Did you know muscle’s only job is to get shorter? That’s it. That’s its whole job and understanding how it does that, why it does that and what limitations it has can help you understand how your body works in the pool. While there are three types of muscle in the body, we are only going to talk about skeletal muscle, aka striated muscle (we will know why shortly). The other two types are smooth muscle and cardiac muscle, both of which do not produce movement and you have no voluntary control over. As you can imagine, skeletal muscle attaches to the skeleton. It almost always crosses a joint (or two joints) and brings those two bones closer together. That’s how you move, simple right?
Alright, let’s zoom in to see the basic functioning unit of all muscle. What the cell is to the organism, so the sarcomere is to each muscle cell. The sarcomere contains the sliding filament theory (who knew muscle was so fancy). Here’s a picture to help you out:
See those Z-lines? That’s what comes closer to each other. Even though each sarcomere is only micrometers long and only shortens a few nanometers, when you place millions of them end to end (as below), you get an additive effect, allowing each muscle cell to shorten many inches. This is also what give skeletal muscle its “striated” quality.
Of course, one long train of sarcomeres, in “series” can’t move much weight (or water), so we need a whole bunch of sarcomeres in “parallel,” or all next to each other working together. The raw strength of a muscle is determined by how many sarcomeres are in parallel…otherwise known as bigger muscles.
Ok, so muscle gets shorter by moving the Z-lines together…but how does that happen? Let’s take a closer look at what goes on between the Z-lines, where those thin and thick filaments are the picture.
The thin filaments, called actin, are attached to the Z-lines from both ends of the sarcomere. The thick filaments, called myosin (myo=muscle) overlap the actin from the middle, but they do NOT attach to the Z-line.
Now, we zoom in more.
Here is where the magic happens. Coming off all along the myosin proteins are the myosin heads which act like caterpillar legs and “crawl” their way towards the Z-line along the actin filaments. Think of the Z-lines as two brick walls with ropes attached to them going inwards. The ropes are the actin. Now imagine two groups of swimmers grabbing onto the ropes facing each wall. Now these are super swimmers, so when each group starts pulling on the actin…I mean ropes; the walls actually move and come closer together.
That’s how muscle works, and now that you understand that, I can start explaining why it matters to you.
When a sarcomere is activated, it’s an “all or nothing” event (actually the entire motor unit activates, but that’s another show). All of the myosin heads start pumping along and crawl their way to the end of the actin, bringing the Z-lines closer together.
BUT, not all myosin heads are created equal. When myosin heads are activated, it costs energy. Some myosin heads use up a lot of energy and they crawl real fast (imagine bodybuilders pulling on the ropes), and others spend a little energy and move slowly (marathon runners on the ropes). This plays a HUGE role is what we call fast twitch and slow twitch muscle fibers (also another show).
There are more factors that play in, but as you can imagine if you have a muscle fiber with 100% fast twitch myosin heads, that muscle fiber is going to spend a lot of energy, move itself quickly down the actin, and generate a lot of force. Versus a slow twitch fiber which will have mostly slow twitch myosin heads, which eats up energy slowly, generates much less force, but can make those energy reserves last much longer.
Again, remember that myosin head type (slow vs fast) is only one factor that plays into whether a muscle fiber (the entire muscle cell) is slow or fast twitch. More on that later.
To complicate things further, a single muscle fiber can have any combination of fast and slow myosin heads making up its power producing ability. This gives any muscle in the body a wide range of abilities as far as power production and endurance. Some muscles are specifically engineered to have a dominant type of myosin heads. The soleus, one of your calf muscles, is almost all slow twitch myosin heads (good for walking miles). While the outer quad muscle, called the vastus lateralis, is almost all fast twitch (good for jumping a few times). Most muscles in the body of a normal person start with a relative equal amount of slow and fast myosin head fibers.
What initially determines which muscles get what type of myosin heads? Genetics. Not the way you work out (sprint vs. distance), not what you eat or how much you lift but genetics is the biggest factor. Your baseline muscle fiber composition is based on genetics. This is part of the reason some people are naturally good at the 100 meter dash, and others are great at marathon running. The difference doesn’t come out as much in swimming since our events are not as extreme as running. BUT, as I said before, it’s waaay more complicated than that, so we have another show just talking about slow vs. fast twitch muscles.
