•Sensible advice for aches, pains & injuries

Muscles cells and the sarcomeres insides them, the potent little bundles of protein that power muscle tissue. Artist unknown, unfortunately.

Dance of the Sarcomeres

A mental picture of muscle knot physiology helps to explain four familiar features of muscle pain

2,750 words, updated Jan 16th, 2014
by Paul Ingraham, Vancouver, Canada bio
I am a science writer, a former massage therapist, and the Assistant Editor of Science-Based Medicine since 2009. I am nearly done with a long-procrastinated Bachelor of Health Sciences degree. I am a middle-aged runner and ultimate player with plenty of personal experience with athletic injury and chronic pain. Readers often want to know more about me and my qualifications, because my style and subject matter is controversial. Most importantly, yes, I used to actually believe and practice almost everything that I now debunk and criticize. I live by the ocean with my wife in beautiful downtown Vancouver.

EXCERPT This page is an adapted and somewhat trimmed down excerpt from my ebook about myofascial trigger points (muscle knots), which creatively explores many other aspects of the science of trigger points. I chose this excerpt because it contains some of the best basic biology writing I think I’ve ever done. Sarcomeres make it easy: they are extremely interesting!

Sarcomeres are the molecular engines that power muscle tissue. Think of them as little microsopic muscles-within-muscles. Micro muscles.

They may also tie our muscles into “knots,” and understanding them may be the key to common muscle pain. What’s in a knot? Here’s the oversimplified, conventional, controversial wisdom since about 1995: a trigger point is an unholy clump of contracted sarcomeres living in a swamp of their own garbage molecules, waste metabolites. Unfortunately, this “energy crisis hypothesis” is imperfect, and could well turn out to be wrong.1 Even normal muscle physiology is still full of mysteries. But almost no matter where the march of scientific progress takes us, it will be worth understanding trigger points in this way for many years to come.

And it will always be worth understanding sarcomeres themselves.

Trigger points are like pimples — everyone has at least a few, and everyone gets a bad one every now and then. Knowing what makes them tick is great “owner’s manual” knowledge!

Trigger points are like pimples — everyone has at least a few, and everyone gets a bad one every now and then. Knowing what makes them tick is great “owner’s manual” knowledge!

The significance of sarcomeres: to biology and to muscle pain

I still remember the day I first learned about sarcomeres, and if you’re encountering them for the first time right now, I hope I can make it just as memorable for you. They were the best example I’ve ever heard, before or since, of how life is chemistry. They are a rare explanatory bridge between something as ordinary as wiggling your toes and an exotic, dazzling protein performance. Without sarcomeres, your heart could not beat, your guts could not digest, your jaw could not flap.And there’s something unusual and beautiful about the way sarcomeres are like an extremely miniature version of the muscles they power. There’s really nothing else going on in our bodies microscopically that so perfectly mimics the macroscopic.

You know how kids are so good at asking a chain of “why” or “how” questions? Well, sarcomeres are the final answer to the chain of kid-questions that starts with, “How do we move?” Sarcomeres are how chemistry lifts barbells. Without sarcomeres, your heart could not beat, your guts could not digest, your jaw could not flap. You would never blink, breathe, or burp. Sarcomeres are the ultimate source of all movement. And they are pure organic chemistry.

And when they get messed up, maybe they hurt. Understand sarcomeres and their failure, and you can make sense of muscle knots, if the energy crisis hypothesis is actually correct. Specifically, troubled sarcomeres could explain (at least) four distinctive clinical characteristics of trigger points:

  1. why trigger points can be so stubborn
  2. why applying pressure often helps
  3. why stretching feels good (but also does not work any miracles)
  4. why they make your muscles weak and heavy

This sarcomere science below is a just a primer for beginners and a refresher course for professionals. I do want you to appreciate just how weird and wonderful sarcomeres are, but what we’re really interested in is how sarcomeres have a starring role in your muscle knots.

Sarcomere size

Sarcomeres are long and thin. Wrap a few hundred of them together like a bundle of firewood, and then line that bundle up end to end with a few thousand other sarcomere bundles, and you’ve got yourself a single muscle cell or fibre. Every muscle consists of many muscle fibres, and therefore of many millions of sarcomeres.

Sarcomeres are too small for microscopes. They are closer to the size of molecules than cells. Compared to a muscle cell — which is already mind-bogglingly small, you understand, about 10,000 of them across the width of a fingernail — a single sarcomere is like a grain of wheat in a silo.2 If you were the size of a water molecule, you could wander around inside a sarcomere like a mouse in Grand Central Station On the other hand, sarcomeres are pretty large as molecular-scale structures go. Every sarcomere is a tidy little package of well-organized proteins, and proteins are massive molecules generally, and sarcomere proteins are big even for proteins. If you were the size of a water molecule, you could wander around inside a sarcomere like a mouse in Grand Central Station.3

How sarcomeres work

You wouldn’t think that a package of proteins, not even big proteins, could be all that clever, but never underestimate organic molecules: they have a way of being even more freakishly amazing than suspected by the last generation of molecular biologists — who were already pretty impressed — and sarcomeres in particular can make hardened researchers cry. People who study these things face the possibility of never really understanding their subject, of never even seeing a live specimen doing its thing — live sarcomeres cannot be directly observed.4

Nevertheless, the internal structure of a sarcomere is well understood: imagine overlapping chains of proteins, like the tines of two forks meshed together. To contract the sarcomere, the proteins grab onto each other and pull, increasing the overlap of the tines. To relax, the proteins “just” let go.5

A (ridiculously) simplified model of a sarcomere.

