What is your feedback? When your Carbs and muscle glycogen stores mucle, like during a glgcogen session, a cascade of signals activates or shuts down metabolic pathways, controlling gene expressions and protein turnover. This is exactly why we built the INSCYD muscle glycogen calculator! Potential impact of nutrition on immune system recovery from heavy exertion: a metabolomics perspective.

Carbs and muscle glycogen stores -

You might not need to store carbs as glycogen or even digest them to benefit exercise performance. Rinsing your mouth with a carbohydrate-rich liquid for 10 seconds every five to ten minutes during a workout seems to affect the central nervous system and your performance positively, even if you spit instead of swallowing.

Most mouth rinse-studies use cycling as the exercise of choice. One meta-analysis found that carbohydrate mouth rinses improve cycling power, but that this does not translate into decreased time to complete a cycling time trial.

How is this relevant to glycogen? You see, carbohydrate mouth rinsing is more effective if you exercise during a fast or when you eat a carbohydrate-restricted diet. When your muscle glycogen levels are low.

That might sound counter-intuitive, but it seems to force your muscles to adapt to the situation, leading to better results in the long run. You improve your exercise capacity when your muscles adapt to the demands you put on them.

Adaptations include things like enhanced fat oxidation, angiogenesis the process of creating new blood vessels from existing ones , and a larger mitochondrial mass. Almost all the ATP, the primary energy source for your cells, is manufactured inside your mitochondria: the larger your mitochondrial mass, the more effective your ATP production.

Signals from your working muscles control these effects. When your muscles contract, like during a training session, a cascade of signals activates or shuts down metabolic pathways, controlling gene expressions and protein turnover.

Many decades of exercise physiology research, beginning in the early s, show us methods to provide exercising muscle with as much carbohydrate as possible, before, during, and after workouts.

A plentiful supply of carbs is key to optimal performance. At the same time, more recent research suggests that your training results might improve if you regularly train without that plentiful supply of carbs.

You rob your muscles of their preferred fuel and force them to adapt to lesser sources. You also get a more effective fatty acid turnover in your muscles and your entire body. The glycogen content in your muscles and how much carbs you eat add to these effects.

That kind of carbohydrate restriction can improve your performance and training capacity over time. In other words, you train without a lot of carbs leading up to a competition or an important event, and then you make sure you load your muscles with glycogen and eat plenty of carbs when it counts.

That way, you combine the greater training adaptations from carbohydrate restriction with the benefits of carbohydrate loading, giving you the best possible performance when you want it and need it the most.

If restricting carbohydrates means better results, no carbohydrates do not mean even better results. That could have the opposite effects, leading to low energy availability, fatigue, and even loss of muscle mass and depressed immune functions. Training without enough carbohydrates might be something for elite athletes who need optimal results at all costs to consider.

However, the casual athlete likely finds that method of training less than fun. And fun is integral to regular exercise habits. It has been busy keeping your blood sugar stable while you were snoring.

You force your body to use more fat as fuel during your workouts, increase the activity of enzymes controlling muscle glucose uptake, improve fat oxidation, and optimize mitochondrial function, compared to always loading up on carbs before your training sessions.

Exercising before breakfast like this leads to similar training adaptations in the long run as more dedicated carbohydrate restriction. As usual, strength training research is less abundant, and that research tends to be ambiguous.

There is no consensus yet. You get the same anabolic effects and stimulate muscle protein synthesis just as well regardless. The anabolic response to a strength training session is mainly dependent on signaling mechanisms and metabolic pathways, just like endurance training.

However, the two different types of exercise activate different pathways. One of the most powerful ones for building muscle is the so-called mTOR-complex.

Signaling pathways activated by low energy availability and depleted glycogen reserves inhibit mTOR. Muscle protein synthesis is the essential part of the muscle protein balance for building muscle mass. Muscle protein breakdown also factors in.

Research from Swedish scientists suggests more significant muscle breakdown if you train with depleted muscle glycogen. Insulin, in turn, reduces muscle breakdown and improves nutrient uptake in your muscles. Cut down on carbs, and your insulin levels drop. In theory, that might mean that you break down more muscle mass and provide your tired muscles with fewer nutrients with your post-workout meal.

Keep in mind that these are theoretical effects. Protein also releases plenty of insulin. Also, a very moderate insulin release reduces muscle breakdown maximally, and a normal-sized protein intake is enough for that insulin release.

When you lift weights, you primarily use muscle glycogen to fuel your efforts. If the same goes for strength training is unclear, even though your muscles rely on their glycogen stores to lift weights.

Several studies suggest that you can handle a higher training volume if you eat carbohydrates before hitting the weights. However, that allows you to conduct some unscientific experiments on your own. The same applies if you notice the opposite, that you perform better in a carb-loaded state.

Training with more or less depleted glycogen levels and generally low carbohydrate availability lead to more stress hormones. Markers indicating immune function are also negatively affected.

Even though always exercising with a low carbohydrate availability might depress your immune system, the milder version of carb restriction, training before breakfast, does not seem to have any negative effects in this regard.

If you are a big person, carry around a lot of muscle mass, or are more fit than the ordinary person, your capacity to store glycogen increases. Fat is good enough. At higher intensities, your muscles switch to using an increasing amount of glycogen.

As your glycogen levels deplete, you fatigue and start performing worse. If you only have 24 hours to restore your muscle glycogen following a workout, you better hurry! You have to cram down around 10 grams of carbohydrates per kilogram of bodyweight in that time to make it.

Also, you have to eat at least as many calories as your burn during that day. Glycogen synthesis is more effective if you eat several smaller carbohydrate-rich meals after a workout rather than loading up on one or two hefty ones.

One gram of carbohydrate per kilogram of body weight and hour during the hours following a training session optimizes glycogen restoration. You speed up your glycogen synthesis if you eat protein along with your carbs. Caffeine and creatine also cooperate with the carbohydrates you eat or drink, speeding up the rate at which you store glycogen in your muscles.

Eating 1—4 grams of carbs per kilogram of bodyweight 3—4 hours before a training session likely improves your endurance performance.

As for strength training, the jury is out. Eat before a workout if it feels good, but you can train on an empty stomach if you prefer. If you eat or drink some form of carbohydrates during long workouts, you save your liver and muscle glycogen for later, allowing you to perform at a higher level for a longer time.

Again, as for strength training, research is lacking, but it might be detrimental to go into a lifting session without decent levels of muscle glycogen. That could increase muscle breakdown and impair anabolic signaling. Prolonged or intense workouts with low muscle glycogen might be tough on your immune system, making you more susceptible to catching a cold.

However, if you have very high carbohydrate requirements, you might find it hard to eat enough , if that base consists of boiled potatoes and broccoli.

Also, you might get too much fiber, making your stomach unhappy. That mainly concerns endurance athletes training at a pretty high level. Seeing as you empty glycogen locally, in the working muscles, ask yourself: do you deplete the same muscles every day, or even several times a day?

Then you need that amount of carbs to restore your glycogen levels. If not, those kinds of intakes are probably too much. In the long run, it would likely make you fat rather than a high-performing athlete.

The same goes for weight training. A workout in the gym burns up a lot of muscle glycogen during the sets themselves, but the total amount required to get you through a training session does not amount to that much. However, even if you are not a high-level endurance athlete, your training benefits from glycogen and filled muscles.

An average mixed diet works just fine for your needs. Andreas Abelsson. Maximize your gains and build the body you want with our guide on the best exercises for every muscle group. Workout Log Articles Exercises Squat Squat Programs Squat Strength Standards Squat Depth Smith Machine vs.

