Delayed onset muscle soreness: No pain, no gain? The truth behind this adage

Abstract

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 athletes. The negative implications of DOMS include pain, decreased motivation to continue
training, and decreased performance. While performance issues may be more relevant to the elite athlete, pain and decreased
motivation are particularly relevant to recreational athletes wishing to sustain a regular level of physical activity. The article is aimed
at general practitioners (GPs) who may encounter athletes presenting with DOMS, and who will benefit from understanding the
proposed mechanisms, signs and symptoms of the condition. Numerous researchers have hypothesised that certain interventions
may prevent or minimise the symptoms thereof, and all GPs could benefit from understanding the available options for athletes,
and the scientific evidence that supports these options.

Full text

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Introduction
Delayed onset muscle soreness (DOMS) is muscle pain and
stiness that develops 24-72 hours after exercise involving
unaccustomed muscle loading1 (Table I). It is classied as a
type of exercise-induced muscle damage, but is dierent 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
initiated by eccentric exercise.1-5 This has been demonstrated in
a number of studies that have tested the relationship between
muscle pain and dierent types of eccentric, concentric and
static activities. Since it was rst described, many theories have
been proposed to explain the mechanisms of DOMS, including
lactic acid build-up, muscle spasm, damage to connective tissue,
mechanical muscle damage, cellular infammation and enzyme
eux theories.5 It is most likely that the best explanation and
understanding of DOMS derives from a combination of two or
more of these theories.5 A variety of treatment modalities have
been tested, with post-exercise nonsteroidal anti-inammatory
drugs (NSAIDs), massage and light aerobic activity showing
limited success in reducing the symptoms.1,4-6 The DOMS
phenomenon, which aects both elite and recreational athletes,
remains topical as researchers continue to rene aetiological
models and investigate eective preventative strategies and
treatment modalities.
Proposed mechanisms
Research suggests that eccentric muscle activity is the trigger
activity for DOMS.3,5,7 Eccentric activities are those which cause
the muscles to lengthen while contracting.7 Examples include
lowering a dumbbell or performing a calf press o a ledge.4
Mechanical stress is greater in eccentric exercise, compared to
concentric exercise, as this type of activity recruits fewer muscle
bres, which results in a greater mechanical load per bre and
a higher propensity for cellular damage.8 Although the exact
cellular mechanisms involved in DOMS are unknown, a model
was proposed by Armstrong in 1984,3 and has continued to be
validated and rened by researchers in more recent years.8,9
The proposed cellular mechanisms occur as follows:
• High tension in the muscle bre results in microtrauma.
Abstract
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 athletes. The negative implications of DOMS include pain, decreased motivation to continue
training, and decreased performance. While performance issues may be more relevant to the elite athlete, pain and decreased
motivation are particularly relevant to recreational athletes wishing to sustain a regular level of physical activity. The article is aimed
at general practitioners (GPs) who may encounter athletes presenting with DOMS, and who will benet from understanding the
proposed mechanisms, signs and symptoms of the condition. Numerous researchers have hypothesised that certain interventions
may prevent or minimise the symptoms thereof, and all GPs could benet from understanding the available options for athletes,
and the scientic evidence that supports these options.
Keywords: delayed onset muscle soreness, mechanism, symptoms, treatment, athletes, management
S Afr Fam Pract
ISSN 2078-6190 EISSN 2078-6204
© 2015 The Author(s)
REVIEW
South African Family Practice 2015; 57(3):29-33
Open Access article distributed under the terms of the
Creative Commons License [CC BY-NC-ND 4.0]
http://creativecommons.org/licenses/by-nc-nd/4.0
Delayed onset muscle soreness: No pain, no gain? The truth behind this adage
PC Zondi,1* DC Janse van Rensburg,2 CC Grant,3 A Jansen van Rensburg4
1Lecturer and Clinician
2Head of Department
3Senior Lecturer and Researcher
4Researcher, Section Sports Medicine, University of Pretoria, Pretoria
Correspondence to: *Phathokuhle Zondi, e-mail: phatho.cele@up.ac.za
Table I: Delayed onset muscle soreness explained1
Examples of common activities known to cause delayed onset muscle
soreness include:
• Eccentric strength-training exercises
• Walking or jogging downhill
• Step aerobics.
Causes of muscle pain associated with delayed onset muscle soreness
include:
• Structural damage to the muscle fibre and plasmalemma
• An inflammatory reaction.
Prevention is achieved with:
• Graduated intensity and duration of novel activities and eccentric
exercise over a period of 1-2 weeks.
Treatment strategies include:
• Nonsteroidal anti-inflammatory drugs.
• Massage administered shortly after the eccentric exercise.
• Light aerobic exercise.
• Nutritional supplementation (antioxidants and L-carnitine) shows
promise, but needs to be investigated further in order for the
optimal dosage and timing of intake to be defined.

S Afr Fam Pract 2015;57(3):29-3332
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• Structural damage of the cell membrane disrupts calcium
homeostasis, causing necrosis, that peaks 48 hours post
exercise.
• Intracellular contents, such as histamine, kinins and potassium,
and the products of the inammatory process accumulate in
interstitium, stimulating the free nerve endings, which results
in the pain associated with DOMS.3,8,9
Histology and biochemistry
Biopsies taken from the aected muscles show structural
damage to the muscle bres at the Z-line (Z-line streaming),
as well as leukocyte inltration, mast cell degranulation and
increased plasma substrates in the extracellular space.10,11 The
neutrophil count was shown to peak at six hours, while the
monocyte count decreased 48 hours post exercise in studies that
investigated changes in serum haematology and biochemistry.11
A signicant correlation was found between DOMS and elevated
myoglobin and creatinine kinase 24-96 hours post exercise.3,7,10
Diagnosis
DOMS may occur in recreational athletes embarking on a new
training programme, 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 aected muscle, often combined with tenderness, stiness
and the loss of strength.13 Pain is not felt at rest, but rather
when the aected muscle is activated by either being stretched,
contracted or placed under pressure.13 The initial symptoms
usually start at the musculotendinous junction, and thereafter
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 The symptoms usually increase in
intensity in the rst 24 hours after exercise, peak between 24
and 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 attenuation and peak torque.5 This
reduced function adversely aects athletic performance and
causes distress to many athletes. The diagnosis of DOMS is
made clinically, based on the patient history and symptoms. It
seldom requires special investigations unless complications of
rhabdomyolysis are suspected. Practitioners should have a high
index of suspicion of complications in athletes presenting with
persistent muscle pain, weakness and myoglobinurea (cola-
coloured urine).14 Biochemistry often demonstrates a raised
plasma creatine kinase and myoglobinemia, and raised aspartate
aminotransferase, hyperkalaemia and hypocalcaemia in some
case reports. These athletes may need admission for intravenous
hydration and monitoring.14
Management
A number of treatment strategies have been tested to decrease
severity, improve muscle function and expedite return to play.5
Although numerous practices exist for the management of
DOMS, few are based on scientic evidence.6 Interestingly,
muscle activity is the best known treatment for DOMS.3,5
Endorphins released in the body during exercise increase the
pain threshold and pain tolerance. However, this analgesic eect
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-induced
activity, or alternatively participate in cross-training that targets
other unaected muscle groups so that the aected muscle
can recover.5 Massage administered shortly after exercise has
been shown to decrease the amount of pain and stiness felt.15
Despite a reported improvement in the analgesic symptoms,
massage does not have an eect on muscle function or enzyme
activity in the damaged muscles.15
Some evidence supports the use of NSAID medication, although
the eects have been shown to be dependent on the dose and
timing of ingestion.5 NSAIDs work by inhibiting cyclo-oxegenase
(COX) enzymes, suppressing 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 the occasional short-term use
of NSAIDs does not negatively eect muscle growth, while
the eects of chronic use need further investigation.9 In a
comprehensive literature review in which the role of nutritional
supplements in the prevention and treatment of exercise-
induced muscle damage was investigated, Bloomer found
evidence which supported the use of certain supplements
(vitamin C, vitamin E, avonoids and L-carnitine) in DOMS.
However, the optimal “prophylactic” and treatment dosage has
yet to be dened.16 While supplementation may have shown
promise in attentuating some signs and symptoms of DOMS, it
did not eliminate muscle injury.16 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
condence when treating DOMS.16
Modalities, such as stretching, warming up, cryotherapy,
homeopathy and electrical current treatments, have been
repeatedly tested, but have failed to demonstrate ecacy in
alleviating the symptoms or severity of DOMS.1,5,6 There are
conicting results with respect to hydrotherapy. A reduction in
functional decit after cold water immersion and contrast water
therapy has been reported in some studies,12 while little or no
evidence to support hydrotherapy has been found in others.6
DOMS can be prevented or reduced by gradually increasing
the intensity of a new exercise programme over 1-2 weeks.5
The symptoms usually resolve within 3-7 days if no active
intervention is introduced.13
Conclusion
DOMS has an impact on both recreational and elite athletes,
resulting in pain and functional limitation, which adversely aect
athletic performance. Numerous studies have been conducted
that have investigated the mechanisms and management
of DOMS. However, denitive models that outline aetiology
and treatment are yet to be established. As athletes respond
dierently to treatment, a combination of strategies should

Delayed onset muscle soreness: No pain, no gain? The truth behind this adage 33
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33
be employed when managing this condition. There is scope
for further research to clearly dene structured protocols for
treatment intervention and preventative strategies.
Declaration
The authors did not receive any funding when conducting this
research.
Conflict of interest
The authors declare that there were no competing interests.
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