Is Exercise Induced Muscle Damage a Key Stimulus for Muscle Hypertrophy?

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With a growing demand of clients wanting to develop bigger muscles, is the old theory that we must induce muscle soreness to achieve growth correct? 

Matthew Sills | Mar 2020

It has long been preached by fitness professionals that to achieve muscle growth muscle soreness in the form of DOMS (delayed onset of muscle soreness) must be achieved. There is a body of evidence that suggests exercise induced muscle damage (EIMD) can have a positive effect on muscle growth through various mechanisms (Evans & Cannon , 2012). When exercise induced muscle damage occurs, normally after strenuous exercise, it can lead to inflammation and increased protein turnover. The inflammation response leads to neutrophils and macrophages (part of our immune system) to flood the area of trauma, where they secrete various agents which help with muscle repair. However this response seems to be more about the repair of muscle tissue rather than an increase in its size. Another theory suggests that the flood of neutrophils results in an increase in reactive oxygen species (ROS) to the area. ROS have been linked to promote growth not only of cardiac and smooth muscle (Suzuki & Ford, 1999), but also skeletal (Takarada, et al., 2000). On the other hand certain ROS have been found to interfere with important muscle hypertrophy pathways including calcineurin activation (Carruthers & Stemmer, 2008).

With the relationship between EIMD and muscle hypertrophy not clear, the role of mechanical tension in the facilitation of muscle hypertrophy is. The simple observation that muscles atrophy when immobilized proves the importance of mechanical load. Many indirect studies have found that mechanical loading plays a key role in muscle hypertrophy (Kumar, et al., 2009; Lasevicius, et al., 2018). An interesting in vitro study carried out by Aguilar-Agon et al., (2019) carried out a more direct approach to accurately assess the role of mechanical load. A tissue-engineered skeletal muscle was subjected to mechanical loading which increased its length by 15%. The subsequent adaptions following this manipulation resulted in significant hypertrophy of the myotubes (building blocks of muscle fibres) and an increase in maximal contractile force of 265% (Aguilar-Agon, et al., 2019). 

However if mechanical load alone was the only instigator of muscle hypertrophy why has it been found that submaximal loads can have the same hypertrophic effects as heavier loads?  A clear example of this is Kaatsu or occlusion training. Light loads (20-50% of 1 RM) using a pressure cuff to occlude blood flow to the muscle, have resulted in similar hypertrophic responses as traditional hypertrophy loads (70-80% of 1 RM) (Abe, et al., 2005). Wearing a pressure cuff that occludes blood flow to exercising muscles causes a premature build-up of various metabolites including lactate, alpha-ketoglutarate, phosphatidic acid and lyso-phosphatidic acid. These metabolites have been shown in various studies to be linked with hypertrophy signalling (Wackerhage, et al., 2019). The low pH environment caused by the build-up of metabolites is also know to stimulate growth hormone, a powerful anabolic molecule that has strong links with muscle protein synthesis (Hwang & Willoughby, 2019). 

It is clear from the current scientific literature that mechanical load is the key instigator of muscle hypertrophy. Training loads typically around 70-80% of 1 RM seem to elicit sizable hypertrophic gains, but lighter loads have also been shown to have marked effects (Schoenfled, et al., 2017). However, the presence of EIMD and certain metabolites seem to play a contributing role in the repair and magnitude of muscle fibre adaptions.   

Matthew Sills is the Founder and Head Coach of Trojan Fitness having been a personal trainer since 2013. Matthew holds a BSc in Sport and Exercise Science from the University of Surrey, and guides his personal training based on the latest scientific research and literature.

References

Abe, T. et al., 2005. Skeletal muscle size and circulating IGF-1 are increased after two weeks of twice daily KAATSU resistance training.. International Journal of Kaatsu Training Research, pp. 6-12.

Aguilar-Agon, K. et al., 2019. Mechanical loading stimulates hypertrophy in tissue-engineerd skeletal muscle: Molecular and phenotypic responses. Journal of Cellular Physiology, Volume 235, pp. 23547-23558.

Carruthers, N. J. & Stemmer, P. M., 2008. Methionine oxidation in the calmodulin-binding domain of calcineurin disrupts calmodulin bindng and calcineurin activation. Biochemistry , Volume 47, pp. 3085-3095.

Evans, W. J. & Cannon , J. G., 2012. The metabolic effects of exercise-induced muscle damage. Journal of strength and conditioning research , 26(5), pp. 1441-1453.

Hwang, P. & Willoughby, D. S., 2019. Mechanisms behind blood flow restricted training and its effect towards muscle growth. Journal of Strength and Conditioning Research , 33(1), pp. 167-179.

Kumar , V. et al., 2009. Age-related differences in the dose response relationship of muscle protein synthesis to resistance exercise in young and old men. journal of Physiology, Volume 587, pp. 211-217.

Lasevicius, T. et al., 2018. Effects of different intensities of resistance training with equated volume load on muscle strength and hypertrophy. European Journal of Sports Science , Volume 18, pp. 772-780.

Schoenfled, B. J., Girgic, J., Ogborn, D. & Krieger, J. W., 2017. Strength and hypertrophy adaptions between low vs. high load resistance training. Journal of Strength and Conditioning Research , 31(12), pp. 3508-3523.

Suzuki, Y. J. & Ford, G. D., 1999. Redox regulation of signal transduction in cardiac and smooth muscle. Journal molecullar and cellular cadiology , 31(2), pp. 345-353.

Takarada, Y. et al., 2000. Rapid increase in plasma growth hormone after low intensity resistance exercise with vascular occlusion. Journal applied physiology, Volume 88, pp. 61-65.

Wackerhage, H. et al., 2019. Stimuli and sensors that initiate skeletal muscle hypertrophy following resistance exercise. Journal of Applied Physiology , Volume 126, pp. 30-43.

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