Wednesday, January 24, 2018

The Science of Muscle Atrophy from Immobilization

An achillies tendon rupture I experienced last month had me in a cast for two weeks and a non weight bearing boot for another 4.  With any injury, you have to define your plan of recovery and the goals for the process of healing and the big concept of return to play.  The biggest goal for me right off the bat was to limit atrophy as much as I could.  Better to preserve muscle then spend months trying to reacquire it.  The last few months of rehab in an achillies rupture is getting the size back to essentially have enough cross sectional area to give the strength back to plantar flexion.  The goal became to fight off atrophy.  Learn your enemy, his tactics and weakness.

What is atrophy?

Atrophy can occur from a few mechanisms.  They are immobilization, spinal cord injury, loss of gravity( space) and aging.  For most of this post will be dealing just with immobilization.

The opposite of atrophy is hypertrophy, or get that muscle bigger.  There is quite a lot of science that shows the model for this, on the contrary and a bit surprising, there isn't a clean model for atrophy.  This is because a chronic decreased use is hard to come by to study.  Most of the research is with rats and dogs.


Limb immobilization has been used for a very long time to protect a broken bone or injured tissue from further injury.  Essentially, one is creating a barrier from movement.  The most common negative consequence of this is muscle atrophy from decreased use.

Muscles respond to the tension they are placed under.  Electrical activity, tension and slight motion can still occur while immobilized, just not gross movement.  Muscle tension hasn't been measured in an immobilized state.  Think of immobilization as reduced, not disused.

(most of these notes will be from the excellent textbook "Skeletal Muscle Structure, Function, and Plasticity" by Richard L. Lieber

There have been some studies that have studied the EMG of muscles in an immobilized state.  One example (that I found especially relevant for my achillies rupture) was implanting  electrodes in a fast twitch medial gastrocnemius and slow twitch soleus muscle of rats.  There was decrease in EMG after just 1 week, greater decrease in the slow twitch medial soleus then the fast twitch gastroc.  The take home for this study was that EMG had nothing to do with atrophy changes.  Just because there was a decrease in EMG didn't mean less atrophy.

There was some interesting relationships between being immobilized in a lengthened, shortened or neutral position.  The soleus immobilized in a neutral position showed 50% atrophy, in the lengthened position it showed no decrease at all, those in a shortened position atrophied the most.

Most of the disuse models have shown that slow twitch muscles atrophy to a greater extent then fast twitch muscles.  Soleus will atrophy more then the gastrocnemius and anti gravity muscles atrophy faster then their corresponding antagonists.  (gastroc will shrink more then tibialis anterior)

A few interesting points regarding immobilization of the quadriceps.  Comparing rectus femoris ( a two joint muscle) the vastus lateralis and Vastus medius.  RF underwent the least, this was theorized because it was more "active" as it had access to two joints.  Vastus medius had the greatest atrophy as it had the greatest percentage of slow twitch so it had the greatest response to the decreased use.  For ACL or knee immobilization the vastus medialis traditionally shows the greatest atrophic response.

The takeaway from this is that muscles that are used quite a lot will have more slow twitch muscle fibers and if they are immobilized, expect it to have a greater atrophic response then a fast twitch muscle, or a muscle that was used less on average.  There is also seen a change in fiber type from slow to fast after immobilization.  (This really surprised me)

Muscle power seems to be a direct relationship to the cross sectional area.  Atrophy definitely brings strength loss with it.  Remobilization after the immobilization then brings the therapy goal of  hypertrophy.  There are not a ton of studies done on how long it takes to bring back the tissue to pre immobilized size.  The data just says it takes longer.  (Big help!)  One dog study showed that 10 weeks of immobilization and 4 weeks of active recovery brought with it a 30% reduction from the original size/characteristics.  The fiber type changes are expected to change back.  Extracellular connective tissue also returns to baseline.

At the cellular level muscle protein turnover is occurring.  Degradation is happening faster then synthesis.  After only one day of immobilization the soleus muscle can decrease their protein synthetic rate by 50%.  This decrease is seen continuously for around 30 days, then the muscle mass stayed around constant.  In other words it took about a month for the muscle to reach homeostasis.

Two genes have been credited with universal regulation of atrophy, MuRF1 and MAFbx.  These enzymes are used to mark proteins for degradation.  ( In the future, maybe they will be used to prevent atrophy!)  The number one player for the regulation of these enzymes is the transcription factor Foxo.

Foxo, interestingly, can be used for atrophy and hypertrophy.  Things that cause atrophy, like immobilization, activate Foxo to upregulate MuRF1 and MAFbx and stimulate protein degradation and thus atrophy.  Things that stimulate hypertrophy, exercise, electrical stimulation, overload, cause an activation of another factor called akt, which inhibits Foxo and stimulates protein synthesis and thus hypertrophy.

