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Morphologic and Mechanical Basis of Delayed-Onset Muscle Soreness

  • Shirley Ryan Ability Lab (Formerly the Rehabilitation Institute of Chicago)

Abstract and Figures

Muscle pain after unaccustomed exercise is believed to result from repetitive active lengthening of skeletal muscle. This "eccentric exercise" initiates a sequence of events that includes muscle cytoskeletal breakdown, inflammation, and remodeling such that subsequent exercise sessions result in less injury and soreness. Recent studies of eccentric exercise using well-defined animal models have identified the mechanical and cellular events associated with the injury-repair process. In addition, neurophysiologic studies have elucidated mechanisms of pain that operate in skeletal muscle. Taken together, these studies improve our understanding of the muscle injury process and will lead to rational therapeutic interventions to facilitate recovery.
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Vol 10, No 1, January/February 2002 67
Delayed-onset muscle soreness
(DOMS), or what is commonly
described as postexercise muscle
soreness, is the sensation of muscu-
lar discomfort and pain during
active contractions that occurs in a
delayed fashion after strenuous
exercise. Usually, the initial symp-
toms are most evident at the mus-
cle tendon junction and thereafter
spread throughout the entire mus-
cle. Skeletal muscle soreness and
injury are associated with intense
exercise. The soreness and accom-
panying muscle damage are even
more pronounced if the exercise
performed is new to the individual.
Thus, even individuals who are in
excellent athletic condition may ex-
perience muscle soreness and dam-
age when performing exercise to
which they are unaccustomed. The
relationship between the develop-
ment of DOMS and the loss of mus-
cle strength has yet to be explicitly
Sore muscles after exercise are usu-
ally described as stiff, tender, or
aching. The stiffness associated with
DOMS is not a function of antago-
nistic muscular action but is proba-
bly caused by edema occurring in
the perimuscular connective tissue.1
The symptoms of DOMS develop
during the first 24 to 48 hours, peak
between 24 and 72 hours, and disap-
pear within 5 to 7 days,2,3 usually
without intervention. Regardless of
the exact location of the palpable
region of soreness, passive stretch-
ing and renewed activity aggravate
the pain. Some controversy exists
regarding the relationship between
maximum voluntary force and
symptoms of soreness. Ebbeling
and Clarkson3suggested that there
is very little or no relationship be-
tween the development of soreness
and a decrease in muscle strength.
Newham et al4demonstrated return
of maximum quadriceps strength to
pre-exercise levels within 24 hours
after step exercise, while others have
reported that a period of >2 weeks is
necessary to recover maximum iso-
metric strength. In addition to ten-
derness with palpation, the examiner
also will find prolonged strength
loss, a reduced range of motion, and
elevated levels of serum creatine
kinase (CK).
Many studies have reported that
eccentric exercise results in a signifi-
cant increase in CK levels 24 to 48
hours after the exercise session5that
may peak between 3 to 6 days, de-
pending on the precise nature of the
exercise (Fig. 1, open circles). CK is
an intramuscular enzyme responsi-
ble for maintaining adequate adeno-
sine triphosphate levels during
muscle contraction. Its appearance
in the serum is interpreted as indi-
cating an increased permeability or
breakdown of the membrane sur-
Dr. Lieber is Professor of Orthopaedics and
Bioengineering, Veterans Affairs Medical
Center, and Department of Orthopaedics and
Bioengineering, University of California, San
Diego, Calif. Dr. Fridén is Professor of Hand
Surgery, Department of Hand Surgery,
Göteborg University, Göteborg, Sweden.
Reprint requests: Dr. Lieber, University of
California San Diego School of Medicine, 3350
La Jolla Village Drive, San Diego, CA 92161.
Copyright 2002 by the American Academy of
Orthopaedic Surgeons.
Muscle pain after unaccustomed exercise is believed to result from repeti-
tive active lengthening of skeletal muscle. This “eccentric exercise” initi-
ates a sequence of events that includes muscle cytoskeletal breakdown,
inflammation, and remodeling such that subsequent exercise sessions result
in less injury and soreness. Recent studies of eccentric exercise using well-
defined animal models have identified the mechanical and cellular events
associated with the injury-repair process. In addition, neurophysiologic
studies have elucidated mechanisms of pain that operate in skeletal muscle.
