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by Tahira Collier
Delayed onset muscle soreness (DOMS)
is a sensation felt in exercised muscles between 8 hours
and 3 days following unaccustomed heavy exercise. Although
muscle soreness usually occurs in less physically trained
individuals, most people, including elite athletes can experience
this soreness as well. The mechanisms involved in DOMS are
still being studied and refined, however researchers strongly
suggest that certain exercises can generally cause damage
to muscle fibers, resulting in soreness. The body responds
to that damage by producing the common symptoms associated
with DOMS shortly after the exercise. These symptoms include
pain, decreased range of motion, decreased output of muscle
force, and some swelling. The body then helps repair the
damage and the muscles are able to function normally again
(i.e., return to their function before exercise) without
pain.
The topic of delayed onset muscle soreness
is of interest for two reasons. One is that most individuals
who engage in some physical activity, especially one they
are not accustomed to, may experience some degree of DOMS.
Depending on how much time passes before exercising again,
DOMS could occur several times in one individual. For those
who experience DOMS, or in cases where DOMS can play a critical
role in performance (i.e., sports), learning more about the
mechanisms of muscle soreness can help people understand
how the body responds to certain physical activities. One
that has an understanding of these general mechanisms can
perhaps learn to deal with the effects of muscle fiber damage.
Another reason the topic of delayed
muscle soreness is of interest is because of the slight uncertainty
in the mechanisms of soreness. Several studies, of which
many are supported, have hypothesized the causes of soreness,
which is initiated by muscle fiber damage, and the body’s
response to it. For example, most studies suggest an acute
inflammatory response while others find no specific indicators
of such response. Although there has been much agreement
on the general causes of muscle fiber damage and the body’s
general response, some questions on both mechanisms remain
unanswered. The goal of this paper is to explore some of
the main studies on the causes of delayed onset muscle soreness.
It will specifically look at the mechanical factors suggested
to play a role in DOMS and how the body responds to the muscle
damage from these factors.
To discuss the mechanical factors involved
in delayed onset muscle soreness, it is necessary to discuss
the types of exercise most associated with soreness, and
the effects this exercise has on muscle fibers. In general,
three main types of exercise can cause muscle soreness. These
include isometric, concentric, and most commonly, eccentric
exercises. Isometric and concentric exercises involve contractions
that make the muscle either shorten or stay the same length.
Examples would be trying to lift a heavy table without actually
moving it (isometric) or bringing a barbell to the chest
during a biceps curl (concentric). An eccentric exercise
on the other hand causes the muscle to lengthen during contraction
(e.g., lowering a barbell to the thigh during a biceps curl).
Eccentric exercises tend to cause more soreness than isometric
and concentric exercises because the muscles endure higher
forces during contraction.
Since the beginning of the twentieth century,
it has been hypothesized and well supported that general
muscle soreness indicates some form of damage to muscle fibers
and/or connective tissue (Hough, 1902). In his study of muscle
soreness and workloads, Hough hypothesized that muscle tissues
were torn after performing exercise with heavy workloads
and this resulted in pain. As several other studies were
conducted to investigate this hypothesis, researchers have
learned more specifically what parts of the fibers may become
injured and have determined eccentric exercises to cause
the most damage (Armstrong et al. 1983; Clarkson et al. 1986;
Sargeant and Dolan, 1987). (This explains why eccentric exercises
generally create soreness more often than isometric and concentric
exercises).
To determine muscle fiber damage and where
it occurs after doing certain exercises, many researchers
use markers of certain enzyme activities in the muscle and
take muscle biopsies to examine the cell patterns, before
and after exercise. For example, Armstrong and his colleagues
(1983) conducted a study to examine the effects of eccentric
exercise on injury in skeletal muscle in rats. They examined
the muscle fibers of rats that ran up a 16ƒ incline (primarily
concentric contractions), at 0ƒ incline (similar amounts
of concentric and eccentric contractions), and down a 16ƒ incline
(primarily eccentric contractions) on a treadmill.
