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How Your Muscles Break Down to Build up

Jan 29, 2017

Think about how many times you’ve told your trainer on Wednesday, “Wow, I still feel sore from Monday.” Ever wonder why that happens to your muscles? Well, it’s due to muscle damage. Yes, when exercising, one often overloads his or her muscles to the point where they become physically altered and impaired. There are ways to track this damage as it heals; specifically there are three factors scientist like to point to as indicative of muscle damage. The three markers are decrements in maximum voluntary muscle contraction strength, elevated creatine kinase levels in the blood, and self-reported delayed-onset muscle soreness. As muscles rebuild themselves, we see an adaptive affect of training on these markers known as the repeated bout effect (RBE). Understanding what triggers these mechanisms, and what the RBE does to them, reveal the adaptive power of the body, and also lets you the client rest in the fact that all that pain is natural, and beneficial.

How your muscles move

Your muscles are capable of performing three types of contractions: concentric contractions, isometric contractions, and eccentric contractions. Concentric contractions occur when a muscle is producing force to shorten itself. Think of a bicep curl; the movement of the curl -bringing the weight from down at the hips with the arms straight, and curling up at the elbows- brings the muscle from an elongated position, to a shortened position. This is the most common example of a concentric contraction. The second type, isometric, is producing a contracting force in a similar manner to the concentric contraction, but without any movement. Think of a wall sit or a plank. You have muscles contracting, but they are not producing any movement in any joints. Both these types of contractions produce force in similar manners. Their mechanisms and operations are well understood. Eccentric contractions however, are less understood. What we do know about them is eccentric contractions are how we slow down lowering a weight against gravity, that they are the most powerful form of muscle contraction (up to two times stronger than concentric and isometric contractions), they put the working muscle(s) under the greatest amount of tension, and as a result inflict the most damage to the muscle(s). The reason for this damage stems mainly from the excessive mechanical load that muscles often handle when contracting eccentrically.

When muscles become damaged through contracting, the body initiates the three markers named previously as protective mechanisms to shield the muscles from any further damage. Common parameters directly dictate the extent each of these mechanisms manifest themselves: exercise intensity (how much weight was lifted and how many times it was lifted), what type of contractions were involved (again mainly as a result of eccentric contractions), and the level of training one has achieved; if one is new to eccentric-heavy training, these effects will be more readily seen, and felt.

Maximal Voluntary Contraction (MVC) Strength

This one is fairly intuitive; if a muscle is damaged, it won’t contract with as much force. This effect can continue to manifest itself for weeks after the initial bout of exercise. This has much to do with the nervous system in addition to the actual mechanical damage to the muscle. In undamaged, healthy muscle, neural firing is actually in maximal eccentric contractions, neural firing is actually inhibited. Once muscles become damaged, this inhibition increases, thus significantly reducing the force produced by a MVC. This reduction is also not just restricted to eccentric actions, but it will also effect concentric and isometric contractions, and can last for up to 10 days post exercise.

Creatine kinase (CK)

This is really only relevant in laboratory setting, but it does play a role in explaining the mechanical damage that can happen to muscles during heavy exercise. Creatine kinase (CK) is an enzyme found in muscle cells. An enzyme is a chemical that accelerates chemical reactions in the body. When muscles become damaged, CK is leaked into the blood, and we can measure that with a quick blood test that is commonly used to diagnose the severity of heart attacks. When we measure CK, we’re actually not interested in CK; what we are interested in is myoglobin. Myoglobin is a structural protein found in muscles that correlates very closely with CK blood levels. Elevated myoglobin in the blood is the true indicator of muscle damage. Think of a building that’s getting torn down; if your muscles are the building, then myoglobin is the rubble left over from the demolition. So the degree to which CK is present in the blood, gives us clues to its level of activity, and from that, we can measure (albeit indirectly) the extent of muscle damage after exercise. There is a lot we don’t know about what triggers CK in the context of muscle damage. There is some debate over what CK’s exact role and influencing factors are in muscle damage because it seems to be a very multifactorial component and can be influenced by many things including genetic factors like ethnicity, all the way down to hydration status prior to exercise.