Free Barbell? Squat Variations Bench Press Bench Press Programs Bench Press Strength Standards How to Bench lb Close-Grip vs Wide Grip Bench Press Incline vs Flat Bench Press Bench Press Variations Bench Press Accessory Exercises Deadlift Deadlift Programs Deadlift Strength Standards How to Grip the Bar Trap Bar vs.

Glycogen — Key Points: Your muscles and your liver are your two main stores of glycogen. You fill them up by eating carbohydrates. Your body prefers to use muscle glycogen to fuel intense workouts and other demanding physical work.

The average person can store a little more than grams of glycogen in the muscles and grams in the liver. However, low-intensity workouts during long periods of time will certainly require a higher daily intake of carbs. High-intensity workouts rely on glucose almost exclusively — there is always a high degree of glycogen depletion and, therefore, a higher carbohydrate intake.

We tried these new recommendations in with the Garmin Pro cycling team, and it worked really well. This method was proven during the Tour de France, with no GI disturbances from the athletes.

We have since tried these recommendations with many athletes of different sports and competition levels with great success and performance results. A mixture of simple and complex carbohydrates is the most efficient way to go.

Asker Jeukendrup, one of the top experts in the world of sports nutrition, has also observed similar findings. The graph below shows how Dr. Jeukendreup and his group observed that higher carbohydrate intake was associated with faster finish times at the Triathlon World Championships in Kona.

Daily intake of CHO varies depending on the level and duration of activity. An excessive carbohydrate diet without the right amount of exercise would lead to an increase in body fat due to the conversion of CHO to fat.

Onywera, V. Food and macronutrient intake of elite Kenyan distance runners. San Millán I, González-Haro C, Hill J. Indirect Assessment of Glycogen Status in Competitive Athletes. Med Sci Sports Exerc. Goodman, MN.

Amino acid and protein metabolism. In Exercise, nutrition and energy metabolism,eds. Horton, R. TErtujn, New York: Macmillan. Sherman WM. Metabolism of sugars and physical performance. Am J Clin Nutr. Kjaer M, Kiens B, Hargreaves M, Richter EA.

Influence of active muscle mass on glucose homeostasis during exercise in humans. Katz A, Broberg S, Sahlin K, Wahren J. Leg glucose uptake during maximal dynamic exercise in humans.

Am J Physiol. Costill DL, Hargreaves M. Carbohydrates for training and competition. Jeukendrup A. A step towards personalized sports nutrition: carbohydrate intake during exercise.

Lambert CP, Flynn MG, Boone Jr JB, Michaud TJ, Rodriguez-Zayas J. Effects of carbohydrate feeding on multiple-bout resistance exercise. Haff G, Schroeder C, Koch A, Kuphal K, Comeau M, Potteiger J.

The effects of supplemental carbohydrate ingestion on intermittent isokinetic leg exercise. J Sports Med Phys Fitness. Haff GG, Stone MH, Warren BJ, Keith R, Johnson RL, Nieman DC, et al. The effect of carbohydrate supplementation on multiple sessions and bouts of resistance exercise.

Kulik JR, Touchberry CD, Kawamori N, Blumert PA, Crum AJ, Haff GG. Supplemental carbohydrate ingestion does not improve performance of high-intensity resistance exercise. Haff GG, Koch AJ, Potteiger JA, Kuphal KE, Magee LM, Green SB, et al.

Carbohydrate supplementation attenuates muscle glycogen loss during acute bouts of resistance exercise. Margolis LM, Pasiakos SM. Optimizing intramuscular adaptations to aerobic exercise: effects of carbohydrate restriction and protein supplementation on mitochondrial biogenesis.

Adv Nutr. Jager S, Handschin C, St-Pierre J, Spiegelman BM. AMP-activated protein kinase AMPK action in skeletal muscle via direct phosphorylation of PGC-1alpha. Proc Natl Acad Sci U S A. Psilander N, Frank P, Flockhart M, Sahlin K.

Exercise with low glycogen increases PGC-1alpha gene expression in human skeletal muscle. Drake JC, Wilson RJ, Yan Z. Molecular mechanisms for mitochondrial adaptation to exercise training in skeletal muscle. Faseb J. Mounier R, Theret M, Lantier L, Foretz M, Viollet B.

Expanding roles for AMPK in skeletal muscle plasticity. Trends Endocrinol Metab. Canto C, Gerhart-Hines Z, Feige JN, Lagouge M, Noriega L, Milne JC, et al. Wackerhage H. Molecular Exercise Physiology: An Introduction.

Xiao B, Sanders MJ, Underwood E, Heath R, Mayer FV, Carmena D, et al. Structure of mammalian AMPK and its regulation by ADP. Carling D, Thornton C, Woods A, Sanders MJ. AMP-activated protein kinase: new regulation, new roles?

Biochem J. Chan MH, McGee SL, Watt MJ, Hargreaves M, Febbraio MA. Altering dietary nutrient intake that reduces glycogen content leads to phosphorylation of nuclear p38 MAP kinase in human skeletal muscle: association with IL-6 gene transcription during contraction.

FASEB J. Knutti D, Kressler D, Kralli A. Regulation of the transcriptional coactivator PGC-1 via MAPK-sensitive interaction with a repressor. Cochran AJ, Little JP, Tarnopolsky MA, Gibala MJ. Carbohydrate feeding during recovery alters the skeletal muscle metabolic response to repeated sessions of high-intensity interval exercise in humans.

Mathai AS, Bonen A, Benton CR, Robinson DL, Graham TE. Rapid exercise-induced changes in PGC-1alpha mRNA and protein in human skeletal muscle. Saleem A, Carter HN, Iqbal S, Hood DA.

Role of p53 within the regulatory network controlling muscle mitochondrial biogenesis. Donahue RJ, Razmara M, Hoek JB, Knudsen TB. Direct influence of the p53 tumor suppressor on mitochondrial biogenesis and function. Saleem A, Adhihetty PJ, Hood DA. Role of p53 in mitochondrial biogenesis and apoptosis in skeletal muscle.

Physiol Genomics. Bartlett JD, Louhelainen J, Iqbal Z, Cochran AJ, Gibala MJ, Gregson W, et al. Reduced carbohydrate availability enhances exercise-induced p53 signaling in human skeletal muscle: implications for mitochondrial biogenesis.

MacDougall JD, Sale DG, Moroz JR, Elder GC, Sutton JR, Howald H. Mitochondrial volume density in human skeletal muscle following heavy resistance training.

Med Sci Sports. Chilibeck PD, Syrotuik DG, Bell GJ. The effect of strength training on estimates of mitochondrial density and distribution throughout muscle fibres.

Tang JE, Hartman JW, Phillips SM. Increased muscle oxidative potential following resistance training induced fibre hypertrophy in young men. Appl Physiol Nutr Metab. Pesta D, Hoppel F, Macek C, Messner H, Faulhaber M, Kobel C, et al.

Similar qualitative and quantitative changes of mitochondrial respiration following strength and endurance training in normoxia and hypoxia in sedentary humans.

Jubrias SA, Esselman PC, Price LB, Cress ME, Conley KE. Large energetic adaptations of elderly muscle to resistance and endurance training. Porter C, Reidy PT, Bhattarai N, Sidossis LS, Rasmussen BB.

Resistance exercise training alters mitochondrial function in human skeletal muscle. Irving BA, Lanza IR, Henderson GC, Rao RR, Spiegelman BM, Nair KS. Combined training enhances skeletal muscle mitochondrial oxidative capacity independent of age.