The take aways are if you have the ability to cast or immobilize in a lengthen state do it.  If you can get moveing before the 30 day window do it.  Create muscular movement even if the joint can't be moved.  ISOMETRICS.  If there is a way to use electrical stimulation do it.  Work the contralateral limb.  Upping some protein intake probably won't hurt.  The balancing game of introducing movement and load to protecting the original injury is not a cut and dry situation and is an under studied field.

Sunday, January 14, 2018

Why Do Self Myofascial Work

We live in an age where your health is in your hands.  No longer is inadequate information, tools, or ability an excuse.  Relatively speaking, self myofascial care is one of the biggest health returns for your money and high return on investment from a time/money perspective.

Self Myofascial care is when a person uses a tool or object to influence the muscles, nerves, blood vessels, bones, lymphatic system, and fascia.  Fascia is a big deal as it is literally everywhere in your body.  It covers your body, it's embedded into the muscles, it forms "structures" or thickened areas. It has the ability to contract, relax and move.  It can be dehydrated.  When we target an area, we are essentially working all this stuff and this is globally referred to as connective tissue.

A person can experience restrictions in the connective tissue.  This means that areas, such as between muscle bellies, that should have a slight glide or wiggle room, no longer wiggle or move as smoothly as they should.  Over time, this can lay down fibers that further increases the inability to glide smoothly.  This can also mean these areas are less hydrated.  Dehydrated tissue is one mechanism that can be thought to contribute to muscles strains.

Certain areas of the body can also experience trigger points.  Trigger points are areas that are super sensitive when applied pressure too, and can even express pain at sights elsewhere in the body.  For example a trigger point in the glute medius, a hip muscle on your side, can express pain in the lateral calf and even into the lower back.  Trigger points can be active or latent.  Active means you know this hurts, latent means you were unaware that it hurt until it was pressed on.  Trigger points, while controversial, have been studied and shown that when blood was taken from them a much higher (H+) was in them.  It was more acidic.

Restrictions in movement can also start to lead to congestion from a lymphatic system perspective.  Remember, the lymphatic system works on the muscles actively contracting.  If they can't contract as strongly as they are capable of, the lymphatics can be congested in certain areas.  There is some evidence that this creates muscle inhibition.  (It makes us unable to express the strength we should be able to)  Muscle weakness.  

When the body starts having restrictions in how muscles contract or move and trigger points that unconsciously affect how we feel, we will start to move differently.  This compensation pattern may last weeks or years.  But eventually, this too will have it's own restrictions and inadequacies.  How often do we just chalk it up to moving poorly or sore when we wake up or an increase in nagging injuries to just old age.  Perhaps our connective tissue is just in poor shape?

Do you brush your teeth twice per day?  What did you do for your connective tissue today?


1.  Keep from developing or start to break up the restrictions.  This is going to help you move better.  More easily.  Increased Range of Motion!

2.  Stop Trigger Points, but also become aware of latent ones.  This is going to start to get rid of unconscious avoidance of movement or positions.  It can also drop down peoples pain!

3.  Increase lymphatics and blood flow.  This brings more blood flow (more oxygen) to the tissues, but also gets rid of the metabolic waste products.  Win, win.  It can create stronger muscular contractions!  

4.  It can help get rid of the delayed onset muscles soreness that can be present after hard workouts.  Increase recovery!


1.  It increases circulation of blood flow.  Blood flow is the reason tissues can heal.  Sometimes people have surgeries just to get blood flow to an injured area.  This in itself is such a big reason it can not be overstated.

2.  Connective tissue heats up.  Some famous fascia researches state that when the area hits a certain temperature from myofascial work, the area will move better and have better contraction ability.

3.  Tissue tension changes.  The connective tissue can relax for a bit.  Often times when one area of the body relaxes another area adjacent becomes more active or "stronger."  This is called reflex neural inhibition.  Work your quadriceps and often the lateral hips will feel stronger.


At the end of the day regardless of everything you just read, I believe there are two very unscientific reasons why we should do a self care on our connective tissue.  One, it just feels good.  You will get up and feel better.  Two, it's a gateway habit.  Ever hear of the concept gateway drug?  Haha...yea, gateway habit.  When you start to do self care, I believe it bleeds into other areas of your life from exercise to nutrition to self image.  The snowball effect.

Minutes a day at minimal cost can create huge healthy and lifestyle benefits.  As a plug in we created the MOBI to address all the soft tissue needs for a self maintenance program.  It replaces the foam roller, the ball, the stick and every other odd object you have collected to hit different parts of your body.  It's also a nice self defense tool if the zombie apocalypse hits.

2018 should be the year you develop your Self Myofascial Care Program, your body deserves it, and you only get one of them.