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iii Repair-post-exercise ingestion of high-quality protein and creatine monohydrate benefit the tissue growth and repair; and iv Rest-pre-sleep nutrition has a restorative effect that facilitates the recovery of the musculoskeletal, endocrine, immune, and nervous systems. Recommended carbohydrate intake.

Intake of Carbohydrate ingestion attenuates the inflammatory response to acute exercise through reduced levels of IL-6, total anti-inflammatory IL-1RA, and cortisol.

kg-1 BM each 2 hours , particularly of high glycemic index carbohydrate foods, leading to a total intake over 24 hours of g. kg-1 BM.

early intake of carbohydrate after strenuous exercise is valuable because it provides an immediate source of substrate to the muscle cell to start effective recovery, as well as taking advantage of a period of moderately enhanced glycogen synthesis.

Therefore, strategies that promote carbohydrate availability, such as ingesting carbohydrate before, during and after exercise, are critical for the performance of many sports and a key component of current sports nutrition guidelines. Providing these carbohydrates in the form of glucose—fructose sucrose mixtures does not further enhance muscle glycogen repletion rates over glucose polymer ingestion alone.

After exercise, the body is primed for muscle glycogen resynthesis and the repair of muscle damage. Millard-Stafford , p. Carbohydrate supplementation has the strongest scientific support, and reduces post-exercise stress hormone levels, inflammation, fatty acid mobilization and oxidation.

after the event to optimize post-event repletion of endogenous carbohydrate stores. This review summarizes the current knowledge about the effects of glycogen availability on skeletal muscle adaptations for both endurance and resistance exercise.

Furthermore, it describes the role of glycogen availability when both exercise modes are performed concurrently. Roughly, exercise can be divided in endurance- and resistance exercise.

Endurance exercise can be further subdivided in traditional -endurance exercise and high intensity interval training HIIT. Traditional endurance exercise is characterized by continues submaximal muscular contractions aimed at improving aerobic power production.

Whereas high intensity interval training primarily consists of brief, intermittent bursts of vigorous movements, alternated by periods of rest or low-intensity movements with the purpose to improve both aerobic and anaerobic power production [ 1 ].

The skeletal muscle adaptations are determined by the type, intensity and duration of the performed exercise. In short, endurance exercise training mainly results in mitochondrial biogenesis, increases capillary density and enzymes leading to enhanced skeletal muscle O 2 utilization capacity [ 2 — 4 ].

In contrast, resistance exercise promotes skeletal muscle hypertrophy and strength through increases in myofibrillar volume predominantly in type II fibers [ 5 , 6 ]. It is now widely accepted that nutrition plays an important role in mediating skeletal muscle adaptations [ 7 ].

Carbohydrates and fat are recognized as the main substrates for powering prolonged muscle contractions during endurance exercise [ 8 ]. Although carbohydrates are widely accepted as fuel for skeletal muscle both during [ 8 ] and following endurance exercise [ 8 ], recent investigations introduced a novel approach of exercising with reduced glycogen levels aimed to optimize skeletal muscle adaptations [ 9 , 10 ].

Indeed, several studies have reported that endurance exercise with low glycogen availability may be a strategy to augment the response in exercise-induced signaling associated with improved oxidative capacity [ 11 — 17 ], and potentially enhance exercise performance [ 17 , 18 ].

In contrast, the effects of low glycogen availability on muscular adaptations following resistance exercise remain somewhat unclear. A recent study revealed that performing resistance exercise with low glycogen could improve acute signaling processes that promote mitochondrial biogenesis to a larger extent compared to exercise with normal glycogen levels [ 19 ], whereas another study demonstrated that muscle protein synthesis following a single bout of resistance exercise appeared to be unaffected by the level of glycogen [ 20 ].

A literature review concerning the role of glycogen availability for both endurance- and resistance exercise on skeletal muscle adaptations is at this time absent. Therefore, the purpose of this review is to identify the effects of glycogen availability on skeletal muscle training adaptations and performance with both endurance- and resistance exercise.

Firstly, the role of glycogen in local skeletal muscle fatigue and energy metabolism will be described. Thereafter, the effects of glycogen availability on performance and markers of skeletal muscle adaptations are discussed.

Finally, this review addresses the role of glycogen availability when both exercise modes are performed concurrently. Moreover, it appears that subsarcolemmal, intermyofibrillar and intramyofibrillar glycogen powers different mechanisms in muscle contractions. Intramyofibrillar glycogen is preferably depleted during high-intensity exercise and seems to power cross-bridge cycling [ 23 ].

