The Half-Life of Gains: The Rate of Muscular Atrophy with Injury

As per my previous nine million posts and my forehead tattoo, ya girl has had yet another ACL reconstruction. So as I prepared myself for the immediate loss of glutes, and all my Alphalete leggings to be confiscated from me by the gods of Instagram, I thought I would delve into the reality of muscle loss (atrophy) and just how quickly those hard fought gains will disappear.

The Fundamentals of Skeletal Muscle Loss

Skeletal muscle atrophy (decrease in size) occurs due to immobilization (e.g. injury recovery protocols such as bedrest or crutches), ageing, muscle unloading and several pathological processes[1].

At a cellular level, atrophy results in a smaller cross-sectional area of muscle fibres. It is important to note here that the number of fibres do not decrease, the existing fibres just decrease in diameter[2]. This decrease in size leads to reduced force output (muscle strength) [1],[2]. In humans, this is attributed to being a consequence of decreased protein synthesis[3]. In addition to the reduction in fibre number, the rate of fibre reduction is accelerated in fast-twitch (type II) muscle fibres[4]. This decreases the muscles resistance to fatigue.

The extent of skeletal muscle atrophy differs slightly depending on the cause (disuse or disease). As we are discussing muscle loss due to injury, we will focus on disuse atrophy. Patients can either be fully (bedrest) or partially immobilised (e.g. one limb placed in a cast/crutches etc.) and disuse atrophy is evidenced in both cases. Bedrest is the most deleterious to muscle, and 10 days bedrest can result in the patient losing up to 30% of their muscle mass[5]. Now obviously, bed rest is normally reserved for critically ill patients, and losing all your gains should be the least of your concerns. Partial immobilisation is less drastic, but nonetheless impactful. For example, lower limb immobilization (cast etc.) has been evidenced to decrease the leg volume by 12% and lead to a 46 and 37% reduction in type I and type II fibres respectively[6].

The mechanism of skeletal muscle atrophy is multi-faceted and beyond the constraints of this article.

Some key take away points from this section:

  • Muscle atrophy occurs due to disease or disuse which causes decreased protein synthesis.
  • Muscle atrophy leads to a loss of strength and decreases fatigue resistance.
  • Disuse atrophy (injury) can lead to a rapid loss of muscle mass.

Factors Influencing Atrophy

A number of factors influence the severity and impact of atrophy, and these impact the individual with varying effect.

The Half-Life of Gains: Immobilisation Time

Literature is generally in consensus that the biggest rate of change in the musculature occurs in the acute phase of immobilisation. After this, the rates of change continue to decrease and eventually plateau[7]. The most drastic reduction in muscle strength occurs during the first week of immobilisation. The same is true for muscle protein synthesis[8].

It is important to be careful around interpretation of the research here. The rate of change is greatest in the first week, but shortening the immobilisation phase doesn’t alter the rate of change. AKA: if you mobilise too early you will shoot yourself in the foot (specifically the musculature).

Injury Nature/Location

Whilst not directly influencing the rate of atrophy, the nature of the injury can have a knock-on effect. For example, if you fracture your femur, you will be likely on bedrest post-operatively for a couple of weeks. If you sustain a less severe injury (e.g. broken finger) you will not be immobilised for as long. And as we know at this stage: immobilisation increases the likelihood of muscle loss.

The location of the injury also influences the rate of atrophy, and this is different for both full and single-limb immobilisation methods. In the case of full-body immobilisation, it is the lower limb that preferentially atrophies[9]. In fact, one study found that the upper limb musculature thickness remained unchanged during the first ten days of full body immobilisation[10]. Great, so the upper limb won’t lose any strength if we never move it? Wrong. This study used ultrasound to measure muscle diameter. Ultrasound is very user-dependent (influence of user on results) and can be limited by patient body habitus (bigger patients will degrade the signal and thus the accuracy of the scan. (And who said that four year radiography degree was a waste?). Furthermore, all of the studies above state that if we remove a stimulus (load) from the muscle, it will decrease in diameter.

I also wanted to investigate whether there was a difference in the rate of upper and lower limb atrophy in the case of single-limb immobilisation. Will you lose your upper body gains faster if you break your wrist faster than you’ll lose lower body gains if you break your ankle? The upper limb is far less researched that the lower limb. Casting appears to affect the lower limb more than the upper limb[10]. This makes sense to me, as the tasks demanded of the lower body are much greater in terms of muscular strength and output.

