Muscle Memory

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The concept of muscle memory seems to have a broad reach when it comes to both scientists and gym bros alike. The most accurate way to describe muscle memory is the quick regain in both strength and size in previously trained muscles following a detraining period. As wordy as that description is it’s an important designation because we need to distinguish a couple of different terms and processes to isolate this phenomenon and, of course, see if it even truly exists.

The first concept needing separate distinction is “cell differentiation.” Early scholars thought that cellular memory existed since certain cells would always act the way they were designed to. An example would be if you took a muscle cell from one individual and tried to place it among liver cells of another individual; the muscle cell would still behave as a muscle cell instead of adopting liver cell processes. That’s not really a harbinger of cellular memory, it’s just a trait of the cell – it was only designed to function as a muscle cell and could never function otherwise (11).

The second concept is “motor learning.” This is probably the most common manner in which people inappropriately allege muscle memory. Think about this for a second: say you learned how to play the piano as a child but haven’t played in 15-years. You could probably still sit at a piano and bang out a few decent tunes even without playing for many years. This is not muscle memory, this is motor learning. Some people tend to think that this memory is peripheral, like in your hands, but realistically it’s all in the brain and central nervous system. Your hands would not be able to play the piano without your brain or nervous system (11).

Now we can talk specifically about muscle memory. The true definition of muscle memory, or any type of cellular memory, is a lasting adaptation in the cell even after the stimulus that created the adaptation has stopped (11). Don’t worry about re-reading that sentence 10-times, we’ll slowly and dramatically clarify it for you in the next few paragraphs.

We’re back to the physiological roots of bodybuilding: stimulus and adaptation. The stimulus is, of course, the workout you impose on your body. The adaptation, on the other hand, is the body’s response to the stimulus and this response is always specific to the type of stimulus given (16). This means that strength training induces muscle growth and strength gains while endurance training improves oxygen usage and fatigueability (3,12). By now you’re probably aware of at least a few reasons behind how and why our muscles grow so let’s take a microscopic look at something that precedes this growth.

Our muscle cells are incredibly unique in that they are one of only a few cells in our body that contain multiple nuclei (5,6). This is mainly due to the fact that our muscle cells are, as Zoolander would say, “really, really, ridiculously large” (11,18) when compared to normal body cells. Multiple nuclei are required for large cells according to the Nuclear Domain Theory. This theory states that a cell nucleus can only control a limited portion of the cell (11,17). So for a cell undergoing a growing phase, adding more nuclei is extremely important for the cell to be able to maintain proper function.

This process of adding nuclei is a precursor to muscle cell growth (1,5,9,14,15). Our muscles contain little helpers called satellite cells that, for the most part, just kind of hang out around muscle cells in case they are needed for tissue repair. When you start strength training, eventually your muscle cells will steal the nuclei from these satellite cells to use as their own. This creates an environment for the cell to grow – more nuclei present = more protein synthesis (5,11) which ultimately leads to greater cell growth.

Recall what we touched on above about the strict concept of muscle memory – it’s an adaptation that remains after the stimulus stops. Several studies have shown that the number of muscle cell nuclei does not decrease following a detraining period (5,8,13,19,20). In fact, a cell nucleus is stable for at least 15-years (11) so a trained muscle fiber should hold on to extra nuclei for a very long time.

This appears to be one of the main reasons why we can regain muscle size and strength quickly after a period of detraining – this has been shown in several studies (5,8,10,11,20,21). It even appears that muscles that were enlarged due to resistance training are more resistant to atrophy during periods of detraining or bed rest (4,5,11,13,19,20) and this is likely due to the increased number of cell nuclei.

Why do our cells hold on to these extra nuclei? It might have something to do with the biological evolution of humans (11). Many, many years ago, humans were not blessed with a Chipotle or Starbucks at every corner so food was not quite as abundant as it is today. This means any calories consumed had to be preserved as fat for survival – this is one of the reasons why it’s still easy to gain weight from eating too much. Exercise forces some of these calories to be used to repair and build tissue and from a survival standpoint, that’s not very efficient. So now, imagine our ancient friend, the caveman.

