Does carb-load impairs keto-adaptation?

The cyclical ketogenic diet (CKD) describes those ketogenic diets that provide for the regular reintroduction of high carbohydrate amounts in a short time period (carb load). The classic scheme consists of 5-6 days of ketogenic diet and 1-2 days of carb load/refeed (1).

However, several authors expressed doubts or frowned upon the carb-load for ketogenic diets, judging it as an obstacle to keto-adaptation due to ketosis inhibition (2,3).

In simple words, if 1-2 days of carb-load are implemented every weekend, the body would be forced to re-adapt to ketosis every time, a long process that requires at least 3 consecutive weeks of the ketogenic diet.

The issue has not yet been studied, but the article proposes some physiological bases and different strategies mostly proposed by Lyle McDonald to limit the alleged carb-load inhibitory effect on keto-adaptation.

Cyclical ketogenic diets (CKD)

In the 80s the fitness & bodybuilding field saw the birth of very low carb/ketogenic diet approaches alternated with regular carb-load days, thanks to authors such as Michael Zumpano and Dan Duchaine. This format was highly popularized in the 90s by the Canadian physician and powerlifter Mauro Di Pasquale with the Anabolic diet (1).

In his 1998 book the Ketogenic Diet, Lyle McDonald formalized on a more rigorous scientific basis these very-low-carb diets variants, grouping them under the umbrella term cyclical ketogenic diet (CKD) (1), a term later also recognized by some in research (4).

Unlike many of the modalities mentioned above, the CKD proper as described by McDonald relies on ketosis in the carbohydrate restriction days (1). Even if ketosis is absolutely not a necessary condition for a more efficient fat loss (5,6), and doesn’t give any advantage for performance (5), not reaching ketosis on low-carb days (5-6 out of 7) would not make it a properly ketogenic diet.

Maintaining ketosis on very low-carb days may therefore not be a priority for those who use these cyclical approaches for aesthetic and performance purposes, or just for fat loss (as promoted by Di Pasquale), but it can be for those looking for some of the benefits typically associated with high ketonemia (appetite suppression, potential therapeutic effects, etc.) (7,8).

So then cyclically reintroducing carbohydrates with carb-load could be cause for concern to maintain an intact keto-adaptation, for whatever reason that wants to be maintained. The principles discussed here may be of interest not only for athletes who follow a strict CKD, but also for practitioners and for those who follow a normal ketogenic diet and want to understand the physiological consequences or relative “risks” of short carbohydrate reintroduction episodes.

Physiological basis

Temporary carbohydrate reintroduction during a ketogenic diet inhibits ketosis, “disturbing” the new metabolic balance established over several weeks. The high carbohydrate availability and the high glucose and insulin levels predominate, suppressing glucagon, and saturating liver glycogen, the master regulator that dictates ketogenesis inhibition (ketones production mostly by the liver) (9).

In the early 24 hours of carbohydrate reintroduction (500 g) the metabolism continues to rely on fat so that carbohydrate is partitioned towards the muscle glycogen resynthesis, while the lipid balance remains exceptionally negative. This would suggest that in the short-term (≤24 hours), keto-adaptation is not significantly compromised. By prolonging the carb-load beyond 24 hours, with the saturation of muscle (and liver) glycogen, the energy metabolism begins to be reversed, as indicated by the positive lipid balance (a marker of fat gain) (1).

Furthermore, keto-adaptation alters the enzyme activity so that the metabolism is more efficient in oxidizing fat but less efficient in oxidizing carbohydrates (“inverse” metabolic inflexibility). With the carbohydrate reintroduction, the body starts to reverse these adaptations by upregulating the glycolytic enzymes, and while 5 hours are sufficient for the liver, 24-48 hours are required so that the inversion takes place in the muscle (1).

These are just some of the many factors altered by keto-adaptation and carb-load, and it’s not possible to know all those numerous changes and give a full answer. For example, some adaptations induced by the ketogenic diet may take much longer to be fully reversed.