J Clin Endocrinol Metab. Coffey VG, Zhong Z, Shield A, Canny BJ, Chibalin AV, Zierath JR, et al. Early signaling responses to divergent exercise stimuli in skeletal muscle from well-trained humans. Gordon PM, Liu D, Sartor MA, IglayReger HB, Pistilli EE, Gutmann L, et al.

Resistance exercise training influences skeletal muscle immune activation: a microarray analysis. Burd NA, Tang JE, Moore DR, Phillips SM. Exercise training and protein metabolism: influences of contraction, protein intake, and sex-based differences. Rennie MJ, Wackerhage H, Spangenburg EE, Booth FW.

Control of the size of the human muscle mass. Annu Rev Physiol. Lemon PW, Mullin JP. Effect of initial muscle glycogen levels on protein catabolism during exercise. J Appl Physiol Respir Environ Exerc Physiol. Van Hall G, Saltin B, Wagenmakers AJ.

Muscle protein degradation and amino acid metabolism during prolonged knee-extensor exercise in humans. Clin Sci Lond. Howarth KR, Phillips SM, MacDonald MJ, Richards D, Moreau NA, Gibala MJ. Effect of glycogen availability on human skeletal muscle protein turnover during exercise and recovery.

Howarth KR, Moreau NA, Phillips SM, Gibala MJ. Coingestion of protein with carbohydrate during recovery from endurance exercise stimulates skeletal muscle protein synthesis in humans.

Pasiakos SM, McClung HL, McClung JP, Margolis LM, Andersen NE, Cloutier GJ, et al. Leucine-enriched essential amino acid supplementation during moderate steady state exercise enhances postexercise muscle protein synthesis. Glass DJ. Skeletal muscle hypertrophy and atrophy signaling pathways. Int J Biochem Cell Biol.

Philp A, Hamilton DL, Baar K. Signals mediating skeletal muscle remodeling by resistance exercise: PI3-kinase independent activation of mTORC1. Wojtaszewski JF, MacDonald C, Nielsen JN, Hellsten Y, Hardie DG, Kemp BE, et al. Regulation of 5'AMP-activated protein kinase activity and substrate utilization in exercising human skeletal muscle.

Churchley EG, Coffey VG, Pedersen DJ, Shield A, Carey KA, Cameron-Smith D, et al. Influence of preexercise muscle glycogen content on transcriptional activity of metabolic and myogenic genes in well-trained humans.

Creer A, Gallagher P, Slivka D, Jemiolo B, Fink W, Trappe S. Pasiakos SM, Vislocky LM, Carbone JW, Altieri N, Konopelski K, Freake HC, et al. Acute energy deprivation affects skeletal muscle protein synthesis and associated intracellular signaling proteins in physically active adults.

J Nutr. Bell GJ, Syrotuik D, Martin TP, Burnham R, Quinney HA. Effect of concurrent strength and endurance training on skeletal muscle properties and hormone concentrations in humans.

Dolezal BA, Potteiger JA. Concurrent resistance and endurance training influence basal metabolic rate in nondieting individuals. Hakkinen K, Alen M, Kraemer WJ, Gorostiaga E, Izquierdo M, Rusko H, et al.

Neuromuscular adaptations during concurrent strength and endurance training versus strength training. Kraemer WJ, Patton JF, Gordon SE, Harman EA, Deschenes MR, Reynolds K, et al. Compatibility of high-intensity strength and endurance training on hormonal and skeletal muscle adaptations.

Leveritt M, Abernethy PJ, Barry BK, Logan PA. Concurrent strength and endurance training. A review. Chromiak JA, Mulvaney DR. A review: the effects of combined strength and endurance training on strength development.

Hennessy LC, Watson AW. The interference effects of training for strength and endurance simultaneously. Wilson JM, Marin PJ, Rhea MR, Wilson SM, Loenneke JP, Anderson JC.

Concurrent training: a meta-analysis examining interference of aerobic and resistance exercises. Hickson RC. Interference of strength development by simultaneously training for strength and endurance.

Baar K. Using molecular biology to maximize concurrent training. Fyfe JJ, Bishop DJ, Stepto NK. Interference between concurrent resistance and endurance exercise: molecular bases and the role of individual training variables.

Perez-Schindler J, Hamilton DL, Moore DR, Baar K, Philp A. Nutritional strategies to support concurrent training. Bolster DR, Crozier SJ, Kimball SR, Jefferson LS. AMP-activated protein kinase suppresses protein synthesis in rat skeletal muscle through down-regulated mammalian target of rapamycin mTOR signaling.

J Biol Chem. Wang L, Mascher H, Psilander N, Blomstrand E, Sahlin K. Resistance exercise enhances the molecular signaling of mitochondrial biogenesis induced by endurance exercise in human skeletal muscle. Apro W, Wang L, Ponten M, Blomstrand E, Sahlin K.

Resistance exercise induced mTORC1 signaling is not impaired by subsequent endurance exercise in human skeletal muscle. Carrithers JA, Carroll CC, Coker RH, Sullivan DH, Trappe TA. Concurrent exercise and muscle protein synthesis: implications for exercise countermeasures in space.

Aviat Space Environ Med. Coffey VG, Pilegaard H, Garnham AP, O'Brien BJ, Hawley JA. Consecutive bouts of diverse contractile activity alter acute responses in human skeletal muscle.

Coffey VG, Jemiolo B, Edge J, Garnham AP, Trappe SW, Hawley JA. Effect of consecutive repeated sprint and resistance exercise bouts on acute adaptive responses in human skeletal muscle.

Havemann L, West SJ, Goedecke JH, Macdonald IA, St Clair Gibson A, Noakes TD, et al. Fat adaptation followed by carbohydrate loading compromises high-intensity sprint performance. Download references. We would like to thank T. Maas HAN University of Applied Sciences Institute for Studies in Sports and Exercise for his fruitful input and feedback on the manuscript.

Division of Human Nutrition, Wageningen University, Bomenweg 4, HD, Wageningen, The Netherlands. Pim Knuiman, Maria T. Radboud University, Radboud Institute for Health Sciences, Department of Physiology, Geert Grooteplein-West 32, GA, Nijmegen, The Netherlands.

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Knuiman, P. Glycogen availability and skeletal muscle adaptations with endurance and resistance exercise. Nutr Metab Lond 12 , 59 Download citation. Received : 19 August Accepted : 11 December Published : 21 December 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. Skip to main content. Search all BMC articles Search. Download PDF. Download ePub. Review Open access Published: 21 December Glycogen availability and skeletal muscle adaptations with endurance and resistance exercise Pim Knuiman 1 , Maria T.

Abstract It is well established that glycogen depletion affects endurance exercise performance negatively. Background Roughly, exercise can be divided in endurance- and resistance exercise.

Glycogen and energetic demands with exercise Glycogen is an essential substrate during high intensity exercise by providing a mechanism by which adenosine tri phosphate ATP can be resynthesized from adenosine diphosphate ADP and phosphate.

Low glycogen and performance with exercise Endurance training performance Low-glycogen availability causes a shift in substrate metabolism during and after exercise [ 30 , 31 ].

Discrepancies between and limitations of the low-glycogen endurance exercise studies A possible explanation for the different outcomes on performance between low-glycogen studies could be differences in the training status of the subjects.

