Modest Glycogen Depletion May Impact Lifting Performance More Than You Think

Some fitness professionals have questioned the importance of dietary carbohydrate, given that resistance training only depletes 24-40% of muscle glycogen. New data suggest that small reductions in muscle glycogen might have bigger performance impacts than once thought. Read on to learn about some very important carbohydrate research.

This article was first published in MASS Research Review and is a review and breakdown of a recent study. The study reviewed is Subcellular Localization- and Fibre Type-Dependent Utilization of Muscle Glycogen During Heavy Resistance Exercise in Elite Power and Olympic Weightlifters by Hokken et al. (2020)

Key Points

  1. The presently reviewed study (1) sought to evaluate the effects of a high-volume resistance training session on localized depletion of distinct muscle glycogen storage depots in type 1 and type 2 muscle fibers.
  2. Total muscle glycogen only decreased by about 38%, but type 2 fibers were depleted far more than type 1 fibers. In type 2 fibers, intramyofibrillar stores dropped by -54%, and 48% of the fibers had very substantial intramyofibrillar glycogen depletion.
  3. Localized glycogen depletion in the intramyofibrillar storage depots can probably start impairing performance at fairly modest levels of whole-muscle glycogen depletion. That’s a pretty big deal for discussions about optimal carbohydrate intake for lifters.

 The last decade or so has been tough for carbohydrates. Back in the 1980s, things were much simpler; dietary fat was vilified for its purported impact on blood lipids and cardiovascular disease risk, and high-carb diets were heavily promoted for the general population and athletes alike. A key focus of the sports nutrition field was focused on glycogen replenishment strategies, as carbs were universally acknowledged as the primary fuel for moderate-to-high intensity exercise. More recently, low-carbohydrate diets have become more and more common among athletes, and specifically among strength and physique athletes. Even extremely low-carb diets, such as ketogenic and carnivore diets, have been embraced by some. One thing that has facilitated the resurgence of low-carb diets for lifters has been a body of literature indicating that a single resistance training session fails to fully deplete muscle glycogen levels. A variety of studies have shown only ~24-40% reductions in muscle glycogen content following resistance training, even when fairly strenuous, high-volume protocols have been employed (2345). This has led to suggestions that traditional resistance training isn’t that glycogen-dependent, most lifters probably have plenty of glycogen left in the tank at the end of their workouts, and carbs aren’t that critical for the maintenance of lifting performance.

This line of thinking overlooks a critical detail about glycogen storage: glycogen particles are stored in multiple distinct compartments within muscle, and different storage depots have different impacts on muscle function and fatigue (6). Total muscle glycogen can be divided up into intramyofibrillar glycogen (located within the myofibrils, mostly near the z-line), intermyofibrillar glycogen (located between the myofibrils), and subsarcolemmal glycogen (located just beneath the sarcolemma). If you’d like to see a visual depiction of these distinct storage depots, check out the images presented in Figure 2 of this open access paper. It appears that intramyofibrillar glycogen most directly relates to muscular fatigue development via impairment of calcium release from sarcoplasmic reticula. So, the current study aimed to assess the effects of high-volume resistance exercise on the utilization of glycogen from various storage depots in competitive male powerlifters and Olympic weightlifters. Results indicated that using typical biochemical assessment methods, whole-muscle glycogen decreased by only 38%. While only intermyofibrillar glycogen dropped substantially in type 1 muscle fibers, all three storage depots were markedly reduced in type 2 fibers, and a decent number of type 2 fibers had almost full depletion of intramyofibrillar glycogen after exercise. Perhaps the biggest implication of these findings is that we can’t simply view glycogen as a “gas tank”; distinct glycogen stores are depleted in a non-uniform manner, and total muscle glycogen content is probably a poor indicator of the risk of performance impairment due to glycogen depletion. We never want to place too much confidence in a small collection of studies, but the evidence for the importance of localized glycogen depletion is mounting. While this finding doesn’t necessarily mean that every lifter needs to adopt a super-high-carb diet, we can no longer assert that lifting-induced glycogen reductions are universally negligible in magnitude, and this will probably influence the way we collectively discuss carbohydrate recommendations for lifters moving forward. Read on to get more details about what these results mean for carbohydrate intake in lifters.

