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.