Resistance exercise performance Resistance exercise is typically characterized by short bursts of nearly maximal muscular contractions. Mitochondrial biogenesis on low-glycogen regimes and molecular pathways involved Endurance exercise PGC-1α Activity of the exercise-induced peroxisome proliferator-activated γ-receptor co-activator 1α PGC-1α has been proposed to play a key role in the adaptive response with endurance exercise Fig.

Full size image. Conclusions To conclude, depletion of muscle glycogen is strongly associated with the degree of fatigue development during endurance exercise.

References Gibala MJ, Little JP, Macdonald MJ, Hawley JA. Article CAS Google Scholar Bebout DE, Hogan MC, Hempleman SC, Wagner PD. CAS Google Scholar Burelle Y, Hochachka PW. Article Google Scholar Charifi N, Kadi F, Feasson L, Costes F, Geyssant A, Denis C.

Article CAS Google Scholar Folland JP, Williams AG. Article Google Scholar Cermak NM, Res PT, de Groot LC, Saris WH, van Loon LJ. Article CAS Google Scholar Coffey VG, Moore DR, Burd NA, Rerecich T, Stellingwerff T, Garnham AP, et al.

Article CAS Google Scholar Cermak NM, van Loon LJ. Article Google Scholar Hawley JA, Burke LM. Article Google Scholar Bartlett JD, Hawley JA, Morton JP. Article Google Scholar Cox GR, Clark SA, Cox AJ, Halson SL, Hargreaves M, Hawley JA, et al. Article CAS Google Scholar Hulston CJ, Venables MC, Mann CH, Martin C, Philp A, Baar K, et al.

Article CAS Google Scholar Morton JP, Croft L, Bartlett JD, Maclaren DP, Reilly T, Evans L, et al. Article CAS Google Scholar Van Proeyen K, Szlufcik K, Nielens H, Ramaekers M, Hespel P.

Article Google Scholar Yeo WK, McGee SL, Carey AL, Paton CD, Garnham AP, Hargreaves M, et al. Article CAS Google Scholar Yeo WK, Paton CD, Garnham AP, Burke LM, Carey AL, Hawley JA.

Article CAS Google Scholar Hansen AK, Fischer CP, Plomgaard P, Andersen JL, Saltin B, Pedersen BK. Article Google Scholar Cochran AJ, Myslik F, MacInnis MJ, Percival ME, Bishop D, Tarnopolsky MA, et al. Article Google Scholar Camera DM, Hawley JA, Coffey VG. Article CAS Google Scholar Camera DM, West DW, Burd NA, Phillips SM, Garnham AP, Hawley JA, et al.

Article CAS Google Scholar Ortenblad N, Nielsen J, Saltin B, Holmberg HC. Article CAS Google Scholar Ortenblad N, Westerblad H, Nielsen J. Article CAS Google Scholar Nielsen J, Holmberg HC, Schroder HD, Saltin B, Ortenblad N. Article CAS Google Scholar Nielsen J, Suetta C, Hvid LG, Schroder HD, Aagaard P, Ortenblad N.

Article CAS Google Scholar Duhamel TA, Perco JG, Green HJ.

Blycogen is a key part of the training regime for any athlete. Not Banned substances in professional sports enough calories Kcalories-Kcal muscel result flycogen a Natural remedies for high cholesterol of important macro Banned substances in professional sports micronutrients. This is especially gpycogen when it comes to carbohydrates CHO. However, from what I have seen, these books and diets lack substantial scientific evidence — especially when it comes to athletic performance. This is especially true for athletes who restrict their carbohydrate intake, as a massive amount of scientific evidence from the past 50 years clearly shows that a good carbohydrate diet is crucial to maintain performance. Home Carbs and muscle glycogen stores Blogs Multivitamin for hangover recovery The Effects of Glycogen on Your Tlycogen Composition. We want to help clear up glycogwn of the confusion. Read on to learn about carbs and its role in energy production i. e glycogen, why you should consider healthy carbohydrates, and what you want to be aware of if you are following a low-carb diet. What about glycogen?

Video

Muscle Glycogen vs Liver Glycogen

Carbs and muscle glycogen stores -

The finding of their study was a significant gain in endurance time till exhaustion in the low-glycogen compared to normal glycogen levels. In addition, they found that low-glycogen improved oxidative capacity citrate synthase activity to a larger extent than commencing all exercise sessions with high-glycogen.

The findings of Hansen et al. Subsequently, other research groups tested the same hypothesis by using an alternative model with trained subjects [ 12 , 16 ]. Yeo et al. Interestingly, following the 3-wk intervention period, several markers of training adaption were increased.

However, min time-trial performance was similar in both the low-glycogen and high-glycogen group. Although speculative, the similar effect in performance suggests that the low-glycogen group showed a greater training adaptation, relative to their level of training intensity.

Hulston et al. Moreover, this was accompanied by increases in oxidation of fatty acids, sparing of muscle glycogen, and greater increases in succinate dehydrogenase and 3-hydroxyacyl-CoA dehydrogenase enzyme activity [ 12 ].

However, with regard to performance, the training with low muscle glycogen availability was not more effective than training with high muscle glycogen levels [ 12 ]. Together, low-glycogen availability affects substrate use during exercise by increasing fatty acid oxidation compared to training with normal glycogen levels; this effect is independent of the subject training status.

Recently, Cochran et al. Both groups trained on a total of 6 d over a 2-wk period, with a minimum of one day of rest between training days. Furthermore, subjects completed two identical HIIT sessions on each training day, separated by 3 h of recovery.

After two weeks of HIIT, mean power output during a kJ time trial increased to a greater extent in the low-glycogen group compared to the high-glycogen group [ 18 ]. A novel aspect of their study was that the subjects performed whole-body exercise for a relatively short period of time 2 weeks , while the study of Hansen et al.

A possible explanation for the different outcomes on performance between low-glycogen studies could be differences in the training status of the subjects. Indeed, it has previously been shown that the effectiveness of nutritional interventions is influenced by the subject training status [ 32 ], possibly because trained subjects depend less on carbohydrate utilization because they have greater metabolic flexibility.

Another methodological issue is the selected test used to determine performance. In some studies, self-selected intensities were used, which could be influenced by carbohydrate manipulation.

Cochran et al. To summarize, although some studies reported that repetitive low-glycogen training leads to improved performance compared with high glycogen [ 17 , 18 ], extrapolating these findings to sports-specific performance should be done with prudence.

First, the study of Hansen et al. Second, as suggested by Yeo et al. Lastly, chronic exercise sessions commencing in the low-glycogen state may enhance the risk for overtraining syndrome [ 35 ] which in turn may result in reduced training capacity [ 36 ].

Resistance exercise is typically characterized by short bursts of nearly maximal muscular contractions. When performing resistance exercise, glycogen is crucial to resynthesize the phosphate pool, which provides energy during high intensity muscle contractions [ 37 ]. According to MacDougall et al.

This reduction in glycogen content during exercise is determined by the duration, intensity and volume of the performed exercise bout.

The largest reductions in glycogen are seen with high repetitions with moderate load training [ 40 ], an effect that mainly occurs in type II fibers [ 39 ]. It has been demonstrated that a reduction of muscle glycogen affects both isokinetic torque [ 29 ] and isoinertial resistance exercise capacity negatively [ 42 ].

However, this effect is not always evident [ 43 ] and is likely to be affected by the protocol used to induce glycogen depletion [ 44 ]. Based on the assumption that pre-exercise glycogen content can influence exercise performance, it seems that the pre-exercise carbohydrate ingestion requires particular attention [ 44 ].

