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 & everyone gets a bad one every now & then. Knowing what makes them tick is great “owner’s manual” knowledge!
Microscopic muscles: the source of all movement
A muscle is made of microscopic contractile units arranged in series and bundles: the sarcomeres, tiny packages of proteins (especially myosin II, a famous molecule). Muscles contract because sarcomeres contract. These molecular machines are the best example of how life is chemistry. Although proteins have many impressive properties and do many dazzling things, none is more defining of living things than this ability to generate movement.
Most molecular biology is amazing if you can understand it, but hard to connect to anything as familiar as wiggling your toes. Sarcomeres are an unusual explanatory bridge between weird science and ordinary experiences because they actually resemble the muscles they power. There’s something simple and beautiful about how they are so much like miniature versions of the muscles they power.
You know how kids are so good at asking a chain of “why” and “how” questions? Sarcomeres are the deepest possible answer to the chain of kid-questions that starts with, “How do we move?” (Well, almost the deepest answer.2)
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 powered by the weird properties of mind-bogglingly complicated molecules.
And sarcomeres can probably screw up.
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!
The clinical relevance of sarcomere mistakes
Understand sarcomeres and their failure, and you might be able to make sense of muscle knots. Specifically, troubled sarcomeres could explain four distinctive clinical characteristics of trigger points:
- why trigger points can be so stubborn
- why applying pressure often helps
- why stretching feels good (but also does not work any miracles)
- why they make your muscles weak and heavy
The sarcomere science here 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.
The size of sarcomeres
Cells are mind-bogglingly small compared to your hand, sarcomeres are mind-boggling small compared to your cells, and atoms and ions are mind-boggling small compared to your sarcomeres.
So sarcomeres are somewhere in the middle of the sizes of things.
They 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. Even small muscles consist of millions of muscle fibres, and therefore millions of millions of sarcomeres.
Sarcomeres are much too small for microscopes. They are closer to the size of molecules than cells. Compared to a muscle cell, which is already crazy small — about 50 micrometres in diameter, so about 10,000 of them could fit in the width of a fingernail — a single sarcomere is like a grain of wheat in a silo.3
As small as sarcomeres are, they are actually quite large as molecular-scale structures go. Every sarcomere is a tidy little package of well-organized proteins, and proteins are massive for molecules, and sarcomere proteins are big even for proteins. And so: if you were the size of a water molecule, about a tenth of a nanometre, you could wander around inside a sarcomere like a mouse in Grand Central Station.4
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.
Despite the limitations of observation, the internal structure of a sarcomere is reasonably well understood from decades of elaborate inference and increasingly sophisticated imaging, even at the nanoscale. We know they look kind of like forks:
A (ridiculously) simplified model of a sarcomere.
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
That’s the structure. What about the function? We do not fully understand how sarcomeres do what they do — we just know what they do in principle. The details of myosin activity happen at the atomic scale and at extreme speeds. It’s like trying to watch a fast-forwarded football game from orbit with a pair of binoculars. And so “the process by which myosin II generates motion is still not completely understood,” Hoffman explains in Life’s Ratchet, “but substantial progress has been made by structural (X-ray, electron microscopy), biochemical, flourescence, and laser tweezer studies.”6 It was the first molecular motor discovered, but “it remains [in 2012] one of the most enigmatic.” Many details of how the stuff works remain surprisingly controversial. And that’s all about pure myosin, a standalone molecular machine in a “test tube,” rather than the intense metabolic environment of living muscle.
Normally, sarcomeres throughout the muscle contract with amazing coordination, and they even sync up with the contraction of sarcomeres in other muscles — precise choreography of action spanning from the nanometre 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.7
Perhaps unsurprisingly, this system isn’t perfect. Sometimes, isolated patches of sarcomeres seem to contract independently of the rest of the muscle. They probably do so briefly all the time, the microscopic version of an eyelid twitch or a shiver. Or they may get “stuck” like that: a trigger point, a sustained, inappropriate contraction, a microscopic version of a long-lasting cramp or the spasticity seen in some diseases.
We don’t know any of this for sure, but it’s all plausible: almost anything that happens as a matter of course in biology can happen too much, too little, or at the wrong time. And we do have some evidence that patches of sarcomeres do indeed malfunction like this. Sometimes the proteins appear to grab onto each other, pull hard, and hang on — the tines of the fork jammed tightly together.
Many experts have speculated about the kinds of stresses that provoke such malfunctions — cold, overstretch, anxiety, trauma, pain, fatigue — but no one really knows.
One: The vicious cycle (why trigger points are stubborn)
I once bit the inside of my cheek seriously while vigorously chewing a steak. 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.8 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.9 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 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 swampy 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.
END OF EXCERPT
To continue reading about the science of sarcomeres, see the full trigger points tutorial, 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 165,000 and 175 chapters. In the full version, you’ll learn about why pressing on patches of stuck sarcomeres “hurts like hell but feels like heaven,” why stretch seems like a great idea but works about as well as trying to stretch out a knot in a bungie cord, and why contracting muscles with trigger points is like trying to pull away from an intersection in third gear. It’s all in the complete tutorial. Buy it now or read the first few sections for free.
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About Paul Ingraham
I am a science writer, former massage therapist, and I was the assistant editor at ScienceBasedMedicine.org for several years. 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 or Twitter.
What’s new in this article?
2016 — Thoroughly rewrote the introduction to sarcomere basics, much of it inspired by the book Life’s Ratchet (Hoffman), about molecular machines.
- Ingraham. The Trigger Point Identity Crisis: The biological evidence that a trigger point is a lesion in muscle tissue. ❐ PainScience.com. 3590 words. ⤻
- The only way to go deeper is to talk about how molecular machines work — how proteins can extract order from the chaos of the molecular storm, the violent vibrations of nanoscale particles (Brownian motion). That’s way above my pay grade, but I can recommend an excellent book on the topic: Life's Ratchet: How molecular machines extract order from chaos, by Peter Hoffman. ⤻
- This was a tough (but fun) 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.” ⤻
- 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. ⤻
- 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 puzzles in 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. ⤻
- In 2001, “the smallest consistent biomechanical event ever demonstrated” was a 2.3-nanometre 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. The field is advancing steadily, but remains limited by the speed of the flourescence techniques used to show the movement of different atomic parts of the molecular machine. ⤻
- Coordination across 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. ⤻
- Travell J, Simons D, Simons L. Myofascial Pain and Dysfunction: The Trigger Point Manual. 2nd ed. Lippincott, Williams & Wilkins; 1999. ⤻
- Previously referenced, Shah JP, Danoff JV, Desai MJ, et al. Biochemicals associated with pain and inflammation are elevated in sites near to and remote from active myofascial trigger points. Arch Phys Med Rehabil. 2008;89(1):16–23. PubMed #18164325. ❐ ⤻