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Purpose and Hypotheses


The presently reviewed study sought to quantify the effects of a high-volume resistance training session on localized depletion of distinct muscle glycogen storage depots in type 1 and type 2 muscle fibers.


The researchers hypothesized that high-volume resistance exercise would lead to different patterns of localized glycogen depletion in specific storage depots and fiber types. Based on the introduction section, it seems safe to infer that they were specifically expecting to see some functionally relevant depletion of the intramyofibrillar storage depot, which has been linked to acute muscular fatigue in previous research.

Subjects and Methods


10 competitive male powerlifters and Olympic weightlifters completed this study. Based on their self-reported 1RMs and years of training experience, it sounds like these participants were pretty solid lifters. Their relevant demographic data are presented in Table 1.


The methods for this study are very intricate, but we can hit the highlights by focusing on a couple simple focus areas: what’s being measured, and what’s being manipulated. On the measurement side, we’re talking about muscle glycogen levels. In many of the previous glycogen depletion studies in this area, the researchers look at estimates of whole-muscle glycogen levels via biochemical analysis of tissue homogenate. They basically take a sample of muscle tissue, grind it up, and see what the glycogen concentration of the ground up muscle tissue is. This precludes them from distinguishing between type 1 and type 2 fibers, let alone distinguishing between distinct glycogen storage depots. In the presently reviewed study, the researchers used this method to take a quick look at overall glycogen depletion, but they also used a more advanced method with microscopic examination of intact samples of muscle tissue (quantitative transmission electron microscopy), which allows them to look at differences between muscle fiber types and specific depots of glycogen storage.

On the manipulation side, the researchers were specifically focused on determining how resistance training impacted glycogen depletion patterns. Participants arrived for testing after an overnight fast and were provided a standardized pre-exercise meal 60-90 minutes prior to a standardized bout of resistance training. The meal provided about 560kcal, with a macronutrient breakdown of 45% carbohydrate, 26% protein, and 29% fat. The exercise session began with some light warmups, followed by three exercises that were intended to target the lower body musculature (since glycogen levels were being assessed using vastus lateralis tissue samples). The workout consisted of back squats (done in accordance with International Powerlifting Federation standards), deficit deadlifts from a 10cm platform, and dumbbell split squats with the rear foot elevated on a standard bench. The exercise bout was designed to last around 70-90 minutes in total, and working sets were performed in rep ranges spanning from 5-12 repetitions per set with loads ranging from 60-75% of self-reported 1RM. A quick overview of the exact exercises, set and repetition schemes, and approximate loads is presented in Table 2. Mean intensity for working sets of back squat and deficit deadlift were 74% and 71%, respectively. During their four sets of split squats, participants were instructed to aim for an RPE of about 8-9 (on a 10-point reps in reserve-based RPE scale) while completing 12 reps per set. Participants rested for 3-6 minutes between sets of squats and deadlifts, and 1-2 minutes between sets of split squats. In order to assess changes in muscle glycogen, muscle biopsies were obtained about 5-10 minutes prior to the onset of exercise and immediately (2-5 minutes) after finishing the exercise session.

In terms of outcome variables, the researchers were primarily interested in assessing total muscle glycogen depletion, fiber-specific glycogen depletion, and location-specific depletion of glycogen from the distinct storage depots within muscle tissue (intramyofibrillar glycogen, intermyofibrillar glycogen, and subsarcolemmal).  