Moreover, depletion of this form highly correlates well with skeletal muscle fatigue [ 24 ]. Reduction of intramyofibrillar glycogen might decrease Na, K-ATPase activity leading to decreased ATP cleavage, and subsequently a lower energy production to power cross-bridge cycling [ 22 ].

Moreover, Duhamel et al. In another study by Ortenblad et al. Based on SR vesicle experiments Ortenblad et al. Moreover, Ortenblad et al. Taken together, the aforementioned findings at both the whole-body and organelle level suggest that the location of the glycogen, especially the intramyofibrillar pool, is important to sustain repeated muscle contractions.

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.

Although the amount of liver and skeletal muscle glycogen is relatively small compared to endogenously stored fat, glycogen is recognized as the major source for fuel during prolonged moderate- to high intensity endurance exercise [ 27 ].

Therefore, glycogen availability is essential to power ATP resynthesis during high intensity exercise which relies heavily on glycogenolysis. Furthermore, it has been well documented that the capability of skeletal muscle to exercise is impaired when the glycogen store is reduced to a certain level, even when there is sufficient amount of other fuels available [ 28 ].

Together, prolonged endurance exercise leads to muscle glycogen depletion, which is in turn linked to fatigue and makes it difficult to meet the energetic requirements of training and competition [ 22 , 29 ]. Low-glycogen availability causes a shift in substrate metabolism during and after exercise [ 30 , 31 ].

In addition, low-glycogen availability induces an increase in systemic release of amino acids and simultaneously increases fat oxidation, and as a consequence exercise intensity drops [ 30 ].

However, the low-glycogen approach seems to promote expression of genes that stimulate fat catabolism and mitochondrial biogenesis and as such improves oxidative capacity [ 10 ]. To date, few studies have found an improved training-induced performance effect of conducting the exercise bouts with low glycogen levels compared with replenished glycogen levels [ 17 , 18 ].

Hansen et al. In their study seven untrained males completed a week training program. Although the total amount of work was the same for each leg, one leg was trained in a glycogen depleted manner, while the contralateral leg was trained with full 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.

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This allows the athlete to start the cycle 9 days prior to competition and still allow 6 days of recovery before the event. A typical glycogen supercompensation cycle would look something like this:. The vigorous exercise should use the same muscles that are going to be used during the competition since it is these muscles that will be depleted and supercompensated.

In other words, if you are a runner you carbohydrate deplete by running. If you are a cyclist you carbohydrate deplete by cycling.

Most of the carbohydrate consumption on day 1 of the high carbohydrate phase should be simple sugars and intake should not exceed 25 grams per hour or 75 grams every three hours.

Carbohydrates should be consumed at least every three hours so that continual glycogen synthesis is occurring. If, as Conlee speculated 4 , some muscle fibers are completely glycogen depleted by high power performances and subsequently are incapable of contributing, one might speculate that power athletes could benefit by glycogen supercompensation.

For many athletes, however, actual performance during competition would not be enhanced by supraphysiological levels of glycogen. For weightlifters, for example, performance is related to the ability to produce force and not the ability to maintain force output over time.

Although glycogen loading can delay the reduction in force output during repeated maximal contractions 14 , no study to date has shown that maximal force production can be enhanced by supraphysiological concentrations of glycogen.

The same logic applies to jumpers and throwers. For high power events lasting less than 10 seconds m sprint the majority of the energy comes from stored Adenosine Triphosphate and Creatine Phosphate with little contribution from carbohydrates Brooks and Fahey For high power events lasting longer than 2 minutes performance is limited by the cardiovascular system Based on these facts and the Heighenhauser study mentioned earlier 30 seconds of maximal pedaling , one might speculate that glycogen supercompensation might be useful for high power events lasting between 10 seconds and two minutes.

However, there is an important distinction between power tests and other 30 second events like a m dash. In a power test power peaks early because subjects are pedaling maximally from the start.

During all but the shortest sprinting events there is some degree of pacing. It is not known if pacing would affect the relationship of glycogen to fatigue during these events.

In addition, no study to date has shown an actual increase in performance in sprinting events either bike, run or swim sprints due to glycogen supercompensation. Also, in some power events, like weightlifting and sprinting, extra bodyweight can be a liability.

Although they should maintain an adequate carbohydrate intake to prevent a decrement in performance, there is no strong evidence to suggest that power athletes would benefit from glycogen supercompensation prior to competition.

Since training can involve repeated high power performances repeated sprints, or sets one might speculate that glycogen supercompensation might be an effective training aid. While training performance might benefit from high concentrations of muscle glycogen, athletes cannot glycogen deplete and supercompensate prior to every training session.