Although it is widely accepted that carbohydrate ingestion before endurance exercise enhances work capacity [ 45 , 46 ], carbohydrate ingestion before resistance exercise has not been studied to the same extent.

The importance of carbohydrates for the resistance exercise-type athlete can be substantiated by the idea that glycogen plays a relatively important role in energy metabolism during resistance exercise. For example, it has been shown that pre-resistance exercise carbohydrate ingestion increases the amount of total work [ 47 — 49 ].

In contrast, other reports show no benefit of carbohydrate ingestion on total work capacity [ 50 , 51 ]. To precisely determine the role of glycogen availability for the resistance exercise athlete more training studies that feature a defined area of outcome measures specifically for performance and adaptation are needed.

Activity of the exercise-induced peroxisome proliferator-activated γ-receptor co-activator 1α PGC-1α has been proposed to play a key role in the adaptive response with endurance exercise Fig. Enhanced activity of PGC-1α and increased mitochondrial volume improves oxidative capacity through increased fatty acid β -oxidation and mitigating glycogenolysis [ 52 ].

As a result, muscle glycogen can be spared which might delay the onset of muscle fatigue and enhances oxidative exercise performance. PGC-1α is responsible for the activation of mitochondrial transcription factors e. the nuclear respiratory factors NRF-1 and -2 and the mitochondrial transcription factor A Tfam [ 53 ].

Schematic figure representing the regulation of mitochondrial biogenesis by endurance exercise. In addition exercise reduces skeletal muscle glycogen in the contracting muscles which in turn activates the sensing proteins AMPK and p38 MAPK.

Both AMPK and p38 MAPK activate and translocate the transcriptional co-activator PGC-1α to the mitochondria and nucleus. The kinases AMPK, p38 MAPK and SIRT 1 then might phosphorylate PGC-1 α and reduce the acetylation of PGC-1 α, which increases its activity.

Thus, endurance exercise leads to more PGC-1 α which over time results in mitochondrial biogenesis. Activation of PGC-1α is amongst others regulated by the major up-stream proteins 5' adenosine monophosphate-activated protein kinase AMPK [ 54 ]. Prolonged endurance type exercise requires a large amount of ATP resulting in accumulation of ADP and AMP in the recruited muscle fibers [ 55 ].

This activates AMPK with the purpose to restore cellular energy homeostasis [ 56 , 57 ]. The rise of ADP and AMP during prolonged endurance type exercise results in the phosphorylation of AMPK at Thr, the active site on the AMPK α subunit [ 58 — 60 ]. Canto and colleagues showed that AMPK action on PGC-1α transcriptional activity is partly regulated by SIRT1, a sirtuin family protein which deacetylates several proteins that contribute to cellular regulation [ 57 ].

Furthermore, it was shown that the acute actions of AMPK on lipid oxidation alter the balance between cellular NAD1 and NADH, which acts as a messenger to activate SIRT1 [ 57 ]. During prolonged endurance type exercise skeletal muscle glycogen reduces, this is sensed by the AMPK β subunit resulting in an activation of AMPK Fig.

The AMPK is then also activated through phosphorylation of Thr and this response is likely dependent on the rise of AMP and ADP during exercise. Chan et al suggested that low muscle glycogen availability associates with the phosphorylation of the nuclear P38 mitogen-activated protein kinases p38 MAPK , rather than translocation of p38 MAPK to the nucleus per se [ 61 ].

Accordingly, p38 MAPK particularly phosphorylate the expression of PGC-1α [ 53 , 62 ], whereas AMPK could both phosphorylate and enhance expression of PGC-1α [ 53 , 62 ]. Restricted CHO availability during or after exercise has also been shown to augment phosphorylation of i.

activate p38 MAPK [ 63 ] and AMPK [ 15 ]. In another study by Mathai and colleagues it was shown that changes in muscle glycogen correlates with the changes in PGC-1α protein abundance during exercise and recovery [ 64 ].

The majority of the studies show that the PGC-1α mRNA content increased during and directly after exercise and returned to resting levels by 24 h after exercise.

However, the studies that measured both PGC-1α mRNA and PGC-1α protein after chronic or acute exercise failed to find increases in both [ 64 ]. Therefore, changes of PGC-1α mRNA content are not necessarily compatible with changes in PGC-1α protein abundance following exercise [ 64 ].

Although these studies suggest that the signalling response to exercise is affected by CHO supply, it remains unclear whether exercise in a glycogen-depleted state can enhance the adaptive signalling response that is required for mitochondrial biogenesis.

Thus, AMPK and MAPK 38 play a key role in the transcriptional regulation of mitochondrial biogenesis trough PGC-1α in response to stress.

However, the precise role of potential regulators which are responsive to glycogen availability, in the processes of mitochondrial biogenesis, needs to be further elucidated. Another described protein that regulates mitochondrial biogenesis is p53, which appears to be sensitive to changes in glycogen availability [ 65 ].

Previous research has shown that p53 is phosphorylated by AMPK and p38 AMPK [ 66 , 67 ]. Furthermore, p53 is implicated in the stimulation of gene expression of mitochondrial function [ 66 , 67 ]. It has been demonstrated that commencing endurance exercise in a glycogen depleted state upregulates p53 to a larger extent than during exercise in a replenished glycogen state [ 68 ].

However, the influence on PGC-1α mRNA expression is difficult to interpret because the subjects involved were not only on an exercise regime with low glycogen availability, but also on a calorie restricted diet. Accordingly, it remains unknown which potent regulator was responsible for the increase in mitochondrial biogenesis in this study.

The precise role of both potential regulators in the processes of mitochondrial biogenesis needs to be further elucidated. Although resistance exercise is mainly recognized as mechanical stimulus for increases in strength and hypertrophy, the aerobic effects following resistance exercise have also been studied.

Early investigations have shown that skeletal mitochondrial volume [ 69 ] and oxidative capacity [ 70 ] are unaltered following prolonged resistance exercise.

However, it has been recently reported that resistance exercise increases the activity of oxidative enzymes in tissue homogenates [ 19 , 71 ] and respiration in skinned muscle fibers [ 72 ]. Moreover, resistance training augmented oxidative phosphorylation in sedentary older adults [ 73 ] and respiratory capacity and intrinsic function of skeletal muscle mitochondria in young healthy men [ 74 ].

Interestingly, following all exercise modalities, concurrent training induced the most robust improvements in mitochondrial related outcomes and mRNA expression [ 75 ]. Notably, the improvements in mitochondria were independent of age.

Therefore, exploring molecular processes regulating the metabolic and oxidative responses with resistance training may lead to a better understanding and eventually to optimized adaptations. Studies examining the effect of low glycogen availability on mitochondrial regulators largely centered on endurance training.

However, Camera et al. It appears that the level of glycogen acts as a modulator of processes regulating mitochondrial biogenesis, independent of the nature of exercise stimuli.

The supposed mechanism by which p53 is translocated from the nucleus to the mitochondria and subsequently enhances mitochondrial biogenesis is through its interaction with mitochondrial transcription factor A Tfam and also by preventing p53 suppression of PGC-1α activation in the nucleus [ 67 ].

According to the findings of Camera et al. Moreover, the acute metabolic response to resistance exercise can be modulated in a glycogen-dependent manner.

However, whether these acute alterations in regulators of mitochondrial biogenesis are sufficient to promote mitochondrial volume and function remains to be elucidated in future long-term training studies.

Skeletal muscle mass is maintained by the balance between muscle protein synthesis MPS and muscle protein breakdown MPB rates such that overall net muscle protein balance NPB remains essentially unchanged over the course of the day.