As one would expect, muscle glycogen concentrations decreased and muscle lactate concentrations increased in response to the training bout. Using biochemical methods, total muscle glycogen decreased by about 38%. Using the more intensive method of glycogen quantification (transmission electron microscopy), they were also able to look at distinct, localized glycogen storage depots in type 1 and type 2 muscle fibers. Expressed as a percentage of total muscle glycogen content, intermyofibrillar glycogen was the largest storage depot, accounting for about 80% of total muscle glycogen. The relative percentage of total muscle glycogen contained within each localized storage depot (intramyofibrillar, intermyofibrillar, and subsarcolemmal) is presented below in Table 3.

In response to the exercise bout, glycogen stores were depleted in a non-uniform manner. When expressed as a percentage in Table 2, the non-uniformity is hard to see, but it becomes more apparent when you look at the raw data and the depot-specific changes from pre-exercise to post-exercise. In type 1 fibers, a significant reduction in intermyofibrillar glycogen was observed (-33%; p < 0.001). While reductions were also observed in the intramyofibrillar (-20%) and subsarcolemmal (-8%) depots of type 1 fibers, these changes were not statistically significant (p = 0.30 and p = 0.51, respectively). In type 2 fibers, statistically significant reductions (p < 0.001) were observed in all three storage depots. Intermyofibrillar stores dropped by -48%, intramyofibrillar stores dropped by -54%, and subsarcolemmal stores dropped by -47%. An interesting observation was that many (48%) of the type 2 fibers demonstrated very substantial depletion of intramyofibrillar glycogen, with post-exercise levels <2 μm3 μm−3 103, whereas such extreme depletion of intramyofibrillar glycogen was far less common in type 1 fibers. The raw changes for each glycogen storage depot within type 1 and type 2 muscle fibers are presented in Figure 1.

The researchers also reported an interesting observation related to the orientation of glycogen storage in the most depleted fibers. In the super-depleted type 2 fibers, the researchers found some crystal-like glycogen structures. These structures were not observed nearly as frequently in type 1 fibers or in fibers with less substantial levels of glycogen depletion. It’s thought that these crystal-like structures bind metabolic enzymes to enhance the initiation of glycogen resynthesis, but they are poorly understood at this time. Since we don’t know much about the practical implications of these crystal-like glycogen structures, I won’t discuss them further in the current article.


I try not to be hyperbolic when discussing new research. If anything, I think I tend to lean a little too hard in the other direction, often opting for a “wait and see” conclusion rather than confidently overstating the impact and utility of new findings. However, I think this is one of the more important papers I’ve seen in recent years, in terms of its potential impact on the way we discuss carbohydrate feeding strategies. It’s very common to see notable figures in the evidence-based fitness and sports nutrition worlds undermine the importance of dietary carbohydrate, primarily based on the fact that prior studies show only 24-40% glycogen reduction in response to single bouts of resistance training (2345). The implied justification is that glycogen depletion induced by traditional resistance training is negligible in magnitude, because lifters still have plenty of stored glycogen to burn through before full depletion occurs and performance is impacted. The current findings cast heavy doubts on this line of thinking and its default justification. To be clear, this isn’t the cathartic practice of seeking out low-hanging fruit and disproving the blatantly wrong assertions made by ill-informed influencers and heavily biased charlatans. We’re talking about claims made by the cream of the crop in the sports nutrition and evidence-based fitness communities; authority figures who do rigorous work and rightfully command a great deal of respect in the area. So, these findings are important, not because they bust a myth that the evidence-based fitness world already abandoned long ago, but because they have potential to shift the high-level, nuanced discussions about dietary carbohydrate moving forward. These results don’t necessarily imply that lifters need to carb-load before each training session as if they’re about to run a marathon, but they suggest that modest glycogen depletion from traditional resistance training could be more impactful than once thought, and that lifters in certain scenarios (e.g., carb restriction, energy restriction, and high-frequency training) might want to shift a little more attention toward mindfully replenishing muscle glycogen in a strategic manner.