How to limit the anti-ketogenic effect of carb-loading

In his classic textbook, McDonald provided various suggestions to limit the risk that carb-load hinder keto-adaptation, and additional practices may be added to minimize the anti-ketogenic effect of carbohydrate reintroduction.

1. Avoid the carb load in the early 3 weeks

McDonald’s first suggestion concerns the optimal establishment of the initial keto-adaptation. In the early 3 weeks, carb-load should be avoided to speed up the process and allow adaptation to take place without any hindrance.

It’s better to introduce the carb-load only once the metabolism has well adapted to this new condition (1). However, this point refers only to the early phase, that is, the one concerning the beginning of the diet.

2. Reduce the carb-loading phase duration

A rather logical suggestion is to reduce the duration of the carb-load. This would serve to allow the liver to anticipate glycogen depletion, which normally should take around a maximum of 24 hours: the sooner the liver can be depleted and the sooner ketogenesis will be recovered (1). As seen above, the more prolonged the carbohydrate is available, the more the adaptations are gradually reversed, therefore reducing the carb-load period minimizes this reversal.

3. Prolong ketogenic cycles length

Another logical suggestion is to prolong the ketogenic phases, in other words, increase the spacing between carb loads (1). Normally the CKD is structured by 5-6 consecutive ketogenic days (keto-days), constantly alternated with 1-2 days of carbohydrate load/refeed (usually in the weekend) (1).

Technically, the more keto-days are held consecutively, the deeper the state of ketosis may become day after day. The CKD could, therefore, become a mode where carbohydrates are introduced on occasion, or only when high glycogen availability is really needed (as before a single episode of intense depleting workout).

4. Control the carbohydrates amount during the carb-load

A further suggestion is to have greater control of carbohydrate ingested during the carb-load. Although McDonald had already established a given carbohydrate threshold in CKD, in this case, he set the limit of 10 g/kg of lean body mass within 24 hours (~650 g/day for a normal weight 75 kg person) (1).

The extension of the carb-load period was designed to supercompensate muscle glycogen stores in order to have the greatest availability as possible during the training session over the ketogenic phase (or just for temporary aesthetic purposes), but by reducing carbohydrate amounts this effect wouldn’t get, leading to a muscle glycogen compensation (‘normal’ levels) at best.

5. Carbohydrate type selection

Another dietary factor to limit the carb-load inhibitory effect is the quality of carbohydrates, or more properly, the nature of the monomers from which they are made.

Since fructose is mainly metabolized by the liver, further promoting the re-synthesis of liver glycogen (10) (the main ketogenesis inhibitor), sources of fructose such as fruit, honey, sucrose, and pure fructose should be avoided or severely restricted (1).

Since galactose also undergoes a metabolic fate similar to that of fructose (10), even high amounts of milk and carb containing dairy products wouldn’t be ideal.

6. Increase LISS cardio and/or NEAT the day after carb-load

An intelligent strategy to restore ketogenesis as soon as possible is to accelerate the liver glycogen depletion rate through physical activity beyond that foreseen by the resistance training program. Adding low-intensity cardio (<50 VO2max) the morning after the carb-load, or just keeping non-exercise activity (NEAT) high, will speed up the liver glycogen depletion compared to a low activity state (1).

It’s important to choose low-intensity activities so as to depleting glycogen stored in the liver and not that stored in the muscle (11,12) since the latter is significantly affected in the moderate-intensity range and above (i.e. MISS, HISS, HIIT, resistance training, etc). By doing so is possible to spare muscle glycogen for the actual training sessions over the week.

7. Carb-load within 24 hours of the last glycogen-depleting workout

Exercise boosts muscle-specific insulin sensitivity for approximately 24 hours post-workout (13). That means that if the carb-load falls within this period of time, the muscle will be more efficient in uptaking the ingested glucose than delaying it the next day. The enhanced glycogen re-synthesis capacity doesn’t seem to be much influenced by how the same amount of carbohydrates are distributed within this period of time (13), but precautionary, it may make sense to place the greater amount in the early few hours.