The two main potent stimuli for MPS are food ingestion and exercise [ 78 ]. Nutrition, proteins in particular, induces a transient stimulation of MPS and is therefore in itself, i.

in the absence of exercise, not sufficient to induce a positive NPB. Likewise, resistance exercise improves NPB, however, the ingestion of protein during the post-exercise recovery period is required to induce a positive NPB [ 79 ].

Thus, both exercise and food ingestion must be deployed in combination in order to create a positive NPB [ 78 ]. To date, only a few studies examined the role of glycogen availability on protein metabolism following endurance exercise [ 30 , 80 , 81 ]. It seems that glycogen availability mediates MPB.

An early study from Lemon and Mullin showed that when exercise was performed with reduced glycogen availability nitrogen losses more than doubled, suggesting an increase in MPB and amino acid oxidation [ 80 ]. Subsequently, two other studies [ 30 , 81 ] used the arterial-venous a-v difference method to explore whether exercise in the low glycogen state affects amino acid flux and then estimated NPB.

In both studies subjects performed an exercise session in the low-glycogen state, the researchers found a net release of amino acids during exercise indicating an increase in MPB.

However, these studies may be methodologically flawed because the a-v balance method only allows for the determination of net amino acid balance. Conclusions about changes in MPS and MPB are therefore of a speculative nature [ 82 ].

A more recent study by Howarth et al. They found that skeletal muscle NPB was lower when exercise was commenced with low glycogen availability compared to the high glycogen group, indicating an increase in MPB and decrease in MPS during exercise. It appears that endurance exercise with reduced muscle glycogen availability negatively influences muscle protein turnover and impairs skeletal muscle repair and recovery from endurance exercise.

As described previously, low glycogen could be used as a strategy to augment mitochondrial adaptations to exercise, however, protein ingestion is required to offset MPB and increase MPS.

Indeed, recent evidence reported that protein ingestion during or following endurance exercise increases MPS leading to a positive NPB [ 83 , 84 ]. The Akt-mTOR-S6K pathway that controls the process of MPS has been studied extensively [ 85 , 86 ]. However, the effects of glycogen availability with resistance exercise and its effects on these regulatory processes remains to be further scrutinized.

Furthermore, work by Churchly et al. did not enhance the activity of genes involved in muscle hypertrophy. Creer et al. mTOR phosphorylation was similar to that of Akt, however, the change was not significant.

In a comparable study from Camera et al. Muscle biopsies were taken at rest and 1 and 4 h after the single exercise bout. Although mTOR phosphorylation increased to a higher extent in the normal glycogen group, there were no detectable differences found in MPS suggesting that the small differences in signaling are negligible since MPS was unaffected.

However, it should be noted that being in an energy deficit state does not necessarily reflects glycogen levels are low. Hence, the total energy available for the cell to undertake its normal homeostatic processes is less. Summarized, it seems that glycogen availability had no influence on the anabolic effects induced by resistance exercise.

However, aforementioned studies on the effects of glycogen availability on resistance exercise-induced anabolic response do not resemble a training volume typically used by resistance-type athletes.

Future long-term training studies ~12 weeks are needed to find out whether performing resistance exercise with low glycogen availability leads to divergent skeletal muscle adaptations compared to performing the exercise bouts with replenished glycogen levels.

Vice versa, the effect of resistance exercise on endurance performance and VO 2max appears to be marginal [ 95 , 96 ]. However, some studies reported compromised gains in aerobic capacity with concurrent training compared to endurance exercise alone [ 97 , 98 ].

Following the work of Hickson et al. Since a detailed analysis on the interference effect associated with concurrent training is beyond the scope of this review, we refer the reader to expert reviews on the interference effect seen with concurrent training Baar et al. It is thought that endurance exercise results in an activation of AMPK, which inhibits the mTORC1 signaling via tuberous sclerosis protein TSC , and this will eventually suppress MPS resulting in a negative net protein balance.

In addition, a higher contractile activity also results in a higher calcium flux, which decreases peptide-chain elongation via activation of eukaryotic elongation factor-2 kinase eEF2k leading to a decreased MPS [ 89 , , ].

However, whether the exercise-induced acute interference between AMPK and mTORC1 entirely explains the blunted strength gains seen with concurrent training is to date obscure. To optimize skeletal muscle adaptations and performance, nutritional strategies for both exercise modes should differ.

Indeed, it was recently proposed that, when practicing endurance and resistance exercise on the same day, the endurance session should be performed in the morning in the fasted state, with ample protein ingestion [ ].

While the afternoon resistance exercise session should be conducted only after carbohydrate replenishment with adequate post-exercise protein ingestion [ ].

Furthermore, whether such a nutritional strategy leads to improved performance compared to general recommendations for carbohydrate and protein intake remains elusive.

Interestingly, it has been demonstrated that a resistance exercise session subsequently after low-intensity endurance, non-glycogen depleting session could enhance molecular signaling of mitochondrial biogenesis induced by endurance exercise [ ].

Furthermore it is currently unclear whether performing resistance exercise with low-glycogen availability affects the acute anabolic molecular events and whether the effects of these responses possibly result in improved or impaired training adaptation.

Furthermore, whether low-glycogen availability during the endurance bout amplifies the oxidative resistance exercise induced response remains to be investigated.

It seems that both modes of exercise in a low glycogen state as part of a periodized training regime are interesting in terms of acute expressions of markers involved in substrate utilization and oxidative capacity.

However, on the other hand, a sufficient amount of glycogen is essential in order to meet the energetic demands of both endurance and resistance exercise. Most existing information on nutrition and concurrent training adaptation is derived from studies where subjects performed exercise in the fasted state [ — ].

Coffey and colleagues investigated the effects of successive bouts of resistance and endurance exercise performed in different order in close proximity on the early skeletal muscle molecular response [ 76 ].

Although the second exercise bout was performed with different levels of skeletal muscle glycogen content, the subsequent effects on Akt, mTOR and p70 signaling following the second exercise bout remained the same. Prospective long-term concurrent training studies may help to understand the complexity of the impaired adaptation with concurrent training and further determine to what extend the acute signaling antagonism contributes to this.

Moreover, the role of nutritional factors in counteracting the interference effect remains to be further elucidated. In this review we summarized the role of glycogen availability with regard to performance and skeletal muscle adaptations for both endurance and resistance exercise.

Most of the studies with low-glycogen availability focused on endurance type training. The results of these studies are promising if the acute molecular response truly indicates skeletal muscle adaptations over a prolonged period of time.

Unfortunately, these results on low-glycogen availability may be biased because many other variables including training parameters time, intensity, frequency, type, rest between bouts and nutritional factors type, amount, timing, isocaloric versus non-isocaloric placebo varied considerably between the studies and it is therefore difficult to make valid inferences.

Furthermore, the majority of the studies with low glycogen availability were of short duration [ 18 ] and showed no changes [ 11 — 17 ], or showed, in some cases decreases in performance [ ]. Nevertheless, reductions in glycogen stores by manipulation of carbohydrate ingestion have shown to enhance the formation of training-induced specific proteins and mitochondrial biogenesis following endurance exercise to a greater extent than in the glycogen replenished state [ 11 — 16 , 18 , 68 ].

For resistance exercise, glycogen availability seemed to have no significant influence on the anabolic effects induced by resistance exercise when MPS was measured with the stable isotope methodology. However, the exercise protocols used in most studies do not resemble a training volume that is typical for resistance-type athletes.

