ATP-supplementation makes muscle cells thriftier with energy


All sports scientists and nearly all strength athletes are familiar with adenosine triphosphate or ATP [structural formula shown here] and regard it as the energy source that muscle fibres turn to when they contract intensively. It’s less well known that you can also use ATP as a supplement. Researchers at the University of Louisville will soon publish in the Journal of Surgical Research a study that suggests that ATP supplementation may indeed be effective.

ATP is not unknown in doping circles, and the supplements industry assessed the potential of ATP after researchers showed that oral administration of ATP boosted the maximal strength of strength athletes, enabling them to do more reps per set. ATP is found in various supplements including Gaspari Nutrition’s SizeOn and Berry de Mey Nutrition’s Beta-Alanine ProElite.

But exactly how ATP is capable of helping strength athletes is not known. All that scientists know is that orally administered ATP does not make its way to muscle cells. The research done at the University of Louisville may shed some light on the matter, even though it had nothing to do with strength sports. The researchers were looking for better ways of storing limbs destined for transplants, where muscle tissue needs to be kept in good condition for long periods of time.

When muscles or other tissues are cut off from their blood supply, the ATP concentration in the cells goes down. If the concentration dips below a certain level the cells start to die off. Cells try to maintain the ATP concentration as long as they can, and first go through their glycogen supply and phosphocreatine before starting on the ATP.

So maybe adding ATP to the fluid in which the tissues are stored can extend tissue quality, the researchers reasoned. To test their theory they did an experiment with muscle tissue from rats.

The figure below shows that the concentration of phosphocreatine [black circles] declined rapidly when the researchers used ordinary preserving fluid. Ultimately the concentration of ATP also went down [white circles]. The concentration of inorganic phosphate [white squares] increased rapidly.


Addition of ATP to the preserving fluid delayed the decrease in phosphocreatine and ATP and the increase in organic phosphate. So ATP helped the muscle cells to be thriftier with their energy.



The effect almost disappeared when the researchers added the adenosine receptor blocker MRS-1523 to the ATP. From this they conclude that the protective effect of ATP is to a large extent due to the fact that the ATP molecule breaks down into adenosine.

When the researchers then looked at whether adenosine would also protect muscle tissue they discovered, however, that adenosine offers less protection than ATP. Exactly how ATP protects muscle tissue remains to some extent a mystery.

Administration of exogenous adenosine triphosphate to ischemic skeletal muscle induces an energy-sparing effect: Role of adenosine receptors.

Maldonado C, Pushpakumar SB, Perez-Abadia G, Arumugam S, Lane AN.


Department of Physiology and Biophysics, University of Louisville, Louisville, Kentucky. Electronic address: cjmald01@louisville.edu.



Ischemia-reperfusion injury is a devastating complication that occurs in allotransplantation and replantation of limbs. Over the years, several preservation strategies have been used to conserve the critical levels of intracellular adenosine triphosphate (ATP) during ischemia to sustain the ion gradients across the membranes and thus the tissue viability. The administration of exogenous ATP to ischemic tissues is known to provide beneficial effects during reperfusion, but it is unclear whether it provides protection during ischemia. The purpose of the present study was to determine the effect of ATP administration on high-energy phosphate levels in ischemic skeletal muscle and to examine the role of purinergic and adenosine receptors in mediating the response to exogenous ATP.


The extensor digitorum longus muscles of Fischer rats were subjected to ischemia and treated with different concentrations of ATP with or without purinergic and adenosine receptor blockers. Phosphorus-31 nuclear magnetic resonance spectroscopy was used to measure the rate of decay of ATP, phosphocreatine (PCr), and the formation of adenosine monophosphate and acidification. Phosphorylated compounds were analyzed using a simple model of energy metabolism, and the PCr half-life was used as an index of internal depletion of ATP to distinguish between intracellular and extracellular ATP.


PCr decay was rapid in all muscle groups and was followed by gradual ATP decay. The half-life of PCr was significantly longer in the ATP-treated muscles than in the vehicle controls and was maximally prolonged by treating with slow hydrolyzing adenosine 5′-O-(3-thio)triphosphate. Purinoceptor (P2X) blockade with ATP treatment significantly increased the half-life of PCr, and adenosine receptor blockers blunted the response. Administration of adenosine to ischemic muscles significantly increased the half-life of PCr compared with that in the vehicle controls.


Exogenous ATP administration to ischemic skeletal muscles appears to spare intracellular energy by acting primarily through adenosine receptors.

PMID: 22795271 [PubMed – in process] PMCID: PMC3494764 [Available on 2014/5/1]

Source: http://www.ncbi.nlm.nih.gov/pubmed/22795271

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