Their study produced several results that
suggested muscle fiber damage, especially from eccentric
exercise. One was a significant increase in plasma enzyme
activities, particularly in the rats that ran downhill. (Although
there is some uncertainty on why there is an increase in
these activities, this increase has been well observed in
the presence of tissue damage in other studies (Altland and
Highman, 1961; Evans et al., 1986; Schwane et al., 1983)).
There was also an increase in serum creatine kinase (CK)
activity, which studies suggest has a direct relation to
the extent of fiber degeneration. The results also showed
an increase in macrophages and mononuclear cells, cells usually
present when tissue damage occurs. Examinations of the muscle
cells following exercise, showed disruption of some muscle
cell membranes (sarcolemma), as well as disruption of the
bands connecting the individual muscle fibers (Z-lines).
Armstrong and colleagues noted the biggest changes of enzyme
activities and fiber disruption in the muscles that underwent
the most eccentric contractions. They interpreted this by
suggesting there was a greater tension per cross-sectional
area of these fibers, causing structural damage and leakage
of the muscular enzymes mentioned.
Friden and his colleagues (1981) conducted
another study that showed similar results to Armstrong’s.
They attempted to look at the morphological changes of cells
of the soleus muscle (part of the calf muscle) in human males,
before and after running down stairs (primarily eccentric
exercise). Upon examination of the exercised muscle cells
two days after exercise (when the subjects complained of
the most soreness), their study found no rupture or fiber
degeneration at the cellular level. At the subcellular level
however, there were disturbances to the Z-lines, showing
widening and streaming, and in some cases total disruption.
The tissues adjacent to the Z-lines were also disorganized
and damaged. Friden and his colleagues explained these results
by suggesting that a high muscle fiber tension developed
during the exercise, causing an overload in the Z-lines.
They concluded that a weak link existed between the chain
of muscle fibers (which is connected by the Z-lines), thereby
causing disruption.
In summary, evidence from studies on
skeletal muscle after heavy exercise suggests some disruption
of muscle fibers. The studies by Hough, Armstrong, and Friden
demonstrate muscle fiber damage especially after eccentric
exercises, which place high mechanical forces on the fibers.
While there seems to be enough evidence to support the hypothesis
that muscle fiber injury occurs during heavy exercise, there
are still questions on exactly how the fibers are
disrupted and to what extent. To determine the mechanisms
by which the fiber degeneration or Z-line disruption occurs,
further studies have to be conducted.
In terms of the physiological factors
associated with delayed onset muscle soreness, the body undergoes
several changes in response to the muscle fiber damage. Most
studies suggest the body undergoes an inflammatory response,
which can be characterized by symptoms of pain, some swelling
or tightness, and decreased function in the muscle. Inside
the body, specific cells associated with the immune system
provide more solid evidence of this type of response, often
referred to as a classic inflammatory response. Although
some studies do not support this response hypothesis, other
physiological evidence shows the muscles fibers undergo repair
and adaptation, such that they are temporarily protected
from further damage.
When tissue damage occurs, the body responds
by sending specific cells and nutrients to the injury site
to get rid of damaged cells, decrease further damage, and
help repair. For tissue injury, these cells generally include
monocytes, neutrophils, macrophages, and lymphocytes. The
body usually alerts the brain of this injury through pain
receptors, which in turn may decrease the functioning of
the injured area to promote healing. Swelling may also occur
to help flush out any damaged cells of the area and promote
nutrient and blood flow to aid in healing.
The vast majority of studies on DOMS and
muscle tissue injury indicate the presence of a general inflammatory
response through pain, swelling and decreased muscle function.
Although the classic inflammatory response (characterized
by the presence of the specific cells mentioned) is not as
universally accepted, many studies do support this idea.
One such study is that by Bruunsgaard and his co-workers
who studied the increases in serum interleukin-6 (a type
of messenger involved in the regulation of immune response)
in exercise-induced muscle injury (1997). Human male subjects
performed 30 minutes of concentric and eccentric exercises
on a bike, two weeks apart. Examination of blood samples
during and after the exercises showed significant increases
in the serum interleukin-6, particularly after the eccentric
exercise. More specifically, the results indicated an increase
in total concentration of lymphocytes, due to a greater recruitment
of natural killer (NK) cells. (NK cells, a type of lymphocyte,
are responsible for killing infected cells).
