycogen stores through the muscle contraction stimulus per se and throughthe increase of calcium release 27 27 Jeon SM.

Regulation and function of AMPK in physiology and diseases. Exp Mol Med. Nature Publishing Group; ;48 7 :e Continuous and repetitive muscle contractionthat is characteristic of exercise acts as a stressor agent.

This activity causes depletion momentary or extended of ATP levels, which are rapidly resynthesized. However, at any given time, cellular ATP resynthesis becomes insufficient due to decreased levels of the enzyme creatine phosphate CP or even glucose, causing an increase in the ADP:ATP ratio and, consequently, in the AMP:ATP ratio.

This phenomenon promotes the phosphorylation of LKB1 liver kinase B1 - B1 liver kinase which phosphorylates and activates AMPK, which can finally phosphorylate the AS protein 28 28 Stanford KI, Goodyear LJ.

Exercise and type 2 diabetes: molecular mechanisms regulating glucose uptake in skeletal muscle. Adv Physiol Educ. AMPK-mediated AS phosphorylation in skeletal muscle is dependent on AMPK catalytic and regulatory subunits.

The AS can act in various ways to translate GLUT4-containing vesicles to the periphery. One is through the activation of Rab-GTP protein, which will trigger signal for the translocation of GLUT4 30 30 Cartee GD.

Mechanisms for greater insulin-stimulated glucose uptake in normal and insulin-resistant skeletal muscle after acute exercise. American Physiological SocietyAm J Physiol Endocrinol Metab; ; 12 :E Another way is by reducing the TUG activity, protein "tethering" which binds to the vesicles, preventing its translocation 31 31 Bogan JS, Hendon N, McKee AE, Tsao TS, Lodish HF.

Functional cloning of TUG as a regulator of GLUT4 glucose transporter trafficking. Additionally, AMPK phosphorylates HDAC5 histone deacetylase 5 , which is exported from the nucleus promoting the activation of MEF2 stimulating factor of myocyte 2 and GEF stimulating factor GLUT4 as well as their combination.

Both these transcription factors are related to the GLUT4 expression in skeletal muscle 32 32 McGee SL, Sparling D, Olson AL, Hargreaves M. Exercise increases MEF2- and GEF DNA-binding activity in human skeletal muscle. FASEB J. Thus, in addition to causing the translocation of GLUT4 molecules to the membrane, AMPK in its active form is also capable of regulatingthe expression of new GLUT-4 molecules.

Calcium ions have gained attention in recent decades due to their contribution to glucose uptake. Early studies found their participation in glucose homeostasis, when Sartorius muscle of frogs were incubated with caffeine 33 33 Holloszy JO, Narahara HT.

Enhanced permeability to sugar associated with muscle contraction. J Gen Physiol. Based on these results, it was observed that caffeine stimulates calcium release from the sarcoplasmic reticulum without plasma membrane depolarization and that this influx per se was sufficient to stimulate glucose uptake.

Subsequently, studies with rat muscles incubated with caffeine or a chemical compound, which also stimulates calcium release in sufficient levels to promote muscle contraction 34 34 Holloszy JO, Narahara HT.

Nitrate Ions: Potentiation of Increased Permeability to Sugar Associated with Muscle Contraction. Since the increase in energy expenditure is responsible for the activation of AMPK, and it triggers processes that signalfor the translocation of GLUT4 from intracellular vesicles to the plasma membrane, glucose uptake will be stimulated 15 15 Witczak CA, Fujii N, Hirshman MF, Goodyear LJ.

Calmodulin-dependent protein kinase kinase-β is an alternative upstream kinase for AMP-activated protein kinase. Due to this, some studies were developed to examine this pathway in muscle tissue of rodents, but they showed controversial results 15 15 Witczak CA, Fujii N, Hirshman MF, Goodyear LJ.

Calcium stimulates glucose transport in skeletal muscle by a pathway independent of contraction. Exercise and Regulation of Carbohydrate Metabolism.

Prog Mol Biol Transl Sci. Some studies suggested the role of ROS in glucose uptake in response to muscle contraction, due to the fact that exercise increases significantly and transiently the production of ROS 38 38 Reid MB. Free radicals and muscle fatigue: Of ROS, canaries, and the IOC.