Cavemen would hunt and gather during times of good weather and would then have to mostly hide in their caves during winter. This means they spent all summer “exercising” to have enough supplies to ride out the winter. We can also assume then, that the caveman is eating less during winter to make his supplies last longer. With this calorie restriction it would be very tough for the caveman to maintain any muscle mass he built during the summer. When spring rolls around again though, he’s got to be ready to get back to it. If his muscle cells did not retain the extra nuclei they gained from the summer before, the caveman could be looking at a rough couple of months for hunting since he’s in such bad shape from winter. But! The extra nuclei he stored help his muscle cells regain strength and size much quicker which makes him ready to hunt and gather at peak performance again in no time. This is all just a theory, but many aspects of human biology and physiology trace back to our needs for surviving and thriving with much less than what we have today.

So, after a long and complex discussion, there seems to be a good case for muscle memory being a real thing. Just remember to differentiate between motor learning and legitimate cell memory. Motor learning absolutely has its place in regaining muscle strength as learned movements will be much more efficient than novel movements which can lead to quick strength gains upon retraining (11). Cell memory is an incredibly complex topic and ideas and theories on it change daily. Regardless, it seems that the increase in muscle cell nuclei plays a huge role in hypertrophy and is probably the main sign of “memory” within a muscle cell.

References:

  1. Allen, D. L., Roy, R. R., & Edgerton, V. R. (1999). Myonuclear domains in muscle adaptation and disease. Muscle & Nerve, 22(10), 1350-1360.
  2. Alway, S. E., & Siu, P. M. (2008). Nuclear apoptosis contributes to sarcopenia. Exercise and Sport Sciences Reviews, 36(2), 51.
  3. Åstrand, P. O., Rodahl, K., Dahl, H. A., & Strømme, S. B. (2003). Textbook of Work Physiology: Physiological Bases of Exercise. Human Kinetics.
  4. Bruusgaard, J. C., & Gundersen, K. (2008). In vivo time-lapse microscopy reveals no loss of murine myonuclei during weeks of muscle atrophy. The Journal of Clinical Investigation, 118(4), 1450-1457.
  5. Bruusgaard, J. C., Johansen, I. B., Egner, I. M., Rana, Z. A., & Gundersen, K. (2010). Myonuclei acquired by overload exercise precede hypertrophy and are not lost on detraining. Proceedings of the National Academy of Sciences, 107(34), 15111-15116.
  6. Bruusgaard, J. C., Liestøl, K., Ekmark, M., Kollstad, K., & Gundersen, K. (2003). Number and spatial distribution of nuclei in the muscle fibres of normal mice studied in vivo. The Journal of Physiology, 551(2), 467-478.
  7. Bruusgaard, J. C., Liestøl, K., & Gundersen, K. (2006). Distribution of myonuclei and microtubules in live muscle fibers of young, middle-aged, and old mice. Journal of Applied Physiology, 100(6), 2024-2030.
  8. Egner, I. M., Bruusgaard, J. C., Eftestøl, E., & Gundersen, K. (2013). A cellular memory mechanism aids overload hypertrophy in muscle long after an episodic exposure to anabolic steroids. The Journal of Physiology, 591(24), 6221-6230.
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  15. McCall, G. E., Allen, D. L., Linderman, J. K., Grindeland, R. E., Roy, R. R., Mukku, V. R., & Edgerton, V. R. (1998). Maintenance of myonuclear domain size in rat soleus after overload and growth hormone/IGF-I treatment. Journal of Applied Physiology, 84(4), 1407-1412.
  16. Nader, G. A. (2006). Concurrent strength and endurance training: from molecules to man. Medicine and Science in Sports and Exercise, 38(11), 1965-1970
  17. Pavlath, G. K., Rich, K., Webster, S. G., & Blau, H. M. (1989). Localization of muscle gene products in nuclear domains. Nature, 337(6207), 570.
  18. Rudin, S., Stiller B., Cornfield, S. (Producers) & Stiller, B. (Director). Zoolander. Motion Picture. United States: Paramount Pictures.
  19. Smith, K., Winegard, K., Hicks, A. L., & McCartney, N. (2003). Two years of resistance training in older men and women: the effects of three years of detraining on the retention of dynamic strength. Canadian Journal of Applied Physiology, 28(3), 462-474.
  20. Staron, R. S., Leonardi, M. J., Karapondo, D. L., Malicky, E. S., Falkel, J. E., Hagerman, F. C., & Hikida, R. S. (1991). Strength and skeletal muscle adaptations in heavy-resistance-trained women after detraining and retraining. Journal of Applied Physiology, 70(2), 631-640.
  21. Taaffe, D. R., & Marcus, R. (1997). Dynamic muscle strength alterations to detraining and retraining in elderly men. Clinical Physiology, 17(3), 311-324.

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