By Safiya Aldris
Many people fear that if they begin working out and are unable to maintain their programme, all their previously gained strength and stamina will vanish, making their efforts a waste of time. The “myonuclear domain hypothesis” backs this up, stating that a nucleus controls a defined volume of cytoplasm; when muscles experience hypertrophy or atrophy, the number of myonuclei changes accordingly. Recent research has shown that this is not wholly the case.
There is a general agreement that when a body goes through training periods and the muscles increase in size, there is an increase in the number of myonuclei (coming from stem cells) to enable the muscles to meet the demands of their growing cells. Controversy arises in stating that as muscles shrink, so does the number of myonuclei. While some research has shown that atrophy is triggered by detraining for long periods of time, bringing about a dramatic loss of myonuclei via apoptosis (Tews, 2005), the methods used do not distinguish the true myonuclei from those of surrounding mononuclear cells. Newer research has been done which focuses on and differentiates the myonuclei alone, without room for confusion between the muscle fibres and neighbouring cells.
To test the validity of the myonuclear domain hypothesis, a study was done on the intersegmental muscle (ISM) of insects (Schwartz et al., 2016); this muscle does not contain satellite cells, capillaries, or endothelial cells, allowing for the results to purely reflect the changes of the nuclei in the muscle fibres. As the muscles underwent atrophy and apoptosis, the mass and cross-sectional areas of the fibres decreased, but the nuclear count was unchanged. Specifically, there was an 84% reduction in the myonuclear domain after the atrophy, with more myonuclei controlling smaller amounts of cytoplasm as the muscles decreased in mass. Further studies have shown that until a certain point, pre-existing myonuclei are able to control a greater volume of cytoplasm up until a certain point (Kadi et al., 2004). If training is consistent, these nuclei will be placed under strain and the addition of new myonuclei is triggered to sustain further hypertrophy of muscles. Both of these studies oppose the theory of myonuclear domains, as a set ration of nuclei to cytoplasm is not maintained.
To observe the effects of retaining myonuclei through atrophy, a study was done on individuals who completed 20 weeks of strength training before experiencing a long period of detraining, then retraining (Staron et al., 1991). The results showed that the speed with which the women were able to get back to their previous form was quicker in those who had completed the 20 weeks strength training compared to those who did not. To further support this study’s results Bruusgaard et al. (2010), observed that an increase in nuclei is lasting and independent of the maintenance of muscle hypertrophy. This led to a proposal that untrained muscle fibres fuse with satellite cells when they first go through strength or resistance training, increasing the number of nuclei in the fibres. Upon detraining, the fibres then maintain their elevated number of myonuclei, and if retraining occurs this increase in myonuclei increases the protein synthesis rate, so increase in muscle size and volume occurs faster, skipping the step of adding newly formed nuclei.
A maintained increase in myonuclei may also be a contributor to what is known as ‘muscle memory’. Whilst the majority of what we understand to be muscle memory occurs in the nervous system, myonuclei appear to play a role. Bruusgaard’s results show that the myonuclei simply shrink without disappearing as muscles atrophy, and have a high resistance to apoptotic measures within the muscle. This means that muscle built is not only easier to get back, but strength training throughout adolescence and adulthood may be incredibly beneficial later on in life, as a store of myonuclei will be within your muscles, improving your physical health and enabling higher levels of strength in older years.
Despite a continued controversy around whether myonuclei remain in muscles after a period of hypertrophy then detraining, there is overwhelming evidence that building muscle will be solely beneficial, through creating long lasting stores of myonuclei. As myonuclei are the synthetic engines of muscle fibres, higher levels of remaining myonuclei will enable muscle size and strength to be recovered more quickly, even if long breaks from training are had.
Tews, D., 2005. Muscle-fiber apoptosis in neuromuscular diseases. Muscle & Nerve, 32(4), p.443-458. Available at: https://onlinelibrary.wiley.com/doi/abs/10.1002/mus.20348 [Accessed 30th August 2020].
Schwartz, L., Brown, C., McLaughlin, K., Smith, W. and Bigelow, C., 2016. The myonuclear domain is not maintained in skeletal muscle during either atrophy or programmed cell death. American Journal of Physiology-Cell Physiology, 311(4), p.C607-C615. Available at: https://journals.physiology.org/doi/full/10.1152/ajpcell.00176.2016 [Accessed 30th August 2020].
Kadi, F., Schjerling, P., Andersen, L., Charifi, N., Madsen, J., Christensen, L. and Andersen, J., 2004. The effects of heavy resistance training and detraining on satellite cells in human skeletal muscles. The Journal of Physiology, 558(3), p.1005-1012. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1665027/ [Accessed 30th August 2020].
Staron, R., Leonardi, M., Karapondo, D., Malicky, E., Falkel, J., Hagerman, F. and Hikida, R., 1991. Strength and skeletal muscle adaptations in heavy-resistance-trained women after detraining and retraining. Journal of Applied Physiology, [online] 70(2), pp.631-640. Available at: https://journals.physiology.org/doi/abs/10.1152/jappl.1918.104.22.1681 [Accessed 31 August 2020].
Bruusgaard, J., Johansen, I., Egner, I., Rana, Z. and Gundersen, K., 2010. Myonuclei acquired by overload exercise precede hypertrophy and are not lost on detraining. Proceedings of the National Academy of Sciences, [online] 107(34), pp.15111-15116. Available at: https://doi.org/10.1073/pnas.0913935107 [Accessed 30th August 2020].