What is DOMS, and what does it mean for muscle growth?
DOMS stands for “delayed onset muscle soreness.” For a long time we thought it was induced by micro-traumas to the muscles after exercising, causing us pain typically for 1-3 days after training. Muscle soreness has been thought (though somewhat undefinitively) to be one of the drivers of muscle hypertrophy.
A recent study by Sonkodi et al (2020), hypothesized that there may be more to it than just trauma to the muscle. In fact, trauma to the muscle does not even have to occur to experience DOMS. The study concluded, "DOMS is an acute compression axonopathy of the nerve terminals in the muscle spindle caused by the repetitive superposition of compression with a coinciding cognitive demand, coupled with possible micro-injury to the surrounding tissues and enhanced by immune-mediated inflammation. Our theory states that DOMS happens only if the superposition of compression reaches the muscle spindle and micro-injuries the nerve terminals under cognitive demand."
Going through this paper lets us know the underlying mechanisms of DOMS are not just muscle damage, but more a result of pressure on the nerves. The presence of this pressure explains why our output would be downgraded due to DOMS. It also shows why when we get back into training or elicit a novel stimulus to get DOMS that we end up holding on to some water. It further demonstrates the role the sympathetic nervous system plays in blunting pain signals that allow us to push to the point that causes this trauma to the neural area.
Sonkodi, et al. also conclude that DOMS can play an important role in muscle growth and adapting the nervous system. Understanding that DOMS is not solely caused by muscle damage will allow us ways to look into all the mechanisms more and to really see if it can help stimulate muscle growth.
Sonkodi, B., Berkes, I., & Koltai, E. (2020). Have we looked in the wrong direction for more than 100 years? Delayed onset muscle soreness is, in fact, neural Microdamage rather than muscle damage. Antioxidants, 9(3), 212. https://doi.org/10.3390/antiox9030212