Does Caffeine Reduce Blood Flow and Muscle Pumps?

If you want to know whether or not caffeine acts as a vasoconstrictor, limiting blood flow, muscle pumps, and performance, then you want to read this article.

 

Caffeine is purely awesome. Just ask anyone who’s worked the late shift, raised an infant, or spent their days training at 4am.


Caffeine gives us energy and focus; it boosts our mental and physical performance, and it can even make us a bit more pleasant to be around, too.


But, as great as caffeine is, it’s not a perfect chemical. It does come with a few drawbacks, including the dreaded tolerance build up and nasty withdrawal symptoms. There are also a few other negatives that have been associated with caffeine consumption that have been promoted by various experts and gurus over the years.


One of the most common potential negatives regarding caffeine is regarding its purported ability to constrict blood vessels, which in the world of athletic performance and weight lifting equates to decreased performance, stamina, and nutrient delivery as well as massively reduced muscle pumps -- something none of us really want.


But, is this statement actually based on any science?


Or, is it just one of the many myths thrown around by “gurus” and “experts”?


Let’s take a look at the belief that caffeine constricts blood vessels and see what the research has to say.


So...


Does Caffeine Constrict Blood Vessels?


YES….and….


No.


You see, caffeine (and coffee) does both constrict and dilate blood vessels.


How is this possible?


To answer that question, let’s take a deeper look into exactly how caffeine works in the body and what areas of the body are affected.


What Does Caffeine Do?


Undoubtedly when asked this question, people will quickly say that caffeine gives them energy or “wakes them up”, but how does it actually do this?


Well...


Caffeine is a xanthine molecule found in coffee, tea, and cocoa which acts in the body’s cells via numerous mechanisms of action across a wide range of molecular targets.


First and foremost, caffeine serves as an antagonist of the adenosine receptors. This means that caffeine binds to adenosine receptors, which prevents the actual adenosine molecule from binding to its partner receptor.


Secondly, caffeine inhibits phosphodiesterase (PDE) enzymes. Yes, these are the same family of enzymes that are the target of male enhancement products, such as Viagra.


Thirdly, caffeine acts as a sensitizer of calcium liberation channels, meaning that caffeine increases release of calcium, which we’ll discuss more about it a bit.


Caffeine also antagonizes GABA receptors[2] and impacts the cardiovascular system through a number of interesting means, which brings us to the topic at hand...

Caffeine and Blood Flow


Our analysis of how caffeine impacts blood flow begins with a discussion of the endothelium -- a rather extensive tissue in the human body that forms the barrier covering the walls of your blood vessels and arteries.


Blood vessels (and arteries) are composed of several different cell types. The outer layer is made up primarily of connective tissue, which helps the blood vessels stick (adhere) to tissues within the body. The middle layer of cells consists of smooth muscle cells, which govern how wide or narrow (vasodilation or vasoconstriction, respectively) a blood vessel gets, which means that smooth muscle cells can directly impact blood flow. Keep this in mind, as we’ll bring this up again in a moment.


The final and innermost layer of vessels are comprised of single layer of endothelial cells and other “supporting” cells. Endothelial tissue is both structural and functional as it is serves as the outer layer of arterial walls and selectively permits compounds to pass through it, meaning it’s rather picky in what it allows to cross through it and into or out of the artery.


Here’s a diagram of a blood vessel to help clear things up[5]:

blood-vessel-cell-layer


What does this have to do with caffeine?


Everything…


Caffeine acts directly on the endothelial cell, stimulating the production of nitric oxide.


How does it stimulate nitric oxide?


That’s where things get complicated…


Caffeine stimulates the release of calcium ions (Ca2)+ from the endoplasmic reticulum, leading to an increase in the concentration of intracellular calcium in the cytoplasm, which is typically abbreviated as iCa2+. This release of calciums leads to the formation of a complex with calmodulin (a calcium-binding messenger in our cells) which favors the activation of endothelial nitric oxide synthase (eNOS), resulting in nitric oxide production.


Now, under normal circumstances, there is a minimal amount of calcium residing in the cytoplasm, but not enough to activate eNOS. However, researchers believe that caffeine lowers the threshold required for the “calcium-induced calcium release” mechanism, meaning that this cellular mechanism can be activated when levels of calcium are at their resting value in the presence of caffeine.[4]


Basically, caffeine increases nitric oxide production in vascular endothelial tissue, which leads to vasodilation (widening of blood vessels), and ultimately greater blood flow.


But, that’s not all….


Caffeine doesn’t just impact the endothelial tissue, but actually affects the vascular smooth muscle cells themselves, both directly and indirectly!


The initial action of caffeine on smooth muscle cells results in vasoconstriction!


Immediately, all of those against stimulants, especially caffeine in pre workouts, will immediately say, “SEE! I TOLD YOU CAFFEINE CAUSES SHRINKAGE!”


As famed college football analyst, Lee Corso would say….”Not so fast….”


After this brief constrictive action, caffeine prompts a “significant vasodilator effect”.[1] This happens through a few different mechanisms, which we’ll briefly discuss:


There are various mechanisms that explain these effects.