An apparent increase in muscle mass is certainly a bonus for bodybuilders. Therefore, successfully glycogen supercompensating can certainly be a worthwhile process for these athletes.

Since bodybuilders have much more muscle mass than the average person, larger carbohydrate intakes are likely to be required to maximize glycogen synthesis. Since we are trying to maximize glycogen supercompensation in all muscles, we must glycogen deplete all muscles.

This is accomplished by performing high repetition, high volume workouts for all body parts while on a low carbohydrate diet prior to glycogen loading. A typical regimen might look like this:. The bodybuilder should be training the entire body over the three-day period with a large volume of high repetition exercises to enhance glycogen depletion.

It is the total volume of work that will determine the degree of glycogen depletion so rest between sets should be adequate to allow a large volume of work to be performed. Bodybuilders should avoid lifting very heavy as high force eccentric contractions have been shown to interfere with glycogen synthesis 15 probably due to muscle microdamage.

Additionally Doyle et al. Although the bodybuilder might not normally train three days in a row, it is recommended in this case. This prevents the bodybuilder from having to remain on a low carbohydrate diet for more than three days.

Determining the amount of carbohydrates that should be consumed will require some trial and error but the research literature might provide some clues. A study by Pascoe et al. If you know the molecular weight of glucose and can convert mmol to grams and if we assume that each gram of glycogen is stored with 3 grams of water this would give us a value of approximately.

If we match carbohydrate intake to the glycogen synthesis rate this would equal 43 grams per hour for a pound bodybuilder kg and a total of approximately g Calories from carbohydrates in a 24 hour period. Glycogen replenishment is very rapid for six hours after high intensity exercise 11 and glycogen concentrations can return to baseline levels within this six hour period if adequate carbohydrates are consumed supercompensation occurs in the days that follow.

Therefore providing a bolus as Ivy suggested might speed up the process relative to consuming a predetermined number of grams every 3 hours.

On day 1 most of the carbohydrates should be in the form of simple sugars to enhance glycogen uptake. The degree of glycogen supercompensation can be estimated by the amount of weight gain. Recall that each gram of glycogen is stored with 3 grams of water.

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Accessed 27 May Download references. This supplement is supported by the Gatorade Sports Science Institute GSSI. The supplement was guest edited by Lawrence L. Spriet, who convened a virtual meeting of the GSSI Expert Panel in October and received honoraria from the GSSI, a division of PepsiCo, Inc.

Dr Spriet received no honoraria for guest editing the supplement. Dr Spriet suggested peer reviewers for each paper, which were sent to the Sports Medicine Editor-in-Chief for approval, prior to any reviewers being approached.

Dr Spriet provided comments on each paper and made an editorial decision based on comments from the peer reviewers and the Editor-in-Chief. Where decisions were uncertain, Dr Spriet consulted with the Editor-in-Chief.

The views expressed in this article are those of the authors and do not necessarily reflect the position or policy of PepsiCo, Inc. School of Sport, Exercise and Rehabilitation Sciences, College of Life and Environmental Sciences, University of Birmingham, Birmingham, UK.

You can also search for this author in PubMed Google Scholar. Correspondence to Gareth A. Both TP and GAW planned, wrote and revised the manuscript.

Both authors also read and approved the final manuscript. This article is based on a presentation by Gareth Wallis to the GSSI Expert Panel in October An honorarium for preparation of this article was provided by the GSSI. No other sources of funding were used to assist in the preparation of this article.

and Volac International Ltd. Tim Podlogar has no conflicts of interest of potential relevance to the content of this review. Open Access This article is licensed under a Creative Commons Attribution 4.

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Reprints and permissions. Podlogar, T. New Horizons in Carbohydrate Research and Application for Endurance Athletes. Sports Med 52 Suppl 1 , 5—23 Download citation. Accepted : 11 August Published : 29 September Issue Date : 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. Download PDF. Abstract The importance of carbohydrate as a fuel source for exercise and athletic performance is well established. Influence of Resistance Training Proximity-to-Failure on Skeletal Muscle Hypertrophy: A Systematic Review with Meta-analysis Article Open access 05 November A Perspective on High-Intensity Interval Training for Performance and Health Article Open access 07 October Impact of a short-term nitrate and citrulline co-supplementation on sport performance in elite rowers: a randomized, double-blind, placebo-controlled crossover trial Article Open access 10 February Use our pre-submission checklist Avoid common mistakes on your manuscript.

FormalPara Key Points Athletes should apply a periodized approach to nutrition to ensure dietary carbohydrate intake matches the carbohydrate demand of training or competition. Table 1 Suggested areas for investigation to enhance understanding of the role of carbohydrates in the diet of athletes Full size table.

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