Creatine first gained significant notoriety and popularity in the late ‘90s as a supplement used for strength and power sports. It has subsequently become an increasingly popular supplement in all sports and even for more general health related goals. Recent research has suggested there is a benefit to creatine supplementation in those on a low creatine diet (low meat diets) as well as for an aging population.

Creatine is an amino acid located mostly in your body's muscles as well as in the brain. You can get creatine through seafood and red meat, though at levels far below those found in creatine supplements. The body's liver, pancreas and kidneys also can make about 1 gram of creatine per day. Your body stores creatine in your muscles predominantly, where it's used for energy.

Creatine is used to aid adenosine triphosphate (your body’s energy currency, and ATP for short) production during times of high energy need. Our body stores are generally said to be enough to power around 10 seconds of work before they run out and need replenishment. Supplementing creatine increases your body's ATP stores.

Given the role of creatine in energy production, it is unsurprising that people often ask what the impact of creatine supplementation on their glucose levels will be.

What does creatine do?

Creatine was shown to improve glucose control, in this case a lower average, when combined with aerobic activity, more so than the control condition where creatine wasn’t used. This is in addition to a growing body of evidence in animal models and in human subjects with insulin resistance or Type 2 diabetes.

Another interesting note is that there is evidence that co-ingestion of creatine and carbohydrates increased total muscle glycogen storage. This seems to be a two-for-one situation where the co-ingestion also increases the amount of creatine stored.

The picture is a little harder to decipher in a non-insulin resistant population. There is some conflicting evidence, but the weight of the evidence looks as though there may be a small increase in glucose as a result of creatine supplementation, though no change to insulin secretion. The dose required to elicit this effect is unclear, as are the reasons or implications for this. It may also be population specific (much research is done in those with low creatine diets, mostly vegetarians). The doses in these studies vary from a normal daily dosing of 5 mg/day to one that represents more of a loading dose of 20 mg/day.

The small increase in glucose may be representative of increased anabolism as explained in this article.

What causes creatine to boost glucose levels?

There seems to be a few different mechanisms potentially at play: Changes to insulin sensitivity have repeatedly been shown not to be the case with creatine supplementation. The most likely potential mechanism to decrease glucose is an increase in GLUT-4 transporters, the transporters that allow glucose to enter your muscles.

What are the implications of increased glucose from creatine supplementation?

It is hard to be certain about the implications of any change in glucose as a result of creatine supplementation. The consistency of evidence indicating no change to insulin is a reassuring factor suggesting that any increased glucose levels are not driving insulin when using creatine. Similarly, even a small increase in glucose may be worth the benefits of creatine supplementation on performance and general health.

It does look as though creatine may be a useful supplement in times when the goal is maximizing muscle glycogen content. Creatine has a well known effect of increasing body mass, likely via water retention, something often seen as negative but having potential positives pre-race, including reducing water needs during race.


Takeaways:

  • Taking creatine may increase body mass (fat free mass) and may have other positive health benefits like neuro-protection.
  • Creatine may increase speed, power, and general athletic performance.
  • There seems to be a beneficial effect of co-ingestion of creatine and carbohydrate on muscle glycogen content. So creatine use leading into a key race appears helpful.
  • The effect of creatine on glucose is variable; evidence indicates it likely lowers glucose in animals, people with type 2 diabetes, and those with insulin resistance, whereas others may see an increase in glucose as a response of creatine supplementation. Any effect seems small and insignificant in comparison to the benefits of creatine for racing and health.

References:

  1. Konstantinos I. Avgerinos, Nikolaos Spyrou, Konstantinos I. Bougioukas, Dimitrios Kapogiannis.Effects of creatine supplementation on cognitive function of healthy individuals: A systematic review of randomized controlled trials.Experimental Gerontology, Volume 108. 2018, Pages 166-173. https://doi.org/10.1016/j.exger.2018.04.013
  2. Solis, M.Y.; Artioli, G.G.; Gualano, B. Potential of Creatine in Glucose Management and Diabetes. Nutrients 2021, 13, 570. https://doi.org/10.3390/nu13020570
  3. Rooney, K. B., Bryson, J. M., Digney, A. L., Rae, C. D., & Thompson, C. H. (2003). Creatine Supplementation Affects Glucose Homeostasis but Not Insulin Secretion in Humans. Annals of Nutrition and Metabolism, 47(1), 11–15. doi:10.1159/000068908
  4. Gualano, B., Novaes, R., Artioli, G. et al. Effects of creatine supplementation on glucose tolerance and insulin sensitivity in sedentary healthy males undergoing aerobic training. Amino Acids 34, 245 (2008). https://doi.org/10.1007/s00726-007-0508-1
  5. Nelson, A.G.; Arnall, D.A.; Kokkonen, J.; Day, R.; Evans, J. Muscle glycogen supercompensation is enhanced by prior creatine supplementation. Med. Sci. Sports Exerc. 2001, 33, 1096–1100.
  6. Green, A.L.; Simpson, E.J.; Littlewood, J.J.; Macdonald, I.A.; Greenhaff, P.L. Carbohydrate ingestion augments creatine retention during creatine feeding in humans. Acta Physiol. Scand. 1996, 158, 195–202.
  7. Op’t Eijnde B, Urso B, Richter EA, Greenhaff PL, Hespel P: Effect of oral creatine supplementation on human muscle GLUT4 protein content after immobilization. Diabetes 2001; 50:18–23.