Now for everybody’s favorite: the post exercise soreness. DOMS stands for delayed-onset muscle soreness. DOMS is sort of your muscles’ alarm bell that goes off when there is excessive muscle damage present in a muscle group. Research has shown that DOMS is a signal of more macro-level damage than CK, which deals with damage all the way down at the cellular level. Muscle cells are wrapped together in sheaths of connective tissue and it has been postulated that DOMS is related to inflammation of the connective tissue that holds these bundles together. DOMS typically starts 24 hours post-exercise, and similar to MVC strength decrements, can last for up to a week and a half after the initial bout of exercise, though there is some question as to how closely correlated these two factors are and whether or not one directly causes or affects the other.

The RBE:

What we know is there is an affect of training on these three protective mechanisms, they will improve, in this case they will lessen, over time as your muscles get stronger. This adaptive process is known as the repeated bout effect (RBE). The basic principle is that as muscles are trained and strengthened, the less activation we see of the aforementioned markers of damage in the muscle cells. How we discovered the RBE was simple; researchers would put two people through two identical bouts of exercise with a week or two separating each bout to allow the muscles to fully rebuild and recover, and measured those three muscle damage markers at various points after each bout. Now note that in these studies, the two bouts of exercise that were the exact same in terms of volume. If you add volume (aka weight), it will create more muscle damage beyond what the RBE can protect against. So by matching the bouts, we can more accurately see the effects, and draw conclusions from them

So what have researchers concluded? Multiple studies have shown significant improvements in MVC, CK levels, and DOMS, along with less neural inhibition of muscular contractions after the second bout of exercise. Scientists measure this using something called an index of protection. Basically how the index of protection works is the higher the index value, the greater the influence of the RBE on that particular factor. When we measure RBE, we see that it has the greatest protective effect on CK, followed by MVC, then DOMS. So the RBE is most effective at reducing CK levels after exercise, and inhibiting the decrements in maximal contraction strength after exercise. The fact that the RBE is most effective on CK leads some to believe that the greatest adaptations of the RBE have to do with the actual structure of the muscle.

Muscle cells (also called muscle fibers), are comprised of bundles of smaller units called myofibrils, and myofibrils are divided up into smaller sections called sarcomeres. Think of a myofibril as a chain, and the sarcomeres are the individual links in the chain. Sarcomeres can vary in length, and the longer sarcomere is, the less tension it can withstand before “popping” (yes, that is the scientific term). Thus there is more sarcomere popping associated with eccentric activity because again, eccentric contractions put muscles under the most tension. During the repair process after a bout of training, something happens that allows the muscle to adapt and become stronger. As of now, all we have is theories on what exactly happens in the muscle, although it appears that muscles ascribe to the adage, “Many hands make light work.”

The prevailing theory on this is that the muscle reinforces sections of popped sarcomeres with more, smaller sarcomeres. This allows the muscle to produce more force at longer lengths and higher tension because the sarcomeres in that section won’t become overstretched because there are more of them.

Changes also happen in the connective tissues that bind together the myofibrils in muscles fibers, and the muscle fibers to other muscle fibers. Both of these can explain the possible structural adaptations to the muscle, the neural adaptations are not as clear cut, but there is one that we have solid evidence on that is quite fascinating.

Imagine you’re doing a maximal bicep curl with your left arm. Now a question: is doing a heavy bicep curl with your left arm only, doing anything for your right arm? Turns out the answer is yes, a little bit. A contralateral (opposite side) effect is observable, and this effect appears to double when engaging in eccentric exercise. Again this is a neural adaptation, which seems to confer some cross-over adaptations to, in this example, the non-exercising right arm. This appears to be another effort by which the body protects itself against muscle damage.

So that deep pain that you feel in the morning after a hard workout? Odds are A) the workout you did the night before had lots of eccentric movements, and B) those eccentric actions, while painful in the short term, are the most efficient way to activate a key biological process that muscles rely on to enhance their ability to resist damage, and generate more force.


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