A (ridiculously) simplified model of a sarcomere.

So, we do not completely understand how sarcomeres do what they do — we just know what they do, in principle.

Normally, sarcomeres throughout the muscle contract with amazing coordination, and they even coordinate with the contraction of sarcomeres in other muscles — precise synchronization of activity spanning from the molecular scale to the metre scale! That is, things that are happening at the molecular scale in your shoulder can be synchronized with sarcomere activity in your lower legs.6

Sometimes, however, isolated patches of sarcomeres may spasm independently of the rest of the muscle — just as capriciously as whole-muscle spasms and twitches happen. We know the kinds of stresses that probably provoke this change — cold, overstretch, anxiety, trauma, pain, fatigue — but exactly why these things cause some sarcomeres to over-contract remains a mystery. For whatever reason, the proteins grab onto each other, start to pull, and will not let go. The tines of the fork jam tightly together, completely overlapping and even overshooting each other partially, like interlaced fingers.

One: The vicious cycle (why trigger points are stubborn)

One evening recently, I bit the inside of my cheek while vigorously chewing a steak. (I was a strict vegetarian for a decade and a half, from age 20 to 35. Which isn’t really relevant, but it’s nice to get to know your tour guide.) I swore, rolled my eyes at myself, and carried on chewing … on the other side, carefully avoiding my bitten cheek, which was already swelling. It’s hard to avoid biting a swollen cheek, though. I hit it a couple more times that evening, and then — what really got me — a hard bite around 4am. I woke up with the inside of my cheek blaring pain at me. A flashlight showed a fat white bulge deep in my mouth, back where the big molars are close together even with your mouth wide open: the hardest spot to avoid biting. And the more I bit it, the more swollen it got, and the harder it was to avoid biting again.

It took five days to break the cycle. I chewed on dozens of ice cubes. I applied crushed up ibuprofen pills. I cut little pieces of plastic to wedge between the wound and my molars. I had a dozen infuriating setbacks where I bit myself again just as I thought it might finally be calming down. I finally won the battle of the cheek by upping the bite-avoidance ante so far that I basically stopped using my mouth for anything for several hours — I just did everything slack-jawed until the nightmare was over.

There’s a reason they are called “vicious” cyles. Positive feedback is a bitch.

An even more vicious cycle

Trigger points are probably not only a vicious cycle, but one that is damned hard to interrupt. Tightly contracted patches of sarcomeres generate a lot of tissue fluid pollution, waste products of sarcomeres that are metabolically “revving” … and those “exhaust” molecules are then accumulating, causing pain and other symptoms, and irritating the trigger point even more. This is called a metabolic energy crisis, and it’s why I’ve been informally calling trigger points “sick muscle” syndrome for several years now.

Of course, “the feedback loop suggested in this hypothesis has a few weak links,” wrote David Simons — one of the doctors who invented the hypothesis, and co-author of the “bible” of trigger point therapy.7 Indeed, it does. He was well aware that several links in the chain of causation were simply guesses.

Nevertheless, some recent research has firmed up the theory.8 Starting with a simpler study in 2005, and then a more thorough one in 2008, a group of scientists using “an unprecedented, most ingenious, and technically demanding technique” have confirmed that there really are irritating metabolic wastes floating in the tissue fluids of trigger points: “… not just 1 noxious stimulant but 11 of them,” Simons explains. “Instead of just a few noxious chemicals that stimulate nociceptors [pain sensors], nearly everything that has that effect was present in abundance.”

Basically, the researchers analyzed tissue samples from in and around trigger points and compared them with healthy muscle tissue. The differences were significant. The tissue of myofascial trigger points is rotten with irritating molecules associated with inflammation, with pain, and with immune function.

The vicious cycle explains why trigger points have the potential to last forever. Many times I have worked on people who have had trigger points in the same location for several decades. My own trigger points are impressively long-lived. I’ve had a barely controllable patch of them in my right hip for a decade now.

Positive feedback also helps to explain why trigger points, even when they do go away, strongly tend to come back. Any well-established trigger point has some reason to be there in the first place: it is a predictable response to some chronic stress or vulnerability in the body. Even if a trigger point could be eliminated on Monday, there’s a good chance that it will be back by Friday. Even if it could be completely eliminated on Monday — the sarcomeres’ proteins restored to a healthy separation, and every trace of metabolic waste flushed away — there’s a good chance that the conditions that led to it in the first place will restore it by Friday.

