Guanidinopropionic Acid and Creatine

Many creatine products on the market right now contain an array of ingredients that theoretically help increase the efficiency of creatine, This can be done by either having creatine easily transported into the cell or a new form of it which will provide you with more energy.

One of these ingredients put into creatine blends is guanidinopropionic acid (GPA). GPA has been added to creatine supplements to help in the aid of insulin function. Generally speaking, the more improved function of insulin, the more energy you will have available and the more anabolic one will be. GPA is a creatine analog. However, GPA can be ergolytic, meaning, it will hinder performance and not increase it.

GPA also has the ability to bind to creatine transporters and block their main function, to allow passage of creatine into the cell. (Brault et al., 2003, Williot et al., 1999) When this happens creatine will not be able to get into various tissues. Thus, a blocked creatine transporter can result in lesser intracellular creatine levels, leading to a decreased performance. The consequences of this will be a diminished contractile force (Eijnde et al., 2004). Along with muscle tissue being affected, GPA also has an influence on brain and heart tissue.

The brain is a very well protected organ, and as in muscle tissue, creatine needs a transporter to gain access to neuronal tissue for it to have a beneficial effect. GPA has been shown to inhibit the creatine transporter, but thankfully the brain has the ability to temporarily recover from the decreases in energy induced by GPA use (Lunardi et al., 2006, O’Groman et al., 1996).

As mentioned previously, GPA can manipulate with heart tissue. Numerous studies showed that intracellular creatine concentrations decreased dramatically, nearly 80%. (Boehm, et al 2003, Horn et al., 2001)

Having both GPA and creatine in the same supplement seems counter-productive. Since GPA has the ability to stop creatine uptake into the cells, which could lead to an overall negative effect. It seems to defeat the purpose of what we are taking creatine for, which is usually to better our performance in the gym.


References:

Boehm E, Chan S, Monfared M, Wallimann T, Clarke K, Neubauer S. Creatine transporter activity and content in the rat heart supplemented by and depleted of creatine. Am J Physiol Endocrinol Metab. 2003 Feb;284(2):E399-406.

Brault J, Abraham K, Terjung.R, Muscle creatine uptake and creatine transporter expression in response to creatine supplementation and depletion. J Appl Physiol. 2003 Jun;94(6):2173-80

Eijne B, Lebacq J, Ramaekers M, Hespel P. Effect of muscle creatine content manipulation on contractile properties of mouse muscles. Muscle Nerve. 2004 Marl29(3):428-35.

Horn M, Remkes H, Stromer H, Dienesch C, Neubauer S. Chronic phosphocreatine depletion by the creatine analogue beta-guanidinopropionate is associated with increased mortality and loss of ATP in rats after myocardial infarction. Circulation. 2001 Oct 9;104(15):1844-9.

Lunardi G, Parodi A, Perasso L, Pohvozcheva A, Scarrone S, Adriano E, Florio T, Gandolf C, Cupello A, Burov S, Balestrin M The creatien transporter mediates the uptake of creatine by brain tissue, but not the uptake of two creatine-derived comounds. Neuroscience. 2006 Nov 3l143(4):991-7

O'Gorman E, Beutner G, Wallimann T, Brdiczka D.. Differential effects of creatine depletion on the regulation of enzyme activities and on creatine-stimulated mitochondrial respiration in skeletal muscle, heart, and brain. 1996 Sep 12;1276(2):161-70.

Willott C, Young M. Leighton B, Kemp G, Boehm, E., Radda G., Clarke K., Creatine uptake in isolated soleus muscle: kinetics and dependence on sodium, but not insulin. Acta Physiol Scand. 1999 June;166(2):99-104.


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