Let’s take a look at the evidence that is most commonly used to undermine the importance of dietary carbohydrate for lifters. Tesch et al (5) studied the glycogen-depleting effect of a pretty rigorous exercise bout including five sets each of front squats, back squats, leg presses, and knee extensions. All sets were taken to failure, with somewhere between 6-12 reps per set. After this exercise protocol, total muscle glycogen was significantly reduced; the text of the paper says glycogen dropped by 40%, but my calculations indicate that it was closer to 26%, so I’m not sure what explains the discrepancy there. The post-exercise mean value was 26% lower than the pre-exercise mean value, but it’s possible that they calculated the relative glycogen reduction (as a percentage) within each individual participant, and the average drop was 40% at the individual level. Pascoe and colleagues (4) used an exercise protocol consisting of numerous sets of six leg extensions using 70% of 1RM, with 30 seconds of rest between sets. Participants completed an average of 8.8 sets before reaching failure, and glycogen was depleted by about 29-33%. In a study by MacDougall et al (3), participants completed sets of bicep curls to failure using 80% of 1RM. One set to failure depleted muscle glycogen by 12%, whereas three sets to failure depleted muscle glycogen by 24%. Koopman et al (2) utilized an exercise protocol consisting of 8 sets of 10 on the leg press machine and 8 sets of 10 on the leg extension machine using 75% of 1RM. Whole-muscle glycogen was reduced by 33%, which included 23%, 40%, and 44% reductions in type 1, type 2a, and type 2x fibers, respectively. Finally, Roy and Tarnopolsky (7) assessed muscle glycogen depletion following a full-body workout. While participants completed six upper-body exercises, muscle glycogen was assessed in the vastus lateralis, so the most relevant components of the exercise protocol were three sets of leg extensions, three sets of leg press, and three more sets of leg extension at the end of the workout. All sets consisted of approximately 10 repetitions using 80% of 1RM, and the protocol resulted in a muscle glycogen reduction of approximately 36%. This is by no means an exhaustive list of the studies measuring glycogen reductions following resistance exercise, but it’s a fairly representative list, and the majority of the literature indicates that approximately 24-40% depletion is typically observed, with the magnitude most closely related to the volume of exercise completed (1).

There are two reasons why I love the exercise protocol in the presently reviewed study. First, I think it’s a solid approximation of how many lifters actually train, which gives us some bonus points for ecological validity. The fact that the study was actually conducted in well-trained, competitive lifters is all the better. More importantly (in my opinion), this exercise protocol generally replicates the total degree of whole-muscle glycogen depletion observed in the previous glycogen depletion studies I just outlined. That’s really convenient, because it gives us a decent approximation of how extensive the localized depletion of each specific glycogen storage depot was likely to be in the previous research documenting similar magnitudes of whole-muscle glycogen depletion. With 38% total muscle glycogen depletion observed, the presently reviewed study is at the higher end of the range, but definitely within the same ballpark. Taken together, this small collection of studies suggests that pretty realistic resistance training protocols are able to induce fairly modest depletion of whole-muscle glycogen content, which is sufficient to markedly reduce the storage of intramyofibrillar glycogen. In fact, as depicted in Figure 1, this exercise bout was able to induce extremely low intramyofibrillar glycogen levels in about half of the type 2 muscle fibers measured.

