Muscle memory (strength training)

For the term "muscle memory" as related to motor learning, see Muscle memory.

Muscle memory has been used to describe the observation that various muscle-related tasks seem to be easier to perform after previous practice, even if the task has not been performed for a while. It is as if the muscles “remember”. The term could relate to tasks as disparate as playing the clarinet^[1] and weight-lifting, i. e. the observation that strength trained athletes experience a rapid return of muscle mass and strength even after long periods of inactivity.^[2] Until recently all such effects was largely attributed to motor learning occurring in the central nervous system, but long term effects of previous training on the muscle fibers themselves have recently been observed, in particular related to strength training.^[3]

Until recently it was generally assumed that the effects of exercise on muscle was reversible, and that after a long period of de-training the muscle fibers returned to their previous state. For strength training this view was recently challenged by using in vivo imaging techniques revealing specific long lasting structural changes in muscle fibers after a strength-training episode.^[4] The notion of a memory mechanism residing in the muscle fibers might have implications for health related exercise advice, and also for exclusion times after doping offences. Muscle memory is probably related to the cell nuclei residing inside the muscle fibers, as is described below.

The muscle cells are the largest cells in the body with a volume thousands of times larger than most other body cells.^[5] To support this large volume, the muscle cells are one of the very few in the mammalian body that contains several cell nuclei. Such multinucleated cells are called syncytia. Strength-training increases muscle mass and force mainly by changing the caliber of each fiber rather than increasing the number of fibers. During such fiber enlargement muscle stem cells in the muscle tissue multiply and fuse with pre-existing fibers as to support the larger cellular volume. It has often been assumed that each nucleus can support a certain volume of cytoplasm, and hence that there is a constant volume domain served by each nucleus, although recent evidence suggests that this is an oversimplification. Until recently it was believed that during muscle wasting (atrophy) muscle cells lost nuclei by a nuclear self-destruct mechanism called apoptosis, but recent observations using time laps in vivo imaging in mice do not support this model. Direct observation indicated that no nuclei are lost under such conditions,^[6] and the apoptosis observed in the muscle tissue were demonstrated to occur only in other cell nuclei in the tissue, e.g. connective tissue and muscle stem cells called satellite cells. Since in vivo imaging have confirmed that cell nuclei are added during strength training and not lost upon subsequent detraining,^[7] the nuclei might provide a mechanism for muscle memory. Thus, upon retraining the extra nuclei are already there and can rapidly start synthesizing new protein to build muscle mass and strength. The extra muscle nuclei obtained by a strength training episode, seems to be very long lasting, perhaps permanent, even in muscles that are inactive for a long time.^[8] The ability to recruit new nuclei is impaired in the elderly,^[9] so it might be beneficial to strength train before senescence. Doping with anabolic steroids also seem to act partly by recruiting new nuclei,^[10][11] so it is possible that doping give offenders a long lasting perhaps life long benefit compared to athletes not cheating.

References

1. ^ Fritz C & Wolfe J. (2005). How do clarinet players adjust the resonances of their vocal tracts for different playing effects? J Acoust Soc Am 118, 3306-3315.
2. ^ Staron RS, Leonardi MJ, Karapondo DL, Malicky ES, Falkel JE, Hagerman FC & Hikida RS. (1991). Strength and skeletal muscle adaptations in heavy-resistance-trained women after detraining and retraining. J Appl Physiol 70, 631-640.
3. ^ Bruusgaard JC, Johansen IB, Egner IM, Rana ZA & Gundersen K. (2010). Myonuclei acquired by overload exercise precede hypertrophy and are not lost on detraining. Proc Natl Acad Sci U S A 107, 15111-15116.
4. ^ Bruusgaard JC, Johansen IB, Egner IM, Rana ZA & Gundersen K. (2010). Myonuclei acquired by overload exercise precede hypertrophy and are not lost on detraining. Proc Natl Acad Sci U S A 107, 15111-15116.
5. ^ Bruusgaard JC, Liestol K, Ekmark M, Kollstad K & Gundersen K. (2003). Number and spatial distribution of nuclei in the muscle fibres of normal mice studied in vivo. J Physiol 551, 467-478.
6. ^ Bruusgaard JC & Gundersen K. (2008). In vivo time-lapse microscopy reveals no loss of murine myonuclei during weeks of muscle atrophy. J Clin Invest 118, 1450-1457.
7. ^ Bruusgaard JC, Johansen IB, Egner IM, Rana ZA & Gundersen K. (2010). Myonuclei acquired by overload exercise precede hypertrophy and are not lost on detraining. Proc Natl Acad Sci U S A 107, 15111-15116.
8. ^ Bruusgaard JC, Johansen IB, Egner IM, Rana ZA & Gundersen K. (2010). Myonuclei acquired by overload exercise precede hypertrophy and are not lost on detraining. Proc Natl Acad Sci U S A 107, 15111-15116.
9. ^ (Schultz & Lipton, 1982)
10. ^ Kadi F, Eriksson A, Holmner S & Thornell LE. (1999). Effects of anabolic steroids on the muscle cells of strength-trained athletes. Med Sci Sports Exerc 31, 1528-1534.
11. ^ Sinha-Hikim I, Artaza J, Woodhouse L, Gonzalez-Cadavid N, Singh AB, Lee MI, Storer TW, Casaburi R, Shen R & Bhasin S. (2002). Testosterone-induced increase in muscle size in healthy young men is associated with muscle fiber hypertrophy. Am J Physiol Endocrinol Metab 283, E154-164.