Muscle damage is neither good nor bad but more so a biomarker of what may be going on in your body. From a performance standpoint accruing copious amounts of muscle damage every time you train can be a very negative thing as it can decrease range of motion, force production, decrease in economy of movement, impairment of glycogen repletion, alteration in biomechanical execution of movements and potentially increase the risk of injury (Smith, L. 1992). These decrements are not advantageous for anyone so when choosing exercises that typically create more muscle damage than others just to provide an idea of a good workout will be more of a negative thing than a good one. Muscle damage also allows the body to create neural adaptations that can help prevent the damage from occurring at such a high level again. This is termed the repeated bout effect and this refers to the protection or attenuation of muscle damage markers observed following continuous exercise bouts and the benefits appear as early as the second bout of exercise. The mechanisms are a bit unknown at this time but they are believed to stem from heat shock proteins which may protect the muscle by aiding in the refolding of damaged proteins and folding of newly synthesized proteins after exercise. Increases in cytoskeletal proteins such as desmin, titin, and dystrophin can also be a mechanism, this relates to a rise in mRNA after muscle damaging protocols which will help with more protein turnover and thus improve recovery faster and create less damage due to the speedy recovery. Strengthening of the extracellular matrix, research by Mackey et al. 2011 showed that 30 days after the first bout of exercise there was an increase in ECM: Collagen and laminin, matrix growth factors TGF-B, IGF-1, satellite cell content, macrophage content, and myofiber regeneration.
Unaccustomed exercise consisting of eccentric muscle contractions often results in muscle damage (Peake et al. 2016). Exercise induced muscle damage are cellular and subcellular disturbances, particularly Z-line streaming. The exact mechanisms have not been fully fleshed out, the initial damage to the muscle is ascribed to mechanical disruption of the fiber, and subsequent damage is linked to inflammatory processes and to changes of the excitation-contraction coupling within the muscles. This damage to the excitation-contraction coupling complex is disrupted in the connection between the t-tubules and the ryanodine receptors of the sarcoplasmic reticulum. Because lengthening contractions produce greater amounts of force while recruiting fewer motor units to do the job than shortening contractions you get filament damage due to the high amount of tension being placed on the muscle. They also disrupt the intermediate filament system that contributes to the passive stiffness of muscle and maintains the architecture of the myofibrils. Cell membrane of muscle cells get damaged as well and when this happens they allow an unregulated influx of extracellular marker dyes to bind to albumin and an unregulated efflux of creatine kinase. The proteolytic enzymes in muscle fibers start to degrade the injured cell structures. This results in elevated bradykinin, histamine, and prostaglandins which invites monocytes and neutrophils to the injured site (Cheung et al. 2003). Proteases and phospholipases are activated by calcium accumulation after sarcolemma damage with concomitant leukotrienes and prostaglandins production. Leukotrienes increase vascular permeability, in addition to attracting neutrophils. These will feed the inflammatory cycle by phagocytosis, releasing oxygen free radicals and proteases and causing further tissue injury (Best et al. 1999). This type of damage can occur from the number of contractions performed in an exercise or workout. Muscle fiber strains produced during the lengthening contraction due to force being produced and the contraction velocity which is why downhill running can be so damaging. A newer theory presented by Sonkodi et al 2020 proposes that DOMS is an acute compression axonopathy of the nerve endings in the muscle spindle. Caused by the superposition of compression when repetitive eccentric contractions are executed under cognitive demand. The compression could coincide with micro injury of the surrounding tissues and is enhanced by immune-mediated inflammation. This would link the muscle damage to the brain and the neural pathways that may be associated with the down regulation of force production and decrease range of motion. When looking at the pain literature, nociceptors and how that down regulates the same things after a traumatic injury it has some interesting insight. In Sonkodi’s paper they discuss DOMS could have the potential role to play in ontogenesis by triggering nerves and surrounding tissues, such as causing muscles to grow and also adapting the nervous system to comply with the growth process. They propose that sensory nerve guidance in the muscle spindle could have a similar functional and essential role in muscle growth, similar to what has been observed in bone growth. I can get behind that model as tissue becomes damaged it has all these protective mechanisms in place to make sure that the damage does not continue to happen much like bones get stronger and grow through the osteoclast osteoblast remodeling cycle, I can see muscle getting bigger and stronger as a protective mechanism. I don’t however feel it plays a substantial role in growth like mechanical tension does but more so a small amount of growth in the repair process and protective process.
References:
Best TM, Fiebig R, Corr DT, Brickson S, Ji L. Free radical activity, antioxidant enzyme, and glutathione changes with muscle stretch injury in rabbits. J Appl Physiol (1985). 1999 Jul;87(1):74-82. doi: 10.1152/jappl.1999.87.1.74. PMID: 10409559.
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 (Basel, Switzerland), 9(3), 212. https://doi.org/10.3390/antiox9030212
Cheung K, Hume P, Maxwell L. Delayed onset muscle soreness : treatment strategies and performance factors. Sports Med. 2003;33(2):145-64. doi: 10.2165/00007256-200333020-00005. PMID: 12617692.
Mackey, A.L., Brandstetter, S., Schjerling, P., Bojsen-Moller, J., Qvortrup, K., Pedersen, M.M., Doessing, S., Kjaer, M., Magnusson, S.P. and Langberg, H. (2011), Sequenced response of extracellular matrix deadhesion and fibrotic regulators after muscle damage is involved in protection against future injury in human skeletal muscle. The FASEB Journal, 25: 1943-1959. https://doi.org/10.1096/fj.10-176487
Peake JM, Neubauer O, Della Gatta PA, Nosaka K. Muscle damage and inflammation during recovery from exercise. J Appl Physiol (1985). 2017 Mar 1;122(3):559-570. doi: 10.1152/japplphysiol.00971.2016. Epub 2016 Dec 29. PMID: 28035017.
Smith, Lucille L. Causes of Delayed Onset Muscle Soreness and the Impact on Athletic Performance, Journal of Strength and Conditioning Research: August 1992 - Volume 6 - Issue 3 - p 135-141