There is a fairly large hurdle to clear before these findings can actually be applied in practical settings. The presently reviewed study shows that glycogen depletion occurs in a localized, non-uniform manner, with particularly notable depletion occurring in the intramyofibrillar area of type 2 muscle fibers. But to translate that to practical application, we need to know whether or not that intramyofibrillar depletion actually translates to acute fatigue or impaired contractile function of muscle. As summarized in a recent review paper by Alghannam et al (8), I think you can make a strong case that we have the evidence to support this translation. In section 2.1 of the paper by Alghannam and colleagues, they summarize the body of literature as it currently stands (by the way, the body of literature was almost entirely produced by the authors of the presently reviewed study over the last 10+ years). Over a series of studies, this research group has demonstrated that reduced intramyofibrillar glycogen levels are associated with impaired calcium release from sarcoplasmic reticula, which appears to increase muscle fatigue and alter muscle contractility (68). One of the largest sources of ATP consumption during muscle contraction is the sarcoplasmic reticulum-calcium-ATPase enzyme, and the sodium-potassium-ATPase enzyme is another notable ATP consumer. These enzymes depend on locally available glycogen as a major source of energy, which helps elucidate a mechanistic link between intramyofibrillar glycogen depletion, sarcoplasmic reticulum calcium kinetics, and muscle fatigue (6).

While that evidence has largely come from highly mechanistic studies with limited ecological validity, the same research group has translated their line of research to real-world studies in athletic populations. In trained triathletes, this group demonstrated that a large reduction in whole-muscle glycogen content (induced by prolonged cycling) was associated with a significant reduction in sarcoplasmic reticulum calcium release (9). Four hours after the exercise bout, glycogen levels and calcium release were markedly restored by post-exercise carbohydrate ingestion, but remained suppressed when post-exercise carbohydrate was restricted. They reported similar findings in trained cross-country skiers (10), but took the study a step further by specifically assessing localized glycogen depots. While the R2 value wasn’t particularly high, intramyofibrillar glycogen was the only glycogen depot that was significantly correlated (R2 = 0.23, p = 0.04) with calcium release rate in the sarcoplasmic reticula. With any line of research, you prefer to see a huge body of evidence with numerous different lab groups replicating each others’ work, but that might be hard to come by with this topic. This is pretty labor- and resource-intensive research that involves intricate methods and specialized equipment, so we aren’t likely to see a huge wave of quickly conducted studies pouring out from several laboratories over the next few months. However, for the time being, I think these researchers have made a strong case for the idea that intramyofibrillar glycogen is particularly important, and can become depleted to a practically meaningful degree in response to resistance exercise when only modest whole-muscle glycogen depletion is observed.

While I think these findings are both cool and important, I don’t want to overstate their impact on day-to-day carbohydrate feedings strategies. Back in the 1990s and early 2000s, it seemed like a lot of lifters were pretty fond of micromanaging their carbohydrate timing, and unnecessarily so. These findings do not suggest that the typical lifter needs to return to those old habits of stressing over rapid post-exercise consumption of a carbohydrate source with the perfect molecular weight, glycemic load, monosaccharide composition, and molecular configuration. Similarly, these findings do not suggest that all lifters need to adopt a super-high-carb diet. If you’re eating near (or above) maintenance calories, utilizing a moderate- or high-carb diet (let’s say, ≥40% of calories coming from carbohydrate), and resting at least 24 hours between high-intensity exercise bouts with the same muscle group, you probably don’t have to worry too much about glycogen levels. In these circumstances, most lifters will probably have adequate glycogen replenishment by simply consuming at least 3-4g/kg per day of carbohydrate per day (11), given the typical rate of glycogen replenishment in the presence of adequate carbohydrate availability (8). However, if you’re in a big energy deficit, utilizing a low-carbohydrate diet, or performing multiple glycolytic exercise bouts with the same muscle group in a 24-hour period, glycogen replenishment could potentially be an influential factor impacting your training capacity and performance. As the presently reviewed results suggest, even modest whole-muscle glycogen depletion from traditional resistance exercise can induce a notable reduction of intramyofibrillar glycogen content in type 2 fibers, which could negatively impact performance in the absence of replenishment. It’s become increasingly common for lifters to overlook the potential benefits of targeted glycogen replenishment in glycogen-limiting scenarios, largely driven by the assumption that near-maximal glycogen replenishment is unnecessary for traditional resistance training that fails to fully deplete glycogen stores. The results of the presently reviewed study cast major doubts on that logic and highlight the potential benefits of making room for carbs in the typical lifter’s diet, along with the need for focused glycogen replenishment in special scenarios that threaten adequate glycogen replenishment.

