What is DOMS?
DOMS or delayed onset muscle soreness is a sensation felt by a person in the form of pain, discomfort in the muscles whose intensity increases within 24 hours after exercising or exercising. The peak of DOMS is usually felt 24 – 72 hours after exercising, and will disappear by itself in 5 – 7 days.
DOMS is categorized as a grade 1 muscle injury, where there is microscopic stretching or tearing of minor muscle fibers. Stretching of these muscle fibers produces stiffness and pain when touched or moved. Tenderness is usually felt in the distal area of a muscle, and spreads progressively within 24 – 48 hours after training/exercise.
DOMS usually occurs due to heavy muscle work exceeding normal muscle work with a predominantly eccentric type of muscle contraction. Eccentric contractions are characterized as lengthening of the muscle while the muscle is contracting simultaneously. If the external load exceeds the muscle's ability to actively support the load, the muscle is forced to lengthen and active tension develops. As a result, greater tension is placed on the active motor units and there is an increased risk of injury to the myotendinous junction.
Mechanism of occurrence of DOMS
- Lactic Acid Theory
This theory is based on the assumption that lactic acid continues to be produced after exercise. Accumulation of metabolic waste products can lead to noxious stimuli and delayed perception of pain. However, this theory was widely rejected because the higher metabolic rate associated with concentric muscle contractions did not produce the delayed pain sensation similar to DOMS. Lactic acid can cause acute pain associated with fatigue after intense exercise, but it cannot be associated with delayed pain experienced 24-48 hours post-exercise.
- Muscle Spasm
This theory is based on an increase resting muscle activity after eccentric contraction. Increased resting muscle activation indicates tonic local spasm of the motor units. This is thought to cause compression of local blood vessels, ischemia, and accumulation of pain activators. This will trigger a 'vicious circle' because further stimulation of the pain nerve endings causes further reflex muscle spasms and prolonged ischemic conditions.
- Connective tissue damage
This theory assesses the role of the connective tissue that forms around muscle fiber bundles. The composition of connective tissue differs depending on the type of muscle fiber. Type 1 (slow twitch) muscle fibers have a more robust structure compared to type 2 (fast twitch) muscle fibers. Type 2 muscle fibers tend to be more susceptible to injury in the form of stretching and tearing of the connective tissue which will cause muscle pain.
- Muscle injury
This theory focuses on discussing disorders of the contractile components of muscle fibers, especially the z-line area during eccentric contractions. The characteristics of microscopic lesions in the z-line area are widening, smearing or even total myofibrillar disruption in the z-line area, and this will further affect the arrangement of the sarcomeres. This damage occurs as a result of increased stress on each unit area of the muscle due to decreased motor unit activation during eccentric contractions. Mechanical disturbances in structural components increase, especially in type 2 muscle fibers which have thin and weak z-line areas. Nociceptors in the muscle connective tissue in the arterioles, capillaries and musculotendinosus areas will be stimulated and cause a sensation of pain.
- Inflammation
This theory is based on the discovery of inflammatory responses such as swelling and inflammatory cell infiltration that are clearly visible after repeated eccentric contractions. Muscle fibers contain proteolytic enzymes that initiate the degradation of the fat and protein structures of cells after injury. Damage to muscle fibers will trigger the release of bradykinin, histamine and prostaglandins, and will trigger monocyte and neutrophil cells to the injury site. This is followed by an influx of protein-rich fluid (exudate) into the muscle through increased permeability of small blood vessels after eccentric exercise. Ultimately, there will be osmotic pressure and pain will arise if group IV sensory neurons are activated.
- Enzyme efflux theory
This theory is based on the assumption that calcium (which is generally stored in the sarcoplasmic retinaculum), accumulates in the injured muscle as a result of sarcolemma damage. This is thought to cause obstruction of cellular respiration in mitochondria causing the regeneration of adenosine triphosphate (ATP), which is needed for the active transport of calcium back to the sarcoplasmic reticulum to be slow. Calcium accumulation will also activate proteases and phospholipases, which can cause further injury to the saecolema with the production of leukotrienes and prostaglandins. As a result, the amount of degenerated muscle protein in the weak z-line area increases, and chemical stimulation of the pain nerve endings occurs.
Effects of DOMS on Athlete Performance
- Perception of Functional Limitations
Limitations can be defined as changes in human anatomy, physiology and psychological status that can be measured objectively. Examples of limitations are decreased joint range of motion, decreased muscle strength or abnormal electromyographic patterns.
- Joint Kinematics
Kinematic analysis when running in athletes with DOMS conditions shows various results. A study showed that there was a significant difference in maximal ankle dorsiflexion and plantarflexion during the support phase of running, and a decrease in maximal hip flexion after 30 minutes of downhill running. It is thought that this change is a compensatory response to a decrease in joint range of motion in muscle groups experiencing DOMS. The reduced ability of the knee and hip to absorb shock (as a result of decreased joint range of motion of the quadriceps muscle group) is also compensated by the ankle joint with increased dorsiflexion during the support phase.
A significant decrease in joint range of motion was also reported in other studies, after repeated eccentric resistance exercise and maximal eccentric contractions of the elbow flexor muscles. Stiffness/decreased joint range of motion is not due to increased muscle activity, but to a significant increase in tissue swelling, especially in the perimuscular connective tissue and myotendinous junction area. This swelling is characteristic of an acute inflammatory response to muscle damage or injury
- Muscle Strength
A significant decrease in muscle strength in DOMS conditions generally occurs in eccentric contractions, although there is also a decrease in isometric and concentric contractions. The peak decrease occurred 24-48 hours after DOMS occurred. The duration of the decrease in muscle strength is also longer in activities that require eccentric contractions, which take 8-10 days to return to normal, while isometric and concentric contractions take only 4 days.
- Changes in Movement Patterns
Muscle injuries can cause muscle dysfunction. Muscle dysfunction is an unusual pattern of muscle recruitment during a series of movements. Injury to muscles and/or connective tissue during eccentric exercise can result in changes in muscle recruitment or changes in muscle activation patterns.
- Injury Risk Factors
Even though DOMS is a subclinical injury that can generally be tolerated, it does not rule out the possibility that DOMS can cause more serious injuries. It is common for individuals to continue exercising during periods of intense muscle soreness. Those seeking to improve or maintain levels of fitness or performance regularly adhere to the ‘no pain, no gain’ philosophy. As a result, the first instinct is to ‘deal with the pain’ rather than resting the affected area. The potential impact of such behavior can be detrimental to weakened tissues and unusual tissue structures that are forced to compensate during the period of functional deficiency following DOMS.
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Reference :
- 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. https://pubmed.ncbi.nlm.nih.gov/12617692/