Free Radic Biol Med. AMPK alpha1 activation is required for stimulation of glucose uptake by twitch contraction, but not by H2O2, in mouse skeletal muscle.

PLoS One. Some experiments that used donor ROS treatment in isolated skeletal muscle fibers observed that glucose uptake in the treated muscles was higher 39 39 Jensen TE, Schjerling P, Viollet B, Wojtaszewski JFP, Richter EA. Other studies using non-specific inhibitors of ROS found divergent results, with no effect on glucose uptake in both rodents 40 40 Merry TL, Dywer RM, Bradley EA, Rattigan S, McConell GK.

Local hindlimb antioxidant infusion does not affect muscle glucose uptake during in situ contractions in rat. and humans 41 41 Merry TL, Wadley GD, Stathis CG, Garnham AP, Rattigan S, Hargreaves M, et al. N-Acetylcysteine infusion does not affect glucose disposal during prolonged moderate-intensity exercise in humans.

Concerning these studies, it is suggested that the involvement of ROS in muscle glucose uptake would be restricted to conditions observed in vitro intense electrical stimulation of isolated muscles fibers , without affecting the effects of exercise on the subjects.

In a study with type 1 diabetics, administration of natural antioxidants e. Do Reactive Oxygen Species Regulate Skeletal Muscle Glucose Uptake During Contraction? Exerc Sport Sci Rev.

These controversial results suggest the need for more studies to further elucidate this issue. Nitric oxide NO is synthesized by three isoforms of nitric oxide synthase: iNOS inducible nitric oxide synthase , eNOS endothelial nitric oxide synthase , and nNOS neuronal nitric oxide synthase.

The role of NO is commonly related to vasodilation of the endothelium to facilitate the coming of nutrients distribution to the active muscles as well as the removal and transport of metabolites, maintaining cellular homeostasis 43 43 Andrade FH, Reid MB, Allen DG, Westerblad H. Effect of nitric oxide on single skeletal muscle fibres from the mouse.

Role of nitric oxide in skeletal muscle: synthesis, distribution and functional importance. Acta Physiol Scand.

Studies using animals showed that 4 and 8 weeks of treadmill running training 47 47 Balon TW, Nadler JL. Evidence that nitric oxide increases glucose transport in skeletal muscle.

Regulation of nitric oxide production in limb and ventilatory muscles during chronic exercise training. Am J Physiol - Lung Cell Mol Physiol. as 4 weeks of swimming training 49 49 Tatchum-Talom R, Schulz R, McNeill JR, Khadour FH.

Upregulation of neuronal nitric oxide synthase in skeletal muscle by swim training. Am J Physiol Heart Circ Physiol. can upregulatenNOS levels in the skeletal muscle of trained mice.

On the other hand, studies with humans are not clear in showing if there is an increase in the levels of nNOS and NO in skeletal muscle in response to exercise 45 45 Bradley SJ, Kingwell BA, Canny BJ, McConell GK.

Skeletal muscle neuronal nitric oxide synthase micro protein is reduced in people with impaired glucose homeostasis and is not normalized by exercise training. Endurance training does not alter the level of neuronal nitric oxide synthase in human skeletal muscle.

Nitric oxide synthase inhibition reduces glucose uptake during exercise in individuals with type 2 diabetes more than in control subjects. Nitric oxide synthase inhibition reduces leg glucose uptake but not blood flow during dynamic exercise in humans. These results indicate that the inhibition of molecules that produce NO attenuates glucose uptake in skeletal muscle during muscle contraction, without affecting the flow of glucose into muscle.

It is suggested that the release of NO by muscular stimulation occurs only in high-intensity exercises. In humans, the inhibition of NOS in low-intensity exercise did not affect glucose uptake, with significant alterations for moderate intensities 53 53 Ilkka H, Bengt S, Jukka K, Sipilä HT, Vesa O, Pirjo N, et al.

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Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada. You can also search for this author in PubMed Google Scholar. and L. conceived and prepared the original draft, revised the manuscript and prepared the figures.

Correspondence to Mark Hargreaves or Lawrence L. Reprints and permissions. Skeletal muscle energy metabolism during exercise. Nat Metab 2 , — Download citation. Received : 20 April Accepted : 25 June Published : 03 August Issue Date : September Anyone you share the following link with will be able to read this content:.