  • Caffeine, acting on the ryanodine channels of the sarcoplasmic reticulum, generates an increase in intracellular calcium ions (iCa2+) which leads to a brief contraction
    • Note: these effects were observed in isolated cells, when additional work was done on human arteries and animal tissues, these constriction was not observed, leading researchers to conclude that caffeine leads to a transitory constriction[1]

  • Caffeine also inhibits phosphodiesterase (PDE) enzymes, which leads to an increase in cAMP levels. cAMP (cyclic adenosine monophosphate) increases “non-contractile” Ca2+ and at the same time diminishes cytoplasmic Ca2+ (iCa2+). It also inhibits Myosin Light Chain Kinase (MLC Kinase). As a result MLC phosphatase predominates, resulting in vasodilation.

  • Caffeine inhibits inositol triphosphate (IP3). IP3 causes the sarcoplasmic reticulum to release Ca2+, which is required for contraction (constriction), but since caffeine inhibits IP3, it prohibits vessel constriction.

There’s also some “indirect” mechanisms at play here too. Chief among these is the effects of caffeine on the vascular smooth muscle cells by nitric oxide. If you remember, endothelial cells can allow certain molecules to cross through its protective barrier. Nitric oxide is one such compound, and once eNOS in the endothelial cell synthesizes nitric oxide, it quickly diffuses to the smooth muscle cell, leading to vasodilation.


If all of that sounds rather complicated and complex (because frankly, it kind of is), here’s an illustration that should hopefully clear things up a bit[1]:

 

caffeine-direct-actions-endothelial-cell


And here’s another graph showing the indirect actions at work[1]:

 

caffeine-indirect-actions


And...here’s a table summarizing all of the effects caffeine exerts on vascular smooth muscle cells[1]:

 

caffeine-smooth-muscle-cell-actions


Caffeine, Blood Flow, and the Brain


If you’ve ever had a migraine, you’ve undoubtedly felt the searing pain that shoots through your head the instant you see any bright light. And to alleviate that mind-melting pain, you’ve probably taken some migraine medication.


9 times out of 10, the medicine you used to quash that pesky migraine was Excedrin (or the generic store brand).


What is it about Excedrin that makes it so effective for putting a stop to a migraine’s paralyzing effects?


Caffeine.


You see, when you have a migraine, levels of adenosine in the head and neck can increase up to 68% above normal, non-migraine concentrations.[6] And, in the head and neck, adenosine dilates blood vessels.


When caffeine antagonizes adenosine receptors, and subsequently prevents adenosine from binding to its receptor, it causes a reduction in cerebral blood flow, and with that reduction also comes some much needed relief from your headache and migraine.


But that’s not all caffeine does to relieve pain.


It also[7,8]:


  • improves the efficiency of pain-relief compounds (analgesics)
  • Accelerates absorption of the analgesic
  • Allows for a lower dose to be used while still being effective work, which decreases the possibility of side effects from certain analgesics

Takeaway


By now, hopefully you realize that caffeine isn’t the terrible, vasoconstricting, pump-killing stimulant you’ve been let to believe it is. Not only is caffeine not vasoconstrictive, it actually promotes vasodilation through the production of nitric oxide and its effects on smooth muscle cells.


Suffice it to say that this myth has been BUSTED.


You can still enjoy your caffeine pre workout and get massive pumps.

References

  1. Darío Echeverri, Félix R. Montes, Mariana Cabrera, Angélica Galán, and Angélica Prieto, “Caffeine's Vascular Mechanisms of Action,” International Journal of Vascular Medicine, vol. 2010, Article ID 834060, 10 pages, 2010. https://doi.org/10.1155/2010/834060
  2. J. W. Daly, “Caffeine analogs: biomedical impact,” Cellular and Molecular Life Sciences, vol. 64, no. 16, pp. 2153–2169, 2007.
  3. Walsh, M. P. (1983). Calmodulin and its roles in skeletal muscle function. Canadian Anaesthetists’ Society Journal, 30(4), 390–398.
  4. M. Endo, “Calcium release from the sarcoplasmic reticulum,” Physiological Reviews, vol. 57, no. 1, pp. 71–108, 1977.
  5. Alberts B, Johnson A, Lewis J, et al. Molecular Biology of the Cell. 4th edition. New York: Garland Science; 2002. Blood Vessels and Endothelial Cells. Available from: https://www.ncbi.nlm.nih.gov/books/NBK26848/
  6. A. I. Scher, W. F. Stewart, and R. B. Lipton, “Caffeine as a risk factor for chronic daily headache: a population-based study,” Neurology, vol. 63, no. 11, pp. 2022–2027, 2004.
  7. Derry, S., Wiffen, P. J., & Moore, R. A. (2015). Single dose oral ibuprofen plus caffeine for acute postoperative pain in adults. The Cochrane Database of Systematic Reviews, (7), CD011509. https://doi.org/10.1002/14651858.CD011509.pub2
  8. Derry, C. J., Derry, S., & Moore, R. A. (2014). Caffeine as an analgesic adjuvant for acute pain in adults. The Cochrane Database of Systematic Reviews, (12), CD009281. https://doi.org/10.1002/14651858.CD009281.pub3

     

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