Future long-term training studies ~12 weeks are needed to investigate whether performing resistance exercise with low glycogen availability leads to divergent skeletal muscle adaptations compared to performing the exercise bouts with replenished glycogen levels.

The role of glycogen availability on skeletal muscle adaptations and performance needs to be further investigated. In particular researchers need to examine glycogen availability when endurance and resistance exercise are conducted concurrently, for example, on the same day or on alternating days during the week.

To date, only a few studies have investigated the interactions between nutrient intake and acute response following a concurrent exercise model. We recommend that future research in this field should focus on the following questions:.

What is the impact of performing one of the exercise bouts endurance or resistance with low glycogen availability on response of markers of mitochondrial biogenesis of the subsequent endurance or resistance exercise bout? Does the resistance exercise bout need to be conducted with replenished glycogen stores in order to optimize the adaptive response when performed after a bout of endurance exercise?

Is nutritional timing within a concurrent exercise model crucial to maximize skeletal muscle adaptations following prolonged concurrent training?

To conclude, depletion of muscle glycogen is strongly associated with the degree of fatigue development during endurance exercise. This is mainly caused by reduced glycogen availability which is essential for ATP resynthesis during high-intensity endurance exercise. Furthermore, it is hypothesized that other physiological mechanisms involved in excitation-contraction coupling of skeletal muscle may play a role herein.

On the other hand, the low glycogen approach seems promising with regard to the adaptive response following exercise. Therefore, low glycogen training may be useful as part of a well-thought out periodization program.

However, further research is needed to further scrutinize the role of low glycogen training in different groups e. highly trained subjects combined with different exercise protocols e. concurrent modalities , to develop a nutritional strategy that has the potential to improve skeletal muscle adaptations and performance with concurrent training.

Gibala MJ, Little JP, Macdonald MJ, Hawley JA. Physiological adaptations to low-volume, high-intensity interval training in health and disease. J Physiol. Article CAS Google Scholar. Bebout DE, Hogan MC, Hempleman SC, Wagner PD. Effects of training and immobilization on VO2 and DO2 in dog gastrocnemius muscle in situ.

J Appl Physiol CAS Google Scholar. Burelle Y, Hochachka PW. Endurance training induces muscle-specific changes in mitochondrial function in skinned muscle fibers. Article Google Scholar. Charifi N, Kadi F, Feasson L, Costes F, Geyssant A, Denis C.

Enhancement of microvessel tortuosity in the vastus lateralis muscle of old men in response to endurance training. Folland JP, Williams AG. The adaptations to strength training: morphological and neurological contributions to increased strength.

Sports Med. Cermak NM, Res PT, de Groot LC, Saris WH, van Loon LJ. Protein supplementation augments the adaptive response of skeletal muscle to resistance-type exercise training: a meta-analysis. Am J Clin Nutr. Coffey VG, Moore DR, Burd NA, Rerecich T, Stellingwerff T, Garnham AP, et al.

Nutrient provision increases signalling and protein synthesis in human skeletal muscle after repeated sprints. Eur J Appl Physiol. Cermak NM, van Loon LJ. The use of carbohydrates during exercise as an ergogenic aid.

Hawley JA, Burke LM. Carbohydrate availability and training adaptation: effects on cell metabolism. Exerc Sport Sci Rev. Bartlett JD, Hawley JA, Morton JP. Carbohydrate availability and exercise training adaptation: Too much of a good thing? Eur J Sport Sci.

Cox GR, Clark SA, Cox AJ, Halson SL, Hargreaves M, Hawley JA, et al. Daily training with high carbohydrate availability increases exogenous carbohydrate oxidation during endurance cycling. Hulston CJ, Venables MC, Mann CH, Martin C, Philp A, Baar K, et al. Training with low muscle glycogen enhances fat metabolism in well-trained cyclists.

Med Sci Sports Exerc. Morton JP, Croft L, Bartlett JD, Maclaren DP, Reilly T, Evans L, et al. Reduced carbohydrate availability does not modulate training-induced heat shock protein adaptations but does upregulate oxidative enzyme activity in human skeletal muscle.

Van Proeyen K, Szlufcik K, Nielens H, Ramaekers M, Hespel P. Beneficial metabolic adaptations due to endurance exercise training in the fasted state. Yeo WK, McGee SL, Carey AL, Paton CD, Garnham AP, Hargreaves M, et al. Acute signalling responses to intense endurance training commenced with low or normal muscle glycogen.

Exp Physiol. Yeo WK, Paton CD, Garnham AP, Burke LM, Carey AL, Hawley JA. Skeletal muscle adaptation and performance responses to once a day versus twice every second day endurance training regimens. Hansen AK, Fischer CP, Plomgaard P, Andersen JL, Saltin B, Pedersen BK. Skeletal muscle adaptation: training twice every second day vs.

training once daily. Cochran AJ, Myslik F, MacInnis MJ, Percival ME, Bishop D, Tarnopolsky MA, et al. Manipulating carbohydrate availability between twice-daily sessions of high-intensity interval training over two weeks improves time-trial performance. Int J Sport Nutr Exerc Metab.

Camera DM, Hawley JA, Coffey VG. Resistance exercise with low glycogen increases p53 phosphorylation and PGC-1alpha mRNA in skeletal muscle. Camera DM, West DW, Burd NA, Phillips SM, Garnham AP, Hawley JA, et al.

Low muscle glycogen concentration does not suppress the anabolic response to resistance exercise. Ortenblad N, Nielsen J, Saltin B, Holmberg HC.

Ortenblad N, Westerblad H, Nielsen J. Muscle glycogen stores and fatigue. Nielsen J, Holmberg HC, Schroder HD, Saltin B, Ortenblad N.

Human skeletal muscle glycogen utilization in exhaustive exercise: role of subcellular localization and fibre type. Nielsen J, Suetta C, Hvid LG, Schroder HD, Aagaard P, Ortenblad N. Subcellular localization-dependent decrements in skeletal muscle glycogen and mitochondria content following short-term disuse in young and old men.

Am J Physiol Endocrinol Metab. Duhamel TA, Perco JG, Green HJ. Manipulation of dietary carbohydrates after prolonged effort modifies muscle sarcoplasmic reticulum responses in exercising males. Am J Physiol Regul Integr Comp Physiol. van Loon LJ, Greenhaff PL, Constantin-Teodosiu D, Saris WH, Wagenmakers AJ.

The effects of increasing exercise intensity on muscle fuel utilisation in humans. Tsintzas K, Williams C. Human muscle glycogen metabolism during exercise. Effect of carbohydrate supplementation. Bergstrom J, Hultman E. A study of the glycogen metabolism during exercise in man.

Scand J Clin Lab Invest. Jacobs I, Kaiser P, Tesch P. Muscle strength and fatigue after selective glycogen depletion in human skeletal muscle fibers. Eur J Appl Physiol Occup Physiol. Blomstrand E, Saltin B. Effect of muscle glycogen on glucose, lactate and amino acid metabolism during exercise and recovery in human subjects.

Weltan SM, Bosch AN, Dennis SC, Noakes TD. Preexercise muscle glycogen content affects metabolism during exercise despite maintenance of hyperglycemia. Am J Physiol. Porcelli S, Ramaglia M, Bellistri G, Pavei G, Pugliese L, Montorsi M, et al. Aerobic fitness affects the exercise performance responses to nitrate supplementation.

Med Sci Sports Exerc ;47 8 — Stellingwerff T, Boit MK, Res PT, International Association of Athletics F. Nutritional strategies to optimize training and racing in middle-distance athletes.