In the upper limb, it is the elbow flexors, forearm muscles and triceps that appear to be affected preferentially by atrophy[11]. The lower limb literature tends to focus on the quadriceps, and single-limb immobilisation can lead to a 5-10% decrease in size within four weeks[12]. So, the research didn’t really answer my question, but it does mean there is a niche for a study out there!


The older individual is also prone to sarcopenia (loss of muscle mass due to ageing)[13]. Nothing we can do to stop getting older, except die, and that makes for a bleak article. Regardless, within older individuals exhibit decreased rates of protein synthesis[14] and muscle mass[15]. Note: these are not caused by injury, they’re just a part of getting old!

The immobilised individual will be affected differently based on their age. One study found disuse atrophy to affect the neuromuscular function of the muscle more so in the older individual, while younger people were more affected at the muscle level (changes in fibre diameter etc.)[16].

I couldn’t find much evidence to say whether the rate of atrophy is greater as you age or not. I would hypothesise that the rate of atrophy is lower in older individuals, as they are already undergoing some degree of muscle atrophy. I would imagine that whilst the younger individual may lose muscle at a greater rate, they can recover to their pre-injury strength quicker, owing to their youth and capacity for recovery. But that is all poorly-worded speculation.


As we discussed above, a key feature of skeletal muscle atrophy is reduced protein synthesis. Conversely, muscle protein synthesis is stimulated by dietary protein intake[17]. The injured individual will be likely less active, and this period of inactivity can lead to decreased energy requirements and appetite. For most people, their energy intake will generally decline, and this will result in insufficient protein intake from the diet to support muscle maintenance[18].

A sufficient intake of protein can help abate muscle loss[18]. This is widely accepted in literature, however one study did find a caveat. This study studied the effects of supplementing with protein on short-term muscle atrophy. When participants were given 20g of protein twice a day (40g total), the rate of atrophy remained unchanged[19]. This does not refute the claims of other literature. It is highly unlikely that sufficient intake for any grown man (typically 0.8-1g per pound of bodyweight) is 40g of protein.

You can stimulate muscle protein synthesis all you want, but if you don’t have the building blocks to go with it, you’ll get nowhere.

Key points from this section:

  • The first week is where you will take the most L’s, and after that it appears to level off.
  • The nature of injury may indirectly influence the rate of atrophy.
  • Sufficient protein intake can slow the rate of muscular atrophy.

What Can I Do to Stop This?

1.   What you’re told.

This might seem like the most obvious, but it bears highlighting. Do what your medical practitioner recommends. They are the experts. If they tell you you’re in a cast for six weeks, you’re in a cast for six weeks. Simple as. Don’t set back your return from injury for the sake of a fractional loss of muscle. It will return, and it will return a hell of a lot quicker if you are better recovered.

2.   Get moving when you can.

This is an extension to the above point. Mobilise as soon as you can, on the advice of your healthcare professional.

3.   Avoid being in a calorie deficit/keep your protein intake high.

Stimulate that muscle protein synthesis, son. Ensure a sufficient intake to help you retain your gains, particularly during the acute phase of injury, when the muscle is most susceptible to atrophy.


It is shit to be injured. Muscle atrophy is inevitable with injury and recovery. The rate at which skeletal muscle atrophies is influenced by a number of factors, which vary between individuals. We are not entirely powerless to resist the theft of our gains, provided protein intake is kept at a sufficient level, and you follow the advice of your healthcare professionals.