Do an experiment for me. Flex your arm at 90° and have a friend try to pull your arm away. Tough isn’t it. You could probably hold them off pretty well. Now, open your arm until it’s almost straight and repeat. Repeat with your arm all the way flexed. At the extreme two points, you bicep is much weaker and your friend should be able to out-muscle you, if only for an inch or two. Every muscle in the body encounters this phenomenon, including the ones you swim with (which is all of them pretty much). The question is why?
What applies to the microscopic is what occurs at the macroscopic, so let’s get back to our sarcomere. Here is a series of sarcomeres with the muscle stretched at different lengths, from super stretched to super flexed.
Notice anything special about the actin and myosin? In the middle, the actin and myosin are well overlapped and there is maximum “interaction” between the myosin heads and the actin proteins. This means the sarcomere is at its strongest because all the myosin heads have a chance to “crawl”. At the extreme stretch however, the myosin and actin barley overlap, and so only a few myosin heads can crawl along the actin, explaining the weakness at this point. When fully flexed, the actin from either end of the Z-lines get too close and overlap, causing too much congestion and weakness.
This is a big reason why swimmers get short when they get tired!! This is why swimmers get short when training with paddles! You have seen and felt all this happen when you swim, and this is the reason why: your mind says “go faster, more power!!” and your body says “use the best sarcomere length,” so it chooses to get short to maintain power when you’re tired.
Let’s try to draw it out.
When your arm is fully stretched, it’s at its weakest point. This is for multiple reasons (angle of the muscle pulling on the bones, the length of your arm….) but also because the sarcomeres in those muscles (the lats mostly) are fully stretched, and there is little actin and myosin interaction. As another analogy/common experience among swimmers, the toughest part of a pullup is the start for the same reason.
By the time the arm has started pulling a few inches, the actin and myosin are fully overlapped and all the myosin heads available to you are crawling along the actin, producing the maximum power. This is where the greatest acceleration in your stroke occurs (if your forearm is pointing in the right place of course).
If you have not-so-good technique and you let your arm swing all the way back to your hips, you are now on the other side of the graph, where the sarcomeres are squished together too much to create any more force. That’s why coach says “don’t pull back all the way, get your elbow out of the water when you’re at your hips.”
This begs the question, “why am I always working on staying long and out in front with my arms if being short is so much more powerful? Why don’t I just stick my arm straight down where I get the most leverage and just take more strokes?” The biggest reason for staying long is to reduce drag and increase efficiency. Any shortening of the stroke will almost always mean an increase in drag. In swimming, if you choose to increase your power instead of decreasing your drag…the water will always win. We are here to understand why your body is fighting your mind, and hopefully understanding the basics of sarcomere length-tension relations will help.
This brings us to a phenomenon we all see and do. That first 25 of any race is great, you feel strong, long and relaxed. But by the end of the race you look and feel like you’re swimming up instead of forward. Here is an illustration:
The first 25, your muscles are full of energy and without much lactic acid in them (we will discuss where and why this comes in another show), so your muscles are pretty strong throughout the full range of motion. By the last 25, you are neck and neck with your greatest rival, your muscles are not working well and burn like the sun, and your brain is shouting “GO FASTER, GO FASTER, GO FASTER.” Naturally, your body responds to those commands, but not in the way you want. Because your muscles are fatigued, they can no longer maintain the same tempo or strength throughout the entire range of motion. So, your body does the “smart” thing, and sacrifices the length of the stroke in order to maintain tempo and power. By lifting the head and body up vertically in the water, your body shortens the muscle (even with your arms at full extension) and keeps the actin and myosin fully overlapped. You can see how the angle in the picture gets smaller, this means the muscle is shortening a little, even if the arm is straight.
That’s all fine and dandy to maintain power, but your body gave up the battle against drag. That’s why you got out touched! That’s why you work on head position so much. That’s why you practice your finishes with your head down. That is also why some swimmers finish their races with straight arms and heads down, so they can force their body position.
Another time this comes up is using paddles or fins for the first time, or training breastroke kick after months of not swimming breastroke, or any time you do something new in training. The bottom line is muscle soreness is caused by muscle damage (or at least is starts with muscle damage). Yup, your muscle cells actually break when you train. We can even detect how much damage you caused by measuring certain muscle enzymes in your blood (creatine kinase if you’re interested)
Tangent: troponins are another protein found in muscle and leak out if the muscle is damaged or dies. In medicine, we measure these troponins during a heart attack.
And if you damage too much muscle and don’t stay hydrated, certain muscle proteins which are toxic to your kidneys can cause a disease called rhabdomyolysis (rod-muscle-breaking) explaining the “peeing blood” phenomenon when you work out too hard (not actually blood BTW).
No…you don’t get to take this article to your coach and say “See! We can’t work hard otherwise we will die of rhabdo!” We will get back to this, but first let’s go through this step by step. You’re just starting a new season and you work out for a couple hours in the pool. During workout, the first thing to break are the Z-lines we talked about earlier. They are damaged through overstretching with repetitive motions, overloading or even lactic acid (some think so at least) and never return to normal. Once enough sarcomeres are broken, the entire muscle cell loses its structural strength (maintained by a cytoskeleton made of actin interestingly) and the muscle cell membrane breaks open. This does not kill the cell. But it won’t function anymore until it is repaired.
By this time you are getting out of the water. You’re not in much pain though. That’s because muscle cells are not nerve cells, and they don’t transmit pain to your brain. When you get a deep cut through muscle, it hurts because you cut adjacent nerves, but the muscle itself does not feel pain. After about a day the pain starts to set in. That’s because while you were sleeping, your body was busy fixing what you broke. To do that, it had to recruit a whole lot of inflammatory cells who clean up the mess of broken proteins by eating them up. This also causes edema, or the buildup of fluid, and O2 radicles to form. These place tension on the swollen, broken muscle and also release certain chemicals that cause pain just by themselves (like histamine). This also causes the muscle to spasm and contract involuntarily, which may explain why muscle is “tight” when sore. This may also explain why stretching and rolling helps (another show of course).
One day after your first workout of the season, you are in maximum pain. Remember, your body is a machine that takes care of itself, and the best way for it to protect itself from further damage is by telling you to stop breaking things through the message of pain. BUT…in your infinite knowledge, you decided to go back to the pool. By the time warmup is over however, you feel pretty good. That’s because the extra movement has worked out some of the swelling and chemicals causing the pain. Also, warming the muscle helps it relax instead of spasm (just like a hot pack).
After a few days of this, you notice you don’t get sore anymore, even from a two hour butterfly work out (yucky...). What changed to make your muscles not break as much? A few things, but they all have to do with decreasing the amount of breakdown that occurs. First, you’re in better shape, so you don’t make as much lactic acid (or at least, you can get rid of it faster, yes…another show too). Second, the cytoskeleton of the muscle improves, giving muscle cells more structural integrity. And lastly, outside the muscle cell, connective tissue develops to further stabilize the muscle.
Your half way through the season now, and coach decides it’s a good time to start running for dryland. Great…now you’re sore again, and it’s even worse than before! Why? You’re in good shape, you kick a lot in practice, but a couple work outs with gravity and you’re shot again. The big thing to note here is that muscle changes according to the challenge, and nothing else! Your body is lazy, and conserves resources above all else. When muscle adapts, it only adapts to the stimulus it is given (swimming, not running). This means every new challenge (running, paddles, fins, weights...) causes the muscle break in a new way and you get sore all over again.
Tangent: This is why you do NOT do new things during taper time! Even if it is “easy” or not a lot, the newness of the activity will make you sore. Bad bad bad.
One more thing, different types of motions can cause more muscle damage than others. Isometric (iso=same, metric=length) exercises are motions where the muscle is contracting, but not moving. Like pushing against a solid wall, your muscles are working, but nothing is moving.
Concentric (con=together/shortening) motions are where the muscle is contracting and getting shorter. Like curling a weight that is light.
Eccentric (ek=out of/lengthening) motions are where the muscle is contracting and getting longer. Like curling a weight that is too heavy and overcomes your muscle strength.
In an untrained person (or if done for long enough), they all cause muscle damage and soreness. However, eccentric motions cause the most damage, and lead to the most soreness. Can you think of any motions in swimming that are eccentric? Nope, neither can I. This right here is the limiting factor in almost every other sport. Marathon runners, powerlifters and ball sports are all limited in how much they can train because eventually their muscles breakdown too much from the eccentric motions and they have to wait until they heal. Trained swimmers don’t have that limit. That is also why swimmers don’t deal with rhabdomyolysis much either, so no excuses swimmers.
Tangent: eccentric exercise and muscle damage is a big factor in stimulating muscle growth, which is why these exercises are heavily targeted in bodybuilding.