J Sports Sci. Hawley JA. Adaptations of skeletal muscle to prolonged, intense endurance training. Clin Exp Pharmacol Physiol.

Petibois C, Cazorla G, Poortmans JR, Deleris G. Biochemical aspects of overtraining in endurance sports : the metabolism alteration process syndrome. Achten J, Halson SL, Moseley L, Rayson MP, Casey A, Jeukendrup AE.

Higher dietary carbohydrate content during intensified running training results in better maintenance of performance and mood state. MacDougall JD, Ray S, Sale DG, McCartney N, Lee P, Garner S. Muscle substrate utilization and lactate production.

Can J Appl Physiol. Katz A, Broberg S, Sahlin K, Wahren J. Leg glucose uptake during maximal dynamic exercise in humans. Koopman R, Manders RJ, Jonkers RA, Hul GB, Kuipers H, van Loon LJ. Intramyocellular lipid and glycogen content are reduced following resistance exercise in untrained healthy males.

Pascoe DD, Costill DL, Fink WJ, Robergs RA, Zachwieja JJ. Glycogen resynthesis in skeletal muscle following resistive exercise. Tesch PA, Colliander EB, Kaiser P. Muscle metabolism during intense, heavy-resistance exercise. Leveritt M, Abernethy PJ.

Effects of carbohydrate restriction on strength performance. J Strength Cond Res. Google Scholar. Mitchell JB, DiLauro PC, Pizza FX, Cavender DL.

The effect of preexercise carbohydrate status on resistance exercise performance. Int J Sport Nutr. Slater G, Phillips SM. Nutrition guidelines for strength sports: sprinting, weightlifting, throwing events, and bodybuilding. Burke LM, Hawley JA, Wong SH, Jeukendrup AE.

Carbohydrates for training and competition. Jeukendrup A. A step towards personalized sports nutrition: carbohydrate intake during exercise. Lambert CP, Flynn MG, Boone Jr JB, Michaud TJ, Rodriguez-Zayas J. Effects of carbohydrate feeding on multiple-bout resistance exercise.

Haff G, Schroeder C, Koch A, Kuphal K, Comeau M, Potteiger J. The effects of supplemental carbohydrate ingestion on intermittent isokinetic leg exercise.

J Sports Med Phys Fitness. Haff GG, Stone MH, Warren BJ, Keith R, Johnson RL, Nieman DC, et al. The effect of carbohydrate supplementation on multiple sessions and bouts of resistance exercise.

Kulik JR, Touchberry CD, Kawamori N, Blumert PA, Crum AJ, Haff GG. Supplemental carbohydrate ingestion does not improve performance of high-intensity resistance exercise.

Haff GG, Koch AJ, Potteiger JA, Kuphal KE, Magee LM, Green SB, et al. Carbohydrate supplementation attenuates muscle glycogen loss during acute bouts of resistance exercise. Margolis LM, Pasiakos SM. Optimizing intramuscular adaptations to aerobic exercise: effects of carbohydrate restriction and protein supplementation on mitochondrial biogenesis.

Adv Nutr. Jager S, Handschin C, St-Pierre J, Spiegelman BM. AMP-activated protein kinase AMPK action in skeletal muscle via direct phosphorylation of PGC-1alpha.

Proc Natl Acad Sci U S A. Psilander N, Frank P, Flockhart M, Sahlin K. Exercise with low glycogen increases PGC-1alpha gene expression in human skeletal muscle. Drake JC, Wilson RJ, Yan Z. Molecular mechanisms for mitochondrial adaptation to exercise training in skeletal muscle.

Faseb J. Mounier R, Theret M, Lantier L, Foretz M, Viollet B. Expanding roles for AMPK in skeletal muscle plasticity. Trends Endocrinol Metab. Canto C, Gerhart-Hines Z, Feige JN, Lagouge M, Noriega L, Milne JC, et al.

Wackerhage H. Molecular Exercise Physiology: An Introduction. Xiao B, Sanders MJ, Underwood E, Heath R, Mayer FV, Carmena D, et al. Structure of mammalian AMPK and its regulation by ADP. Carling D, Thornton C, Woods A, Sanders MJ. AMP-activated protein kinase: new regulation, new roles?

Horton, R. TErtujn, New York: Macmillan. Sherman WM. Metabolism of sugars and physical performance. Am J Clin Nutr. Kjaer M, Kiens B, Hargreaves M, Richter EA. Influence of active muscle mass on glucose homeostasis during exercise in humans.

Katz A, Broberg S, Sahlin K, Wahren J. Leg glucose uptake during maximal dynamic exercise in humans. Am J Physiol. Costill DL, Hargreaves M. Carbohydrate nutrition and fatigue.

Hermansen L, Hultman E, Saltin B. Muscle glycogen during prolonged severe exercise. Acta Physiol Scand. Coyle EF, Coggan AR, Hemmert MK, Ivy JL. Muscle glycogen utilization during prolonged strenuous exercise when fed carbohydrate.

J Appl Physiol. Coyle EF, Hagberg JM, Hurley BF, Martin WH, Ehsani AA, Holloszy JO. Carbohydrate feeding during prolonged strenuous exercise can delay fatigue. Coggan AR, Khort WM, Spina RJ, Bier DM, Holloszy JO. Endurance training decreases plasma glucose turnover and oxidation during moderate intensity in men J Appl Physiol.

Coggan AR, Coyle EF. Reversal of fatigue during prolonged exercise by carbohydrate infusion or ingestion. Maughan RJ, Greenhaff PL, Leiper JB, Ball D, Lambert CP, Gleeson M.

Diet composition and the performance of high-intensity exercise. J Sports Sci. Sahlin K, Katz A, Broberg S. Tricarboxylic acid cycle intermediates in human muscle during prolonged exercise. McConell G, Snow RJ, Proietto J, Hargreaves M. Muscle metabolism during prolonged exercise in humans: influence of carbohydrate availability.

Sherman WM, Wimer GS. Insufficient dietary carbohydrate during training: does it impair athletic performance?. Int J Sport Nutr. Snyder AC, Kuipers H, Cheng B, Servais R, Fransen E. Overtraining following intensified training with normal muscle glycogen.

Costill DL, Flynn MG, Kirwan JP, Houmard JA, Mitchell JB, Thomas R, Park SH. Effects of repeated days of intensified training on muscle glycogen and swimming performance. Kirwan JP, Costill DL, Flynn MG, Mitchell JB, Fink WJ, Neufer PD, Houmard JA.

Physiological responses to successive days of intense training in competitive swimmers. Lemon PWR, Mullin JP. Effect of initial muscle glycogen levels on protein catabolism during exercise. Tarnopolsky MA, Atkinson SA, Phillips SM, MacDougall JD.

Carbohydrate loading and metabolism during exercise in men and women. Eccentric exercise-induced muscle damage impairs muscle glycogen repletion. Costill DL, Pascoe DD, Fink WJ, Robergs RA, Barr SI, Pearson D.

Muecle Banned substances in professional sports you can use pretty adn anything you Carbohydrate-rich vegetables to fuel them, only glycogen will do if you musccle them to Carbs and muscle glycogen stores work. Glycogen musclle a large polysaccharide Pomegranate Snacks many branches, Carbss illustrated in the picture below. Polysaccharides are carbohydrates made up of simple sugars. Glycogen, in particular, is made up of many molecules of the monosaccharide glucose. The average person carries around about grams of glycogen when those two stores are filled and combined. It depends on many factors, like how much muscle you have, what your diet looks like, your fitness level, and your exercise habits.