A characteristic of ketogenic diets is that they can limit muscle glycogen content, at least partially, which can worsen muscular processes leading to strength production.

Although in strength sports such as Powerlifting or Weightlifting where the effort is of very short duration (1RM) are not too dependent on glycogen, we must know that glycogen fulfills functions far beyond an energy substrate, that is, it is not only something that provides us with energy but regulates multiple processes at the cellular level. Let’s see:

Chin and Allen (1997) demonstrated a clear connection between muscle glycogen content and the process of muscle contraction. A reduction in muscle glycogen leads to a reduction in intramuscular calcium levels and therefore to a decrease in force production (calcium is key to muscle contraction). This has subsequently been confirmed in other studies as it has been shown that low muscle glycogen concentration alters calcium release by the sarcoplasmic reticulum impairing muscle contraction and thus strength (Barnes et al. 2001, Tupling, 2004, Ørtenblad et al. 2011).

In addition, it has been shown that the decrease in force production that occurs when having low muscle glycogen content, something that occurs if we maintain a ketogenic diet over time, is independent of the cellular volume of energy (ATP). What does this mean? Well, even if you are in adequate energy conditions (diets in normo or caloric surplus), if the muscle glycogen content is low, there will be an alteration in the process of muscle contraction and therefore a decrease in the production of force (Barnes et al.2001, Nielsen et al. 2009), suggesting that for the correct and maximum application of force, localized energy (ATP) is required. This means that even if you eat a ketogenic diet with high energy intake from fat, it is likely to be suboptimal for optimizing your maximal strength capacity.

But what’s more, recently Jensen et al 2019 wanted to investigate in a study the effects of glycogen-derived ATP per se on the action potential refractory period (i.e., the estimated time before a second action potential leading to a muscle contraction can occur), on muscle function, including complete muscle fatigue and force production in whole muscles and individual fibers.

These authors assumed that blocking glycogen-derived ATP production (by blocking glycogen phosphorylase, which are glycogenolytic enzymes) would lead to a longer refractory period time at the action potential, a reduction in muscle contraction and force, and an acceleration of fatigue.

The results were that inhibition of glycogen phosphorylase leads to:

  1. Reduced muscle contraction and tetanic force in individual fibers.
  2. Prolonged refractory period of the action potential (i.e., decreased fiber excitability).

Overall, the above and presented results strongly support the model proposed by Epstein et al. 2014. In this model, glycolysis acts as a rapid response to rapid transitions in energy demand, despite high oxygenation. In summary, it is clearly shown that a high overall energy state (energy surplus) is insufficient to maintain muscle function during glycogen phosphorylase inhibition or glycogen disposal. In other words, that even if you ingest sufficient calories through a high-protein and/or high-fat diet, if muscle glycogen levels are low (due to insufficient carbohydrate intake) force production and muscle contraction will not be optimal.

Therefore, despite the fact that some strength sports are only at 1 RM, such as Weightlifting or Powerlifting, understanding that they are basically phosphagenic, a low-carbohydrate or ketogenic diet will inevitably worsen performance if glycogen concentrations fall below a certain threshold (approximately 5g/kg of muscle mass).

Overall, these results support the concept of compartmentalized ATP resynthesis within the fiber and that glycogen plays a crucial role in supporting these compartments. In conclusion, this research demonstrates a functional link between ATP derived specifically from intramuscular glycogen and force production through the refractory period of the action potential, regardless of whether there is a high overall ATP level due to high energy intake through diet, which induces a decrease in force production and an accelerated development of fatigue.

Another interesting issue is that muscle glycogen may mediate the response to muscle protein synthesis. For example, Creer and his team found that mTOR phosphorylation was attenuated at depressed glycogen concentrations (3g/ kg muscle weight), but increased at high glycogen values (Creer A, et al 2005). Other authors such as Lemmon et al 1985 found similar conclusions in their studies. A study by Cameron et al did not find a clear relationship between decreased muscle glycogen and decreased protein synthesis, but it should be noted that the exercise protocols performed in their study were minimal and not at all representative of conventional strength training.

In fact, Knudsen et al 2020 found in a recent study done in rats (it would be interesting to recreate this in humans) that muscle glycogen was intimately linked with the activation of protein synthesis through mTOR. Increasing muscle glycogen concentration above basal levels increased mTORC for up to 4 hours after exercise. Furthermore, they saw that when muscle glycogen stores were restored, the decrease in protein synthesis was completely rescued.

Finally, the first randomized controlled trial (Sjödin et al 2020) investigating the effects of a long-term ketogenic diet on muscle fatigue in young, healthy, normal-weight women has just been published. They were not in caloric deficit to ensure energy intake.

The study was on 24 women for 4 weeks, which although many will say is not enough time to keto-adapt, the reality is that even Volek (one of the world’s leading researchers on ketogenic diets in sports) comments that it is enough time to do so. Still, I wish this study had been longer to see longer term effects. The study that ketoadapted women shifted their metabolism toward increased fat utilization during submaximal exercise, something physiologically evident. On the other hand, the ketogenic diet did not affect maximal isometric strength or muscle fatigue under conditions of sustained low-intensity exercise, i.e., neither improved nor worsened, also physiologically correct. However, the women experienced exercise and normal day-to-day activity as more strenuous. In fact, they became fatigued earlier during exercise and the perception of exertion was greater (see figure in the image), having a negative effect on muscle fatigue and RPE.

Although 4 weeks is sufficient for ketoadaptation, perhaps more time in this condition will alleviate the negative effects mentioned. Still, to say that a ketogenic diet improves performance in relatively high intensity sports is, at least to this day, absurd no matter how you look at it.

As I have said many times, I have nothing against ketogenic diets, I myself sometimes apply them in some patients, but always when the context, subject profile, adherence and the objective sought indicate to me that it could be a good strategy. The problem, as always, is that I use it as a magic tool, that it works for everything and everyone and that it has miraculous effects. Nothing could be further from the truth…

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