Taken together, these studies improve our understanding of the muscle
injury process and will lead to rational therapeutic interventions to facili-
tate recovery.
J Am Acad Orthop Surg 2002;10:67-73
Morphologic and Mechanical Basis of
Delayed-Onset Muscle Soreness
Richard L. Lieber, PhD, and Jan Fridén, MD, PhD
rounding the muscle cell. Increased
CK levels resolve in 7 to 14 days. In
a similar delayed fashion, muscle
pain accompanying eccentric exer-
cise peaks 24 to 48 hours after the
exercise session but resolves more
rapidly compared with CK levels.
Interestingly, peak CK levels are not
strongly correlated with either the
timing of increased muscle pain or
the magnitude of tissue injury.
Another widely agreed-on find-
ing is that training prevents or at
least attenuates the magnitude of
muscle injury that occurs after
eccentric exercise (Fig. 1, solid cir-
cles). This training effect is pro-
duced only after eccentric training
of the specific muscle group being
tested. In other words, there is a
very high degree of specificity
regarding the protective effect of
exercise. General increased aerobic
fitness neither prevents nor attenu-
ates eccentric contraction-induced
muscle injury.
Skeletal Muscle Injury
Injury to muscle fibers can occur as
a result of direct trauma, disease, ap-
plication of myotoxic agents (such as
local anesthetics), inflammatory
processes, or intense exercise. The
association between the type of in-
jury and the nature of the pain that
accompanies it has been studied
using a number of experimental
models. Results from these studies
clarify the various mechanisms of
muscle fiber injury and factors that
influence the type and duration of
pain associated with it. The model
most commonly used to study
DOMS is the eccentric contraction
Muscle Injury Resulting From
Eccentric Contractions
Among the variety of types of
muscle action are the eccentric, con-
centric, and isometric. During an
eccentric action, an activated muscle
is forced to elongate while produc-
ing tension. Its counterpart, concen-
tric action, produces tension during
muscle shortening. The intermedi-
ate, isometric contraction produces
tension while the muscle remains
essentially at a constant length. All
three actions are common compo-
nents of daily movement. The ten-
sion generated during eccentric
action is higher than that for either
of the other actions. Asmussen6es-
tablished that DOMS was primarily
associated with the eccentric com-
ponent of exercise. A muscle injury
model utilizing eccentric contrac-
tion, in which the muscle is actively
generating force during the length-
ening maneuver, has been imple-
mented in animals as well as hu-
Based on experimental studies of
skeletal muscles directly subjected
to eccentric exercise, investigators
believe that the very early events
causing muscle injury are mechani-
cal in nature.7,8 For example, during
cyclic eccentric exercise of the rabbit
tibialis anterior, significant mechan-
ical changes were observed in the
first 5 to 7 minutes of exercise. After
this period, histologic examination
revealed that a small fraction of
muscle fibers appeared to be larger,
more rounded, and more lightly
stained compared with surrounding
normal muscle fibers. Interestingly,
recent immunohistochemical stud-
ies have revealed structural disrup-
tion of the cytoskeleton within the
fibers at these very earlier time peri-
ods9that may provide further in-
sights into the damage mechanism.
Such pathologic changes also can be
seen following either sprint or dis-
tance running in humans and after
resistance training.10,11
Fiber Type-Specific Damage
Both animal and human studies
have provided evidence for selec-
tive damage of fast fiber types after
eccentric exercise.12,13 In human
studies, this damage was confined
Delayed-Onset Muscle Soreness
Journal of the American Academy of Orthopaedic Surgeons
Hours Days
Serum CK (IU/ml, Log Scale)
0 3.75 1235 7911
Figure 1 Time course of serum CK levels after a session of eccentric exercise in untrained
and trained young men. Note that the delayed and prolonged increase in CK levels in
untrained individuals is attenuated after training. (Reproduced with permission from
Lieber RL [ed]: Skeletal Muscle Structure and Function: Implications for Rehabilitation and
Sports Medicine. Baltimore, Md: Williams & Wilkins, 1992.)
