Quads atrophy post ACL repair

[badlybruised]

I am a physio student looking into the different rehab protocols post acl repair.

I was wondering if anyone is aware of why there seems to be a quads atrophy post acl repair, esp vastus medialis, and the mechanisms that cause this.

Thanks :@)

[pcfu]

I'm not a doctor or anything, but i would think that the muscle atrophy is simply because you aren't using those muscles, so they waste away. Try using crutches for more than a few weaks and then you'll see how easy it is to lose muscle

[injuryupdate]

I think studies have shown that knee effusion itself causes specific VMO atrophy. Even when 'recovered' from an injury like an ACL reco, the body probably learns running mechanisms that protect the knee joint against high torques, putting extra stress on other body parts. In this sense the knee doesn't get used as much so the muscles may stay weak.

Interesting letter to BJSM this month showed stats that the non-dominant thigh in soccer players was bigger than the dominant. Wonder why this is (maybe bigger torque on the stance leg in kicking?)?

[hhh]

Most research concerning patterns of muscle wasting in reflex inhibition has been conducted at the knee joint. Evidence of patterns of motor responses have classically been studied with pinching of the joint capusle to replicate a pain situation. This led to inhibition of knee extensors and facilitation of knee flexors. I think the reference Johnny is eluding to was experimentally induced effusion, which was used to stimulate joint receptors in human knees, which led to preferential inhibition of the vastus medialis muscle. Similar findings have been documented in patellofemoral pain syndromes. So initially it is nociceptor generator neurogenic inhibition of the VMO that occurs. Results of animal and human research to date strongly support the concept that lack of information to the body about gravity differentially affects the antigravity (one joint) muscles, which change their patterns of use and display changes in physiology. This change in muscle physiology occurs through a process called neuromuscular plasticity, where the physiological structure of muscles is determined by the pattern of neural impulses delivered to it. As a consequence of this inhibiton and atrophy, the muscle imbalance remains and can be accentuated with exercises that do not specifically target VMO.

If you want a hardcore neuro answer let me know.


I think studies have shown that knee effusion itself causes specific VMO atrophy. Even when 'recovered' from an injury like an ACL reco, the body probably learns running mechanisms that protect the knee joint against high torques, putting extra stress on other body parts. In this sense the knee doesn't get used as much so the muscles may stay weak.

Interesting letter to BJSM this month showed stats that the non-dominant thigh in soccer players was bigger than the dominant. Wonder why this is (maybe bigger torque on the stance leg in kicking?)?

[Jengizu]

I have experienced the same atrophy in the vastus medialis after (and actually prior to) arthroscopy (medial plica removal). I think in my case it's primarily due to the fact that I wasn't able to place the same load on my knee because of pain prior to the arthroscopy. I'm slowly building up that muscle now, using mainly lunges on a Smith machine in conjunction with leg extensions.

[injuryupdate]

Hate to say it (and it wouldn't be true in 100% of cases) but most surgeons believe that medial plica syndrome is a bit of a myth. Good news if they 'took out' your plica was that they couldn't find much else inside your knee, which is great. Keep up the rehab, and you should get better.

[Jengizu]

The only thing I can say is I definitely have less snapping noises coming from my knee during extension after the plica was removed. A lot of other symptoms are gone too, such as an overall feeling of tightness (always felt like I needed to stretch the quads) in the knee joint on the medial side and some discomfort in the back of my knee.