  1. Jackman, R.W., Kandarian, S.C. (2004) ‘The molecular basis of skeletal muscle atrophy’, American Journal of Physiology. Available at:
  2. Brooks, N.E., Myburgh, K.H. (2012) ‘Prevention of Skeletal Muscle Wasting: Disuse Atrophy and Sarcopenia’, Skeletal Muscle – From Myogenesis to Clinical Relations. Available at:
  3. Ferrando, F.F., Lane, H.W., Stuart, C.A., Davis-Street, J., Wolfe, R.R. (1996) ‘Prolonged bed rest decreases skeletal muscle and whole body protein synthesis’, American Journal of Physiology. Available at:
  4. Topp, R., Ditymer, M., King, K., Doherty, K., Hornyak, J. (2002) ‘The effect of bed rest and potential of prehabilitation on patients in the intensive care unit’, AACN Advanced Critical Care. Available at:
  5. Puthucheary, Z.A.,, Rawal, J., McPhail, M., Connolly, B., Ratnayake, G., Chan, P., Hopkinson, N.S., Phadke, R., Dew, T., Sidhu, P.S., Velloso, C., Seymour, J., Agley, C.C., Selby, A., Limb, M., Edwards, L.M., Smith, K., Rowlerson, A., Rennie, M.J., Moxham, J., Harridge, S.D., Hart, N., Montgomery. H.E. (2013) ‘Acute skeletal muscle wasting in critical illness’, Journal of the American Medical Association. Available at:
  6. Sargeant, A.J., Davies, C.T., Edwards, R.H., Maunder, C., Young, A. (1977) ‘Functional and structural changes after disuse of human muscle’, Clinical Science of Molecular Medicine. Available at:
  7. Campbell, M., Varley-Campbell, J., Fulford, J., Taylor, B., Mileva, K.N., Bowtell, J.L. (2019) ‘Effect of Immobilisation on Neuromuscular Function In Vivo in Humans: A Systematic Review’, Sports Medicine. Available at:
  8. Appell, H.J. (2012) ‘Muscular Atrophy Following Immobilisation’, Sports Medicine. Available at:
  9. Turton, P., Hay, R., Taylor, J., McPhee, J., Welters, I. (2016) ‘Human limb skeletal muscle wasting and remodeling during five to ten days intubation and ventilation in critical care – an observational study using ultrasound’, BMC Anesthesiology. Available at:
  10. Nakanishi, N., Oto, J., Tsutsumi, R., Iuchi, M., Onodera, M., Nishimura, M. (2018) ‘Upper and lower limb muscle atrophy in critically ill patients: an observational ultrasonography study’, Intensive Care Medicine. Available at:
  11. Andrushko, J.W., Lanovaz, J.L., Björkman, K.M. (2018) ‘Unilateral strength training leads to muscle-specific sparing effects during opposite homologous limb immobilization’, Journal of Applied Physiology. Available at:
  12. De Boer, M.D., Maganaris, C.N., Seynnes, O.R., Rennie, M.J., Narici, M.V. (2007) ‘Time course of muscular, neural and tendinous adaptations to 23 day unilateral lower-limb suspension in young men’, Journal of Physiology. Available at:
  13. Rong, S., Wang, L., Peng, Z., Liao, Y., Li, D., Yang, X., Nuessler, A.K.,Liu, L., Bao, W., Yang, W. (2020) ‘The mechanisms and treatments for sarcopenia: could exosomes be a perspective research strategy in the future?’, Journal of Cachexia, Sarcopenia and Muscle. Available at:
  14. Volpi, E., Nazemi, R., Fujita, S. (2010) ‘Muscle tissue changes with aging’, Current Opinions on Clinical Nutrition and Metabolic Care. Available at:,to%20disability%20in%20older%20people.
  15. Melton, L.J., Khosla, S., Crowson, C.S., O’Connor, M.K., O’Fallon, W.M., Riggs, B.L. (2000) ‘Epidemiology of sarcopenia’, Journal of the American Geriatric Society. Available at:
  16. Suetta, C., Hvid, G., Justensen, L., Christensen, U., Neergaard, K., Simonsen, L., Ortenblad, N., Magnusson, S.P., Kjaer, M., Aagaard, P. (2009) ‘Effects of aging on human skeletal muscle after immobilization and retraining’, Journal of Applied Physiology. Available at:,affected%20at%20the%20muscle%20level.
  17. Rennie, M.J., Edwards, R.H., Halliday, D., Matthews, D.E., Wolman, S.L., Millward, D.J. (1982) ‘Muscle Protein Synthesis Measured by Stable Isotope Techniques in Man: The Effects of Feeding and Fasting’, Clinical Science. Available at:
  18. Wall, B.T., van Loon, L.J. (2013) ‘Nutritional strategies to attenuate muscle disuse atrophy’, Nutrition Reviews. Available at:
  19. Dirks, M.L., Wall, B.T., Nilwik, R., Weerts, D.H., Verdijk, L.B., van Loon, L.J. (2014) ‘Skeletal Muscle Disuse Atrophy Is Not Attenuated by Dietary Protein Supplementation in Healthy Older Men’, The Journal of Nutrition. Available at:

Published by Michelle Carroll

I am a qualified personal trainer and radiographer. I believe in empowering others to make better choices for their health through education. I think that the fitness industry has created a disconnect between best practices and “evidence-based” practices. I am hoping that by chronicling my experience as a healthcare professional and my education as a fitness professional I can assist others on the path to bettering themselves.

Leave a Reply

Fill in your details below or click an icon to log in: Logo

You are commenting using your account. Log Out /  Change )

Google photo

You are commenting using your Google account. Log Out /  Change )

Twitter picture

You are commenting using your Twitter account. Log Out /  Change )

Facebook photo

You are commenting using your Facebook account. Log Out /  Change )

Connecting to %s

%d bloggers like this: