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What you need to know about muscle wasting (atrophy)

If you have knee arthrofibrosis, or you’re treating somebody with it, you’re probably worried that the muscles of the upper leg aren’t what they used to be before the surgery or injury. There might have been advice to exercise the affected leg even harder in an effort to build muscle, or there might have been accusations of non-compliance and blame. However, it is well known that muscle atrophy is a natural outcome of inflammation and nerve damage from an injury or surgery [1,2]. This post-op pathological atrophy is not the same condition as the physiological atrophy from being sedentary [2] and can’t be successfully treated in the same way with exercise [3] while inflammation is high. This is because skeletal muscle is controlled by motor nerves, and any negative changes in the health of these nerves affects the mechanical forces that can be generated [4] and can significantly impair the ability to contract the muscle.

Peripheral nerve injuries are common after major trauma or surgery. People who have had a major surgery such as a total knee replacement will likely be familiar with numb patches around the knee, and may also experience tingling or burning sensations as a result of damaged nerves. There are a variety of ways in which nerves can be damaged by trauma or surgery, including hypoxia (lack of oxygen from decreased blood flow to cells), crush injuries, compression, stretching and mechanical damage. Nerves can often recover from minor injuries, but complete transection (cutting) of the nerve frequently results in permanent nerve injury. Even with the best of care, only about a third of peripheral nerve injuries recover completely, with the remaining two thirds of people experiencing some degree of nerve fibrosis that can result in muscle atrophy, chronic pain, weakness, poor function and sensory changes [5].

Exercising a joint with arthrofibrosis has very different effects compared to exercising a healthy joint

As with other forms of fibrosis, in nerve fibrosis myofibroblasts are activated by TGF-β and inflammatory cytokines after injury, and produce scar tissue, adhesions and contractions that can tether nerves, cause compression, and impair nerve signalling and conduction [5]. Even minor injuries can cause nerve damage, and carpel tunnel syndromes is an example of nerve fibrosis that can occur even without an obvious injury [5]. In joints that contain scar tissue the increased stiffness and altered mechanical stress further contributes to nerve fibrosis [5].

Upset nerves create inflammation, and exercising a joint with arthrofibrosis or another inflammatory condition has very different effects compared to exercising a healthy joint [1]. In this inflammatory situation all the exercise in the world may not build muscle, and could actually be counterproductive since exercise increases inflammation [6] and the production of TGF-β [7], which are the primary drivers of fibrosis and also cause muscle atrophy [7]. In addition, in knee arthrofibrosis the Hoffa’s fat pad is likely to be pinched while exercising the affected leg, and because this organ is packed full of nerves, pinching increases the inflammatory and fibrotic processes.

We believe that its best not to exercise the affected limb until the inflammation and pain have resolved

So, muscle atrophy will likely occur following joint trauma despite exercise, and we believe that its best not to exercise the affected limb until the inflammation and pain have resolved. Exercise can be carefully introduced as tolerated when inflammation and pain are controlled, while always being careful not to over-do it.

Dietary quercetin, a natural compound found in many plants, including onions, was found to decrease muscle atrophy from denervation in animals [8]. Quercetin is available as a supplement. As always, please consult your doctor before starting a new supplement.


  1. Madaro, L. et al. Denervation-activated STAT3-IL-6 signalling in fibro-adipogenic progenitors promotes myofibres atrophy and fibrosis. Nat Cell Biol 20, 917-927, doi:10.1038/s41556-018-0151-y (2018).

  2. Ji, Y. et al. Inflammation: Roles in Skeletal Muscle Atrophy. Antioxidants11, 1686 (2022).

  3. Lepley, L. K., Davi, S. M., Burland, J. P. & Lepley, A. S. Muscle Atrophy After ACL Injury: Implications for Clinical Practice. Sports Health 12, 579-586, doi:10.1177/1941738120944256 (2020).

  4. Alix-Fages, C., Del Vecchio, A., Baz-Valle, E., Santos-Concejero, J. & Balsalobre-Fernandez, C. The role of the neural stimulus in regulating skeletal muscle hypertrophy. Eur J Appl Physiol122, 1111-1128, doi:10.1007/s00421-022-04906-6 (2022).

  5. Wang, M. L., Rivlin, M., Graham, J. G. & Beredjiklian, P. K. Peripheral nerve injury, scarring, and recovery. Connect Tissue Res 60, 3-9, doi:10.1080/03008207.2018.1489381 (2019).

  6. Nieman, D. C. & Wentz, L. M. The compelling link between physical activity and the body's defense system. J Sport Health Sci8, 201-217, doi:10.1016/j.jshs.2018.09.009 (2019).

  7. Dreher, S. I. et al. TGF-beta Induction of miR-143/145 Is Associated to Exercise Response by Influencing Differentiation and Insulin Signaling Molecules in Human Skeletal Muscle. Cells 10, doi:10.3390/cells10123443 (2021).

  8. Mukai, R. et al. Preventive effect of dietary quercetin on disuse muscle atrophy by targeting mitochondria in denervated mice. J Nutr Biochem 31, 67-76, doi:10.1016/j.jnutbio.2016.02.001 (2016).

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