But more importantly: it’s unlikely that the swamp physiology of the trigger point can be completely eliminated in the first place. No matter what we do to it, there will always be some excessive contraction left, the circulation at least a little restricted, and some junk molecules still floating around in that spot — perfect conditions for the trigger point to flare right back up again.

This squares well with the clinical experience of every patient and professional trying to help: it seems to be easy enough to make trigger points a little better, but incredibly difficult to make them go away completely. Trigger point stubbornness explained. Just like cheek bites.


To continue reading about the science of sarcomeres, see the full trigger points tutorial, Save Yourself from Trigger Points & Myofascial Pain Syndrome This article is just 3,000 words and includes just two out of five chapters sarcomeres and muscle pain. The entire book is 122,500 and 193 chapters. In the full version, you’ll learn about why pressing on patches of stuck sarcomeres “hurts like hell but feels like heaven,” why it tends to make people say funny things, and why contracting muscles with trigger points like trying to pull away from an intersection in third gear. It’s all in the complete tutorial. Buy it now ($19.95) or read the first few sections for free.

Buy! $19.95. All major credit cards and PayPal accepted. Add the trigger points tutorial to your cart.

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About Paul Ingraham

I am a science writer, former massage therapist, and assistant editor of Science-Based Medicine. I have had my share of injuries and pain challenges as a runner and ultimate player. My wife and I live in downtown Vancouver, Canada. See my full bio and qualifications, or my blog, Writerly. You might run into me on Facebook and Google, but mostly Twitter.


  1. I am slowly working on a long article about these concerns and controversies, called Trigger Point Doubts (last updated 2014-01-19). My goal: to take criticisms of the conventional wisdom about trigger points seriously — critically analyzing the “bath” to see how much and what kind of “baby” is really in there … but I am certainly not chucking the whole thing. All that’s really at stake here is an etiologic model (how trigger points work) for a very real and unpleasant experience. My muscles hurt. My patients’ muscles hurt. There's a world full of people with hurtin' muscles! But there may also be some grave problems with how we explain and treat that phenomenon. BACK TO TEXT
  2. This was a tough image to come up with. Sarcomeres are about 2.5 microns long, give or take, depending on whether they are contracted or not. That means you can put about 20,000 of them end-to-end in a 5cm long muscle cell, which is pretty much equivalent to grains of wheat stacked about 15,000 deep into a fifty-foot silo. But the comparison gets confusing when comparing diameters. Muscle cells are only about 40–100 microns wide, which makes them about a thousand times longer than they are wide. A fifty foot grain silo with matching proportions would only be about a half inch wide! More like a grain pipe. Still, sarcomeres are also extremely skinny, just like cells. Laid end-to-end, you could fit only about 40 across the diameter of a muscle cell. But sarcomeres are so skinny that the number you can fit side to side across a muscle cell skyrockets and becomes, once again, comparable to the number of grains across the width of a silo. So you really can think of a sarcomere as being the size of a “grain” in a muscle cell “silo.” BACK TO TEXT
  3. Water molecules are ridiculously small. They are measured on the scale of angstroms, which are 10,000 times smaller than microns. So if you’ve got yourself a sarcomere 2.5 microns long, you could line up about 25,000 1-angstrom water molecules in there. BACK TO TEXT
  4. The only way to “see” them in any detail at all is to use an electron microscope, which requires a dead specimen, and even if you could watch the overall shape of a single sarcomere contracting, it still wouldn’t be enough: all the detailed action happens at the atomic scale. It would be like trying to make sense of a football game from orbit. In 2001, “the smallest consistent biomechanical event ever demonstrated” — not actually “seen,” just demonstrated — was a 2.3-nanometer long step in the length of a sarcomere (see Blyakhman). That is an impressive one-thousandth the size of the sarcomere, but still ten to one hundred times larger than the scale of the smallest units involved, the ions and other smaller non-protein molecules that mediate all of this. And again, this distance was inferred from cryptic and extremely complex data … not “observed.” BACK TO TEXT
  5. Actually, there is nothing “just” about it: how sarcomeres control muscle elongation — what we call an eccentric contraction, which occurs in the biceps when lowering a barbell, for instance — is one of the biggest mysteries of muscle physiology. There is no known mechanism for how a sarcomere’s overlapping proteins can partly hang on to each other, yet still allow themselves to pull apart. See Eccentric Contraction. BACK TO TEXT
  6. Coordination over several orders of magnitude of scale is one of the “holy grails” of robotics — one of the everyday miracles of biology that is extremely difficult to imitate in technology. BACK TO TEXT
  7. Travell et al. Myofascial Pain and Dysfunction. 1999. BACK TO TEXT
  8. Previously referenced, Shah et al. Biochemicals associated with pain and inflammation are elevated in sites near to and remote from active myofascial trigger points. Archives of Physical Medicine & Rehabilitation. 2008. PubMed #18164325. BACK TO TEXT