Signalling pathways of muscular adaptation through strength training

Which signalling pathways lead to muscular adaptation through strength training?

Strength training, combined with the intake of dietary protein, increases muscle protein synthesis via various signalling pathways and thus improves muscle building. Although not all influencing factors and signalling pathways of adaptation through strength training have been researched yet, the increase in mass of the skeletal muscle can largely be described. Three signalling pathways are associated with information transfer in muscle building.

1. mTor signalling cascade

mTor stands for mammalian/mechanistic target of rapamycin, which has nothing to do with protein synthesis but describes the influence of the immunosuppressant rapamycin on the enzyme. It is a serine/threonine kinase, which means that it promotes small modifications (phosphorylations) on the amino acids serine and threonine, which are very important for information transfer via signalling cascade. The activation of mTor is highly complex and will not be discussed in more detail here. However, it should be said that mechanical stress on the muscle fibres has an indirectly positive influence on mTor, while endurance training can cause a negative effect via activation of AMPK. How mechanical load is registered by the muscle cell and which mechanosensors are responsible for it remains the subject of current research and possibly one of the most important unanswered questions in this area of science.

mTor regulates protein synthesis at three different points and therefore plays an important role in adaptation to strength training. On the one hand, it improves mRNA translation at the ribosome and thus accelerates the synthesis process. (increased speed). On the other hand, it increases the capacity of the individual cell for synthesis by increasing ribosome biogenesis. (increased capacity). In addition, mTor has an inhibiting influence on the protein breakdown process called autophagy in some cells (less breakdown). In addition to the direct influence on synthesis speed and capacity, the enzyme also has an indirect effect by modifying cell division and the gene transcription of certain genes (more cell division and increased gene transcription)

2. Myostatin-Smad signalling cascade

After various intra- and extracellular modifications, myostatin leads to activation of Smad and results in growth inhibition. In contrast to mTor, the myostatin-Smad signalling pathway therefore slows skeletal muscle growth. In animal models, myostatin activity was modified or even stopped, which resulted in skeletal muscles that were twice as pronounced compared to the wild type. An important question would now be whether the additional muscle mass also leads to an adequate gain in additional strength. This question could be answered using randomly occurring gene mutants. The additional muscle mass does result in an increase in strength, but the reduced muscular efficiency led to a smaller relative strength compared to the total mass of the individual. This shows that unlimited skeletal muscle growth can also be a disadvantage for individual fitness and explains the relevance of myostatin for human regulatory processes.

It has been shown that strength training lowers the mRNA level of myostatin, which can explain its influence on muscle growth. In what form and to what extent this effect influences the adaptation responses after strength training has not yet been fully clarified.

3. Regulation of satellite cell behaviour

Fully differentiated skeletal muscle cells have already lost their ability to divide and therefore cannot ensure the repair and replacement of damaged muscle cells. This task was transferred to the satellite cells, which are a kind of stem cell of the muscle. These cells are located in the muscle at the periphery between the plasma membrane and the basal lamina.

It has been shown that, despite almost complete removal of the satellite cells (over 90%), normal muscular adaptation through hypertrophy is still possible. This proves that satellite cells have no effect on short-term muscle hypertrophy. 8 weeks later, however, the hypertrophy was greatly reduced, which means that satellite cells are indispensable for the long-term maintenance of the muscle gained. In addition, they are essential for muscle growth after birth and for regeneration after injuries.

Adaptation through strength training - interpretation of the scientific findings

Many further scientific findings, not mentioned here, contribute to a better understanding of muscle plasticity. Using various methods, muscle biologists have searched for further information relevant to muscle growth, such as the optimal duration of load and recovery or movement speed. In summary, however, there are not many rules to follow in order to achieve maximum output with minimum effort. One of the most central factors in strength training is muscle fatigue and the associated recruitment of all motor units specific to the motor task. As fatigue increases, the number of recruited motor units and thus the number of activated muscle fibres increases. This is an important prerequisite for increasing the speed of muscle protein synthesis.

Another central factor is slow execution of the movement. It increases muscle protein build-up more than fast execution of the movement. The exercises should therefore be performed within the given tension duration until exhaustion or fatigue, i.e. until a complete, anatomically correct repetition over the individually possible range of motion is no longer possible. The tension duration required for this (from start to end of the exercise) should lie within a sensible range, between 30 and 180 seconds.

Besides training, optimal protein intake is decisive for adaptation through strength training. Optimal would be consuming approx. 20 g of high-quality protein per serving approx. every 3 - 4 hours.

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Sources

Wackerhage H. Molecular Exercise Physiology. Abingdon: Routledge; 2014. 24-30, 52-65, 133-151 p.

McCarthy JJ, Mula J, Miyazaki M, Erfani R, Garrison K, Farooqui AB, et al. Effective fiber hyperthrophy in satellite cell-depleted skeletal muscle. Development [Internet]. 2011 [cited 2017 Nov 15];138:3657–66. Available from: http://dev.biologists.org/content/develop/138/17/3657.full.pdf