to the type 2 muscle fibers in gener-
al (Table 1), but in animal studies,
damage has been further localized
to the type FG (often equated to
type 2B) fast fiber subtype. In one
study,12 231 “enlarged” rabbit tib-
ialis anterior fibers were observed
from six different muscles; all were
of the FG fiber type. Their average
size was about four times the nor-
mal muscle fiber area. For some
fibers observed in serial section, the
area and shape of the fiber changed
dramatically from one section to the
next12 (Fig. 2). Because FG fibers
are the most highly fatigable muscle
fibers, it has been speculated that
the high degree of fatigability of
these fibers may predispose them to
injury, but this has not been sup-
ported in detailed animal studies.14
At the ultrastructural level, the
most commonly reported morpho-
logic abnormality is the loss of the
regular orientation of Z bands with
the fibers. The most subtle form of
injury is the slight “wavy” appear-
ance of the Z band, while more
severe injury is manifest by com-
plete Z band or A band disruption
(Fig. 3). Despite the numerous re-
ports of this phenomenon, a mecha-
nistic explanation for selective Z
band damage is not available.
Inflammation After
Muscle Injury
Direct evidence of inflammatory
cells within skeletal muscle after ec-
centric exercise has been reported in
both animals and humans.5,15 The
early mechanical events are fol-
lowed by infiltration of circulating
monocytes that become macro-
phages after entering the tissue (Fig.
4). In a study of the rabbit tibialis
anterior,12 the time course of torque
generation in rabbit dorsiflexors
was measured after a single eccen-
tric exercise session; there was a mea-
surable progressive decline in force
that was delayed and occurred over
a 2- to 3-day period. The mecha-
nism for the progressive decline in
force was hypothesized by the au-
thors to be the infiltration of inflam-
matory cells and associated proteo-
lytic degradation of muscle tissue.
In this model, the progressive force
decline was about the same order of
magnitude as the force decline that
occurred as a result of the mechani-
cal injury itself. Cellular infiltration
was uniquely associated with the
eccentric exercise itself in that iso-
metrically exercised muscles were
devoid of infiltrating cells, and the
same force decrement was not ob-
served after isometric exercise of the
same duration. A similar scenario
has been proposed in human exer-
cise studies.16
Because the inflammatory pro-
cess itself can cause damage in ex-
cess of that caused by the exercise, it
is possible that prevention of in-
flammation would improve muscle
status following injury. Based on
this assumption, nonsteroidal anti-
inflammatory drugs (NSAIDs) are
commonly prescribed to provide
analgesia and to improve perfor-
mance. The specific objective effects
of the NSAIDs on muscle function
are, however, poorly understood,
and it is difficult to test muscle func-
tion in humans because the anal-
gesic effect of NSAIDs may itself
permit improved performance by
lessening or eliminating pain. The
anti-inflammatory medication flur-
biprofen was tested in the rabbit
muscle injury model described
above. Muscles were exercised with
a single eccentric exercise session,
after which the anti-inflammatory
medication was given for 7 days.17
Muscle contractile properties were
measured for the 28 days following
the exercise; interestingly, muscles
treated with the NSAID demon-
strated a significant short-term
improvement in contractile function
Richard L. Lieber, PhD, and Jan Fridén, MD, PhD
Vol 10, No 1, January/February 2002 69
Table 1
Characteristics of Human Skeletal Muscle Fiber Types
Type I Type IIA Type IIB
Other names Red, slow twitch (ST) White, fast twitch (FT)
Slow oxidative (SO) Fast oxidative glycolytic (FOG) Fast glycolytic (FG)
Speed of contraction Slow Fast Fast
Fatigability Fatigue-resistant Moderately fatigue-resistant Most fatigable
Aerobic capacity High Medium Low
Anaerobic capacity Low High High
Motor unit size Small Medium Large
