Delayed Onset Muscle Soreness

Delayed Onset Muscle Soreness: what the GP needs to know

Dr Phatho Zondi

MBChB, MSc Sports Medicine, MBA

Sports Science Institute of South Africa

PC Zondia, b

First Published 2014

Section of Sports Medicine, University of Pretoria, Pretoria

Exercise SMART Team, University of Pretoria

The purpose of this article is to provide brief insight into delayed onset muscle soreness (DOMS), a phenomenon that is often experienced by recreational and elite athlete. The article is aimed at general practitioners who may encounter athletes presenting with DOMS and who will benefit from understanding the proposed mechanisms, signs and symptoms and various treatment options available to manage athletes.


Delayed onset muscle soreness (DOMS) is muscle pain and stiffness that develops 24-72 hours after exercise involving unaccustomed muscle loading (1). It is classified as a type of exercise induced muscle damage (EIMD), but is different to muscle fatigue or pain that develops during or immediately after exercise. While the aetiology and exact mechanisms remain unknown, most research acknowledges that DOMS is iniated by eccentric exercise (1-5). This has been demonstrated in a number of studies that have tested the relationship between muscle pain and different types of eccentric, concentric and static activities.  Since it was first described, many theories have been proposed to explain the mechanisms of DOMS including lactic acid buildup, muscle spasm, damage to connective tissue, mechanical muscle damage, cellular infammation and enzyme efflux theories (5). It is most likely that the best explaination and understanding of DOMS would be derived from a combination of two or more of these theories (5). A variety of treatment modalities have been tested, with post-exercise non-steroidal anti-inflammatories, massage, and light aerobic activity showing limited success in reducing symptoms (1,4-6). The DOMS phenomenon, which affects both elite and recreational athletes, remains topical as researchers continue to refine aetiological models and investigate effective preventative strategies and treatment modalities.

Proposed Mechanisms

Research suggests that the trigger activity for DOMS is eccentric muscle activity (3,5,7). Eccentric activities are those which cause muscles to lengthen while contracting (7). Examples include activities such as lowering a dumbbell or performing a calf press off a ledge  (4). Mechanical stress is greater in eccentric exercise compared to concentric exercise as this type of activity recruits fewer muscle fibres which results in greater mechnical load per fibre and a higher propensity for cellular damage (8). Although the exact cellular mechanisms involved in DOMS are unknown, a model was proposed by RB Armstrong in 1984 (3)  and continues to be validated and refined by researchers in more recent years (8,9). Proposed cellular mechanisms occur as follows: 1) high tensions in muscle fibre result in microtrauma; 2) structural damage of the cell membrane disrupts calcium homesostasis causing necrosis that peaks 48 hours post exercise; 3) intracellular contents (such as histamine, kinins, and potassium)  and products of the inflammatory process accumulate in interstitium stimulating free nerve endings which results in the pain associated with DOMS (3,8,9).

Histology and Biochemistry

Biopsies taken in affected muscles show structural damage to muscle fibres at the Z-line (Z-line streaming), as well as leukocyte infiltration, mast cell degraulation and increased plasma substrates in the extracellular space(10,11). In studies that have investigated changes in serum haematology and biochemistry, neutrophil count was shown to peak in 6 hours while monocyte counts decreased 48 hours post exercise(11).  Significant correlations were found between DOMS and elevated myoglobin and creatinine kinase 24 – 96 hours post exercise (3,7,10).


DOMS may occur in recreational athletes who are embarking on a new training programme, or in elite athletes at the beginning of a new season or as a result of repetitive, high intensity contractions (5,12). Patients typically present with complaints of dull, aching pain in the affected muscle, often combined with tenderness, stiffness and a loss of strength (13).  Pain is not felt at rest but rather when the affected muscle is activated by either being stretched, contracted or put under pressure(13). Initial symptoms usually start at the musculo-tendinous junction and therafter spread throughout the rest of the muscle (13). The severity of the symptoms depends on the duration, intensity and type of exercise performed (5,9). Symptoms usually increase in intensity in the first 24 hours after exercise, peak between 24 – 72 hours, then subside without intervention 5 – 7 days after exercise (13). Other than pain, DOMS also causes a reduction in range of motion, shock attenuaton and peak torque (5). This reduced function adversely affects athletic performance and may be a cause of distress to many athletes. The diagnosis of DOMS is made clinicallly, based on patient history and symptoms, and seldom requires any special investigations unless complications of rhabdomyolysis are suspected.


A number of treatment strategies have been tested to decrease severity, improve muscle function and expedite return to play (5). Although numerous practices exists for the management of DOMS, few are based on scientific evidence (6). Interestingly, the best known treatment for DOMS is muscle activity (3,5). Endorphins released in the body during exercise increase pain threshold and pain tolerance, however, this analgesic effect is temporary and the discomfort may return following exercise (3,5). Athletes who train daily should be encouraged to decrease the intensity of their training for 1 -2 days following DOMS-inducing activity or, alternatively, participate in cross-training that targets other unaffected muscle groups so that the affected muscle can recover (5). Massage administered shortly after exercise has been shown to decrease the amount of pain and stiffness felt (14). Despite reported improvements in algesic symptoms, massage does not have an effect on muscle function or enzyme activity in damaged muscles (14).

There is some evidence supporting the use of non-steroidal anti-inflammatory (NSAIDS) medication although effects have been shown to be dependent on dose and timing of ingestion(5). NSAIDS work by inhibiting cyclo-oxegenase (COX) enzymes which suppresses prostaglandin production (9). A theoretical risk exists that NSAIDS may impair the adaptive response to exercise as COX activity and prostanoid-mediated signalling are key processes involved in achieving maximum skeletal muscle hypertrophy in response to functional overload (9). Current evidence suggests that occasional short term use of NSAIDS does not negatively effect muscle growth, while effects of chronic use need further investigation (9). In a comprehensive literature review investigating the role of nuritional supplements in the prevention and treatment of exercise induced muscle damage, Bloomer found evidence supporting the use of certain supplements (vitamin C, vitamin E, flavonoids, and L-carnitine) in DOMS, however, optimal ‘prophylactic’ and treatment dosag remained yet to be defined (15). While supplementation may have shown promise in attentuating some signs and symptoms of DOMS, it did not eliminate muscle injury (15). Studies conducted in this area are limited in number and quality, and further research is needed before the use of nutrients can be recommended with absolute confidence for treating DOMS (15).

Modalities such as stretching, warming up, cryotherapy, homeopathy and electrical current treatments have been repeatedly tested but fail to demonstrate efficacy in alleviated symptoms or severity of DOMS (1,5,6). The results of hydrotherapy are conflicting with some studies reporting a reduction in functional deficits after cold water immersion and contrast water therapy (12) while others studies find little or no evidence supporting hydrotherapy (6).

DOMS can be prevented or reduced by gradually increasing the intensity of a new exercise programme over 1 – 2 weeks (5). If no active intervention is introduced, symptoms usually resolves within three to seven days (13).


DOMS affects both recreational and elite athletes resulting in pain and functional limitation which adversly affects athletic performance. Numerous studies have been conducted investigating the mechanisms and management of DOMS, however, definitive models outlining aetiology and treatment are yet to be established. As athletes respond differently to treatment, a combination of strategies should be employed in managing this condition. There remains scope for further research to clearly define structured protocols for treatment interventions and preventative strategies.