Another study that supported the classic
inflammatory response to muscle fiber injury looked at the
possible causes of pain and the inflammatory response (Davies
et al., 1979). Many studies suggest that a specific type
of prostaglandin (PGE, a hormone) sensitizes pain receptors,
thereby causing pain. Davies and colleagues found that under
inflammatory conditions, macrophages are capable of making
and releasing large quantities of PGE, thereby causing the
sensation of pain. As one particular study showed increases
in PGE after eccentric exercise (Smith et al., 1993), this
suggests that the muscle injury from exercise elicits an
inflammatory response that may cause pain.
One other study that showed support of
the classic inflammatory response was by Armstrong and colleagues
(1983), that examined the muscle injury from eccentric exercise
in rat skeletal muscle (described earlier). Upon examination
of the fibers after exercise, there was an increase in the
number of macrophages and mononuclear cells (a type of lymphocyte).
This increase was even more pronounced in the muscles that
underwent the most eccentric contractions. (Although this
study showed evidence of inflammatory responses, other results
from the study do not fully support the inflammatory response,
as will be explained below).
Studies that do not support the inflammatory
response hypothesis are mainly those that do not show evidence
of the characteristic cells (i.e., monocytes, neutrophils,
macrophages, and lymphocytes). One example is a study that
examined general factors in DOMS in man (Bobbert et al.,
1986). Eleven subjects performed exercise to induce delayed
muscle soreness in one leg while the other leg served as
a control. Blood samples taken before and several times after
exercise were analyzed to determine white blood cell count.
The results did not show an increase in white blood cells,
suggesting there was not an inflammatory response to muscle
damage.
Another study that did not support the
inflammatory response hypothesis was one that observed muscle
fiber damage from eccentric exercise in man (Friden et al.,
1983). Muscle biopsies were taken from the vastus lateralis
muscle in humans (a quadriceps muscle of the thigh) after
performing eccentric exercise. Although the results showed
tissue damage from the exercise, they did not observe the
presence of mononuclear cells or macrophages. Their absence
suggested that inflammation did not occur from the tissue
damage. A third study opposing the inflammatory hypothesis
was Armstrong and colleagues’ study on eccentric exercise
and rat skeletal muscle. As mentioned above, the study showed
some evidence for an inflammatory response, however they
found very small amounts of neutrophils in the muscle tissue.
Since neutrophils are a major component of the inflammatory
response, Armstrong and colleagues suggested that there was
not a classic inflammatory response involved in the tissue
damage.
Although there is still some question on
the type of response the body has to muscle damage (inflammatory
or other), there is strong evidence that the muscle fibers
are repaired so the muscle can return to normal functioning.
One study that supported the idea of muscle repair and adaptation
was that conducted by Clarkson and Tremblay (1988). Eight
college women performed eccentric exercises of their forearm
flexors, at differing numbers of maximal contractions. Five
days after exercise, Clarkson and Tremblay analyzed muscle
soreness, muscle strength, and serum creatine kinase (CK)
activity. Their results suggested that the muscle adapts
to the exercise by becoming more resistant to muscle damage
when subsequent exercise of the same kind was performed.
They also concluded that any damage that did occur was repaired
at a faster rate.
Chen and Hsieh (2001) conducted another
study that supported the idea of muscle adapting to exercise.
They examined the effects of a 7-day eccentric training period
on muscle damage in college-age males. Their results referred
to an effect called the repeated bout effect (RBE), where
after an initial exercise bout that induces soreness, repeating
the same exercises results in less muscle damage. In their
study, they found that the eccentric exercises performed
on days 2-7 did not cause any further damage or soreness
than from the first day of exercise. They also suggested
that the muscle may start to adapt as early as 24hours following
the first bout of exercise.
To summarize, the body displays some inflammatory
responses to muscle fiber damage caused by some exercise.