Earlier this year, Dr. Helms and I published a review paper about bodybuilding nutrition guidelines with Dr. Brandon Roberts and Dr. Peter Fitschen (12). When discussing macronutrient distribution, we acknowledged the obvious challenge faced by lean people that are trying to get leaner: calories get low, and something’s got to give. We generally advocated for an approach that most would classify as low-fat, in order to free up calories for the protein-sparing effects of protein and the performance-preserving effects of carbohydrate. In light of the presently reviewed findings, I’m feeling even more confident that keeping carbohydrate intake as high as feasibly possible (without slowing the rate of fat loss) is a generally advisable strategy for lifters navigating a caloric deficit. Of course, there are circumstances in which other preferences or considerations may lead you to opt for an alternative dietary strategy, but a focused effort toward muscle glycogen maintenance seems like an ideal “default” approach for lifters on lower-calorie diets. In addition, we have previously discussed some of the underwhelming effects of various ketogenic dieting strategies on strength and hypertrophy when compared to higher-carbohydrate approaches (herehere, and here). When interpreting those findings, I highlighted evidence showing that ketogenic diets can impair high-intensity, glycogen-dependent exercise performance. Ketogenic diets have also been shown to reduce muscle glycogen stores by up to 47% in athletes (cyclists) that are regularly training (13). In light of the presently reviewed findings, it seems defensible to infer that such a large degree of total muscle glycogen depletion is likely to involve notable depletion of the intramyofibrillar glycogen stores (which are closely linked to muscle contractile function) in people who regularly exercise. To be extremely clear, I am not suggesting that lifters have no justifiable applications of low-carbohydrate diets. Maintenance of glycolytic exercise performance is just one factor to consider when selecting a diet, along with essential nutrient intake, satiety management, muscle protein accretion, cooking and flavor preferences, and a variety of other considerations. Nonetheless, modest glycogen reductions that were once assumed to be benign might materially impact performance, so eating sufficient carbohydrates to replenish glycogen stores to a maximal (or near-maximal) level should probably be viewed as a relatively high dietary priority for lifters.

Next Steps

Over the last 10-15 years, our understanding of glycogen has changed pretty significantly, in large part thanks to the efforts of this research group. I think they’ve made a strong case that even modest whole-muscle glycogen depletion can result in practically relevant depletion of intramyofibrillar glycogen stores. Moving forward, I’m excited to see future studies shift the conversation from mechanisms to practical application. For example, I’d like to see the magnitude by which the observed degree of intramyofibrillar glycogen depletion impairs maximal strength and strength endurance. I’d also like to see exactly what kind of nutritional interventions are required to replenish intramyofibrillar glycogen enough to fully restore performance. I don’t anticipate future research indicating that all lifters need to go on extraordinarily high-carbohydrate diets or implement extreme glycogen replenishment protocols; after all, the observed magnitude of glycogen depletion is far greater in long-duration endurance events than traditional resistance training, and many lifters have multiple days of recovery between training sessions involving the same muscle group. However, the increasingly popular argument that lifters can largely ignore carbs due to incomplete depletion of whole-muscle glycogen doesn’t seem to hold up, and we need some applied research to tell us how low is too low for maintaining sufficient intramyofibrillar glycogen storage.  