8. Structure a glycogen depleting workout pre-carb-load

Since muscle has priority over the liver in post-workout for uptaking exogenous glucose sources, trying to emphasize this priority may further limit liver glycogen re-synthesis. The extent of muscle glycogen depletion depends on the number, the type, and the volume of the workouts, and on how much the last pre-carb-load workout is glycolytic (i.e. that highly rely on glucose and glycogen as a fuel).

In general, it is suggested to make the last workout highly depleting by involving all the muscles (total body) (1), but since this strategy does not always fit with the training program, it may be enough to follow the previous points. After all, “typical high volume bodybuilding-style workouts involving multiple exercises and sets for the same muscle group would deplete the majority of local glycogen stores” (13).


From the notions discussed here, it appears that the metabolic adaptations induced by the very low carb/ketogenic diet only start to be reversed with the carb-load, and 24 hours would be a too short period of time to impair keto-adaptation. Since this adaptation takes about 3 weeks to be completed, it’s hard to believe that only a 24-48 hours carb-load is enough to start all over again.

If by measuring the ketone concentrations in the urine (a gross ketone concentration estimation) there is a lower value than expected, it’s recommended to assess the strategies proposed above to speed up the ketogenesis re-activation. Most of these strategies are aimed at:

  • enhance muscle-specific insulin sensitivity and glucose uptake pre-carb-load;
  • limit the liver glycogen re-saturation during the carb-load;
  • speed up the liver glycogen depletion post-carb-load;

It is important to keep in mind that the first point (muscle glycogen depletion and enhanced muscle glucose uptake) can be respected practically only with enough intense physical activity, and it’s likely that in sedentary or non-sporty conditions the carb-load inhibitory effect is more pronounced.


  1. McDonald L. The Ketogenic Diet: A Complete Guide for the Dieter and Practitioner. Independently published. 1998.
  2. Tzur ABA, Roberts BM. The ketogenic diet for bodybuilders and physique athletes. Strength Cond J. 2020.
  3. Norton L, Baker A. Fat Loss Forever: How to Lose Fat and KEEP it Off. Independently published. 2019. pp. 188.
  4. Cafri G et al. Pursuit of the muscular ideal: Physical and psychological consequences and putative risk factors. Clin Psychol Rev. 2005 Feb;25(2):215-39.
  5. Hall KD, Guo J. Obesity energetics: body weight regulation and the effects of diet composition. Gastroenterology. 2017 Feb 10. pi:i S0016-5085(17)30152-X.
  6. Freedman MR et al. Popular diets: a scientific review. Obes Res. 2001 Mar;9 Suppl 1:1S-40S.
  7. Gibson AA et al. Do ketogenic diets really suppress appetite? A systematic review and meta-analysis. Obes Rev. 2015 Jan;16(1):64-76.
  8. Puchalska P, Crawford PA. Multi-dimensional roles of ketone bodies in fuel metabolism, signaling, and therapeutics. Cell Metab. 2017 Feb 7; 25(2): 262–284.
  9. Foster DW. Banting Lecture 1984. From Glycogen to Ketones–And Back. Diabetes. 1984 Dec;33(12):1188-99.
  10. Décombaz J et al. Fructose and galactose enhance postexercise human liver glycogen synthesis. Med Sci Sports Exerc. 2011 Oct;43(10):1964-71.
  11. Gollnick PD et al. Selective glycogen depletion pattern in human muscle fibres after exercise of varying intensity and at varying pedalling rates. J Physiol. 1974 Aug;241(1):45-57.
  12. Hultman E et al. Glycogen storage in human skeletal muscle. in: B Pernow, B Saltin (Eds.) Muscle Metabolism During Exercise. Advances in Experimental Medicine and Biology. vol 11. Plenum, New York; 1971:273.
  13. Aragon AA, Schoenfeld BJ. Nutrient timing revisited: is there a post-exercise anabolic window? J Int Soc Sports Nutr. 2013 Jan 29;10(1):5.

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