These inflammatory responses are generally characterized
by the presence of monocytes, neutrophils, macrophages, and
lymphocytes inside the body, and felt as symptoms of pain,
swelling, and loss of function. Although there is still question
on whether there is a classic inflammatory response to muscle
tissue injury, there is general agreement on the idea that
muscle repair and adaptation occur to help prevent further
damage from the same exercise repeated in the near future.
Further studies have to be conducted to determine if the
responses to muscle fiber injury can be classified as inflammatory.
The studies discussed above are examples
of studies that provide evidence supporting the proposed
muscle fiber damage from certain exercise and the body’s
response to that damage. Because several researchers study
related topics, and the goals of their research slightly
differ, it is necessary to consider those differences when
attempting to understand the proposed hypotheses. More specifically,
some of these experimental differences may account for the
inconsistencies in the results and the unanswered questions
of the topics being studied.
Regarding the studies discussed in
this paper, there were three main differences amongst the
studies that could have accounted for some unanswered questions.
One is that Armstrong and his colleagues studied rat skeletal
muscle rather than human muscle. Although several studies
on rodents and other animals, such as frogs, have suggested
strong correlation with very similar studies on humans, it
is not well understood that specific mechanisms in rodents
and humans are the same. Therefore, the mechanisms and extent
of muscle fiber damage, and the presence of certain inflammatory
cells following exercise in the rats may not be that reflective
of what occurs in humans.
Another major difference amongst the
studies was the time of data collection from the subjects
after exercise. In some studies, such as those by Armstrong
et al. and Bruunsgaard et al., the experimental protocol
involved collecting data within the first few hours after
exercise and thereafter. In other studies, such as those
by Bobbert et al. and Friden et al., data collections did
not begin until 24 hours or more following exercise. This
difference in the studies is important because different
levels of plasma enzymes and inflammatory cells, and different
stages of fiber degeneration are present at different times
after tissue injury. For example, neutrophils and monocytes
increase in circulation within a few hours after injury and
then begin to concentrate at the injury site thereafter.
Thus, depending on the stage of fiber damage, or which specific
cells are most present, data collection may not show much
damage or indices of an inflammatory response.
A third difference amongst the studies
that may need to be taken into account is the type of measurements.
This difference may be more relevant to the studies that
assessed the presence of an inflammatory response. In the
studies presented in this paper, researchers used either
muscle biopsies or blood samples to assess the presence of
inflammatory cells, with the exception of Armstrong and colleagues
who used both. These different measurement methods may be
important because as explained above, some inflammatory cells
may only be present in the blood at certain times after the
injury occurs, while others may only be at the injury site.
The differing methods may also be important because there
may not be a precise location where the tissue injury occurred.
Most muscle biopsies are taken from the belly of the muscle
(the bulkier part of the muscle). However, if the injury
site is more near the myotendinous junction (where the muscle
and tendon meet), then there may not be any inflammatory
cells present. Therefore, studies that perform muscle biopsies
away from the injury site may oppose the inflammatory response
hypothesis.
Delayed onset muscle soreness is the result
of muscle fiber injury from unaccustomed exercise, usually
eccentric exercises, which put the most force on the muscle
fibers. Studies suggest that the disruption to the muscle
fibers occurs particularly in muscle cell membranes and the
bands that connect muscle cells. In terms of the body’s
response to this tissue damage, most studies suggest an acute
inflammatory response. Although some question remains on
whether the response is inflammatory in a classic sense (i.e.,
the presence of white blood cells and macrophages), the proposed
inflammatory response helps explain the common characteristics
of DOMS felt 8 hours to 3 days after exercise. These include
pain, loss of muscle function, swelling and reduced muscle
force. The purpose of the response is to prepare the fibers
for repair, so that the muscle can perhaps become protected
from further damage by similar exercise that might be performed
in the near future.
At present, most studies agree on the general
mechanisms causing muscle fiber damage. However, some questions
remain on whether an inflammatory response is involved in
DOMS. To understand some of the inconsistencies of the results,
one should consider looking at some of the main differences
amongst the studies, including the types of subjects used
and the methods of measurements. Perhaps, future studies
with more similar experimental methods and subjects can create
more consistent data to determine the specific mechanisms
of delayed onset muscle soreness.
–copyright © 2008, Tahira
Collier
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