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Abstract The continual supply of ATP to the fundamental cellular processes that underpin skeletal muscle contraction during exercise is essential for sports performance in events lasting seconds to several hours. Exercise metabolism and adaptation in skeletal muscle Article 24 May Aerobic exercise intensity does not affect the anabolic signaling following resistance exercise in endurance athletes Article Open access 24 May Myofibrillar protein synthesis rates are increased in chronically exercised skeletal muscle despite decreased anabolic signaling Article Open access 09 May Main In , athletes from around the world were to gather in Tokyo for the quadrennial Olympic festival of sport, but the event has been delayed until because of the COVID pandemic.

Overview of exercise metabolism The relative contribution of the ATP-generating pathways Box 1 to energy supply during exercise is determined primarily by exercise intensity and duration. Full size image. Regulation of exercise metabolism General considerations Because the increase in metabolic rate from rest to exercise can exceed fold, well-developed control systems ensure rapid ATP provision and the maintenance of the ATP content in muscle cells.

Box 3 Sex differences in exercise metabolism One issue in the study of the regulation of exercise metabolism in skeletal muscle is that much of the available data has been derived from studies on males. Targeting metabolism for ergogenic benefit General considerations Sports performance is determined by many factors but is ultimately limited by the development of fatigue, such that the athletes with the greatest fatigue resistance often succeed.

Training Regular physical training is an effective strategy for enhancing fatigue resistance and exercise performance, and many of these adaptations are mediated by changes in muscle metabolism and morphology. Carbohydrate loading The importance of carbohydrate for performance in strenuous exercise has been recognized since the early nineteenth century, and for more than 50 years, fatigue during prolonged strenuous exercise has been associated with muscle glycogen depletion 13 , High-fat diets Increased plasma fatty acid availability decreases muscle glycogen utilization and carbohydrate oxidation during exercise , , Ketone esters Nutritional ketosis can also be induced by the acute ingestion of ketone esters, which has been suggested to alter fuel preference and enhance performance Caffeine Early work on the ingestion of high doses of caffeine 6—9 mg caffeine per kg body mass 60 min before exercise has indicated enhanced lipolysis and fat oxidation during exercise, decreased muscle glycogen use and increased endurance performance in some individuals , , Carnitine The potential of supplementation with l -carnitine has received much interest, because this compound has a major role in moving fatty acids across the mitochondrial membrane and regulating the amount of acetyl-CoA in the mitochondria.

Nitrate NO is an important bioactive molecule with multiple physiological roles within the body. Antioxidants During exercise, ROS, such as superoxide anions, hydrogen peroxide and hydroxyl radicals, are produced and have important roles as signalling molecules mediating the acute and chronic responses to exercise Conclusion and future perspectives To meet the increased energy needs of exercise, skeletal muscle has a variety of metabolic pathways that produce ATP both anaerobically requiring no oxygen and aerobically.

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Type 2 diabetes T2D is a glucosse disease characterized by obesity, gpucose Ribose sugar and protein synthesis, and the dysfunction of several Respiratory health awareness campaign Ribose sugar and protein synthesis metaabolism. Among these organs, impaired mettabolism function is recognized metabolusm one of the earliest contributors to impaired metabooism glucose homeostasis, with well-characterized hepatic insulin resistance Exercise and glucose metabolism in elevated rates of hepatic glucose production HGP and fasting hyperglycemia. One Exercise and glucose metabolism of this review will metabolismm an andd of how HGP is regulated during the fasted state in healthy humans and how this process becomes dysregulated in patients with T2D. Less well-appreciated is the liver's role in post-prandial glucose metabolism, where it takes up and metabolizes one-third of orally ingested glucose. An abundance of literature has shown that the process of hepatic glucose uptake is impaired in patients with T2D, thereby contributing to glucose intolerance. A second portion of this review will outline how hepatic glucose uptake is regulated during the post-prandial state, and how it becomes dysfunctional in patients with T2D. Finally, it is well-known that exercise training has an insulin-sensitizing effect on the liver, which contributes to improved whole-body glucose metabolism in patients with T2D, thereby making it a cornerstone in the management of the disease. Exercise and glucose metabolism

Author: Yok

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