Application and Takeaways

In many cases, it can be hard to draw practical conclusions from research that is more focused on biochemical changes or mechanistic observations than applied outcomes. However, the presently reviewed study leaves us with some pretty noteworthy takeaways that can probably inform how we discuss carbohydrate feeding strategies. People in the fitness industry often discuss glycogen storage as if it’s a gas tank; if something depletes glycogen levels by 30%, they’d say we can handle two more drops of that magnitude before we start getting nervous. As the research about non-uniform glycogen depletion continues to evolve, we need to have more nuanced discussions about carbohydrate feeding, and we should probably start focusing more on staying near 100% glycogen storage than staying away from 0%. I don’t think this research meaningfully alters our perspective on day-to-day carbohydrate timing for most lifters; as long as you’re not training the same muscle group twice within a single day and your daily carb intake is reasonably matched with your activity level, glycogen resynthesis shouldn’t be a limiting factor. However, it’s common to see people argue that carbs are dramatically overrated for lifters because whole-muscle glycogen concentrations are “only” reduced by 24-40% in response to resistance training. It’s probably time to retire (or heavily revise) that line of thinking, as localized glycogen depletion in the intramyofibrillar storage depots can probably start impacting performance at fairly modest levels of whole-muscle glycogen depletion.


  1. Hokken R, Laugesen S, Aagaard P, Suetta C, Frandsen U, Ørtenblad N, et al. Subcellular localization- and fibre type-dependent utilization of muscle glycogen during heavy resistance exercise in elite power and Olympic weightlifters. Acta Physiol. 2020 Sep 22;e13561.
  2. Koopman R, Manders RJF, Jonkers RAM, Hul GBJ, Kuipers H, van Loon LJC. Intramyocellular lipid and glycogen content are reduced following resistance exercise in untrained healthy males. Eur J Appl Physiol. 2006 Mar;96(5):525–34.
  3. MacDougall JD, Ray S, Sale DG, McCartney N, Lee P, Garner S. Muscle substrate utilization and lactate production. Can J Appl Physiol. 1999 Jun;24(3):209–15.
  4. Pascoe DD, Costill DL, Fink WJ, Robergs RA, Zachwieja JJ. Glycogen resynthesis in skeletal muscle following resistive exercise. Med Sci Sports Exerc. 1993 Mar;25(3):349–54.
  5. Tesch PA, Colliander EB, Kaiser P. Muscle metabolism during intense, heavy-resistance exercise. Eur J Appl Physiol. 1986;55(4):362–6.
  6. Ørtenblad N, Westerblad H, Nielsen J. Muscle glycogen stores and fatigue. J Physiol. 2013 Sep 15;591(Pt 18):4405–13.
  7. Roy BD, Tarnopolsky MA. Influence of differing macronutrient intakes on muscle glycogen resynthesis after resistance exercise. J Appl Physiol. 1998 Mar;84(3):890–6.
  8. Alghannam AF, Gonzalez JT, Betts JA. Restoration of Muscle Glycogen and Functional Capacity: Role of Post-Exercise Carbohydrate and Protein Co-Ingestion. Nutrients. 2018 Feb;10(2):253.
  9. Gejl KD, Hvid LG, Frandsen U, Jensen K, Sahlin K, Ørtenblad N. Muscle glycogen content modifies SR Ca2+ release rate in elite endurance athletes. Med Sci Sports Exerc. 2014 Mar;46(3):496–505.
  10. Ørtenblad N, Nielsen J, Saltin B, Holmberg H-C. Role of glycogen availability in sarcoplasmic reticulum Ca2+ kinetics in human skeletal muscle. J Physiol. 2011 Feb 1;589(Pt 3):711–25.
  11. Kerksick CM, Wilborn CD, Roberts MD, Smith-Ryan A, Kleiner SM, Jäger R, et al. ISSN exercise & sports nutrition review update: research & recommendations. J Int Soc Sports Nutr. 2018 Aug 1;15(1):38.
  12. Roberts BM, Helms ER, Trexler ET, Fitschen PJ. Nutritional Recommendations for Physique Athletes. J Hum Kinet. 2020 Jan;71:79–108.
  13. Burke LM. Ketogenic low CHO, high fat diet: the future of elite endurance sport? J Physiol. 2020 May 2; ePub ahead of print.
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