Delayed onset muscle soreness, also called muscle fever, is the pain and stiffness felt
in muscles several hours to days after unaccustomed or strenuous exercise.
The soreness is felt most strongly 24 to 72 hours after the exercise. It is thought to
be caused by eccentric exercise, which causes microtrauma to the muscle fibers. After such
exercise, the muscle adapts rapidly to prevent muscle damage, and thereby soreness, if the
exercise is repeated. Delayed onset muscle soreness is one symptom
of exercise-induced muscle damage. The other is acute muscle soreness, which appears during
and immediately after exercise.
Characteristics The soreness is perceived as a dull, aching
pain in the affected muscle, often combined with tenderness and stiffness. The pain is
typically felt only when the muscle is stretched, contracted or put under pressure, not when
it is at rest. This tenderness, a characteristic symptom of DOMS, is also referred to as "muscular
mechanical hyperalgesia". Although there is variance among exercises
and individuals, the soreness usually increases in intensity in the first 24 hours after exercise.
It peaks from 24 to 72 hours, then subsides and disappears up to seven days after exercise.
Cause The soreness is caused by eccentric exercise,
that is, exercise consisting of eccentric contractions of the muscle. Isometric exercise
causes much less soreness, and concentric exercise causes none.
Mechanism The mechanism of delayed onset muscle soreness
is not completely understood, but the pain is ultimately thought to be a result of microtrauma
– mechanical damage at a very small scale – to the muscles being exercised.
DOMS was first described in 1902 by Theodore Hough, who concluded that this kind of soreness
is "fundamentally the result of ruptures within the muscle". According to this "muscle damage"
theory of DOMS, these ruptures are microscopic lesions at the Z-line of the muscle sarcomere.
The soreness has been attributed to the increased tension force and muscle lengthening from
eccentric exercise. This may cause the actin and myosin cross-bridges to separate prior
to relaxation, ultimately causing greater tension on the remaining active motor units.
This increases the risk of broadening, smearing, and damage to the sarcomere. When microtrauma
occurs to these structures, nociceptors within muscle connective tissues are stimulated and
cause the sensation of pain. Another explanation for the pain associated
with DOMS is the "enzyme efflux" theory. Following microtrauma, calcium that is normally stored
in the sarcoplasmic reticulum accumulates in the damaged muscles. Cellular respiration
is inhibited and ATP needed to actively transport calcium back into the sarcoplasmic reticulum
is also slowed. This accumulation of calcium may activate proteases and phospholipases
which in turn break down and degenerate muscle protein. This causes inflammation, and in
turn pain due to the accumulation of histamines, prostaglandins, and potassium.
An earlier theory posited that DOMS is connected to the build-up of lactic acid in the blood,
which was thought to continue being produced following exercise. This build-up of lactic
acid was thought to be a toxic metabolic waste product that caused the perception of pain
at a delayed stage. This theory has been largely rejected, as concentric contractions which
also produce lactic acid have been unable to cause DOMS. Additionally, lactic acid is
known from multiple studies to return to normal levels within one hour of exercise, and therefore
can't cause the pain that occurs much later. Relation to other effects
Although delayed onset muscle soreness is a symptom associated with muscle damage, its
magnitude does not necessarily reflect the magnitude of muscle damage.
Soreness is one of the temporary changes caused in muscles by unaccustomed eccentric exercise.
Other such changes include decreased muscle strength, reduced range of motion, and muscle
swelling. It has been shown, however, that these changes develop independently in time
from one another and that the soreness is therefore not the cause of the reduction in
muscle function. Possible function as a warning sign
Soreness might conceivably serve as a warning to reduce muscle activity so as to prevent
further injury. However, further activity temporarily alleviates the soreness, even
though it causes more pain initially. Continued use of the sore muscle also has no adverse
effect on recovery from soreness and does not exacerbate muscle damage. It is therefore
unlikely that soreness is in fact a warning sign not to use the affected muscle.
Repeated-bout effect After performing an unaccustomed eccentric
exercise and exhibiting severe soreness, the muscle rapidly adapts to reduce further damage
from the same exercise. This is called the "repeated-bout effect".
As a result of this effect, not only is the soreness reduced, but other indicators of
muscle damage, such as swelling, reduced strength and reduced range of motion, are also more
quickly recovered from. The effect is mostly, but not wholly, specific to the exercised
muscle: experiments have shown that some of the protective effect is also conferred on
other muscles. The magnitude of the effect is subject to
many variations, depending for instance on the time between bouts, the number and length
of eccentric contractions and the exercise mode. It also varies between people and between
indicators of muscle damage. Generally, though, the protective effect lasts for at least several
weeks. It seems to gradually decrease as time between bouts increases, and is undetectable
after about one year. The first bout does not need to be as intense
as the subsequent bouts in order to confer at least some protection against soreness.
For instance, eccentric exercise performed at 40% of maximal strength has been shown
to confer a protection of 20 to 60% from muscle damage incurred by a 100% strength exercise
two to three weeks later. Also, the repeated-bout effect appears even after a relatively small
number of contractions, possibly as few as two. In one study, a first bout of 10, 20
or 50 contractions provided equal protection for a second bout of 50 contractions three
weeks later. The reason for the protective effect is not
yet understood. A number of possible mechanisms, which may complement one another, have been
proposed. These include neural adaptations, mechanical adaptations, and cellular adaptations.
Prevention Delayed onset muscle soreness can be reduced
or prevented by gradually increasing the intensity of a new exercise program, thereby taking
advantage of the repeated-bout effect. Soreness can theoretically be avoided by limiting
exercise to concentric and isometric contractions. But eccentric contractions in some muscles
are normally unavoidable during exercise, especially when muscles are fatigued. Limiting
the length of eccentric muscle extensions during exercise may afford some protection
against soreness, but this may also not be practical depending on the mode of exercise.
A study comparing arm muscle training at different starting lengths found that training at the
short length reduced muscle damage indicators by about 50% compared to the long length,
but this effect was not found in leg muscles. Static stretching or warming up the muscles
does not prevent soreness. Overstretching can by itself cause soreness.
The use of correctly fitted, medical-grade, graduated compression garments such as socks
and calf sleeves during the workout can reduce muscle oscillation and thus some of the micro-tears
that contribute to DOMS. Proper nutrition to manage electrolytes and glycogen before
and after exertion has also been proposed as a way to ease soreness. Consuming more
vitamin C may not prevent soreness. Treatment
The soreness usually disappears within about 72 hours after appearing. If treatment is
desired, any measure that increases blood flow to the muscle, such as low-intensity
activity, massage, hot baths, or a sauna visit may help somewhat. Immersion in cool or icy
water, an occasionally recommended remedy, was found to be ineffective in alleviating
DOMS in one 2011 study, but effective in another. Counterintuitively, continued exercise may
temporarily suppress the soreness. Exercise increases pain thresholds and pain tolerance.
This effect, called exercise-induced analgesia, is known to occur in endurance training, but
little is known about whether it also occurs in resistance training. There are claims in
the literature that exercising sore muscles appears to be the best way to reduce or eliminate
the soreness, but this has not yet been systematically investigated.
References Kokkinos, Peter. Physical Activity and Cardiovascular
Disease Prevention. Jones & Bartlett Learning. pp. 111–112. ISBN 978-0-7637-5612-3.
Nosaka, Ken. "Muscle Soreness and Damage and the Repeated-Bout Effect". In Tiidus, Peter
M. Skeletal muscle damage and repair. Human Kinetics. pp. 59–76. ISBN 978-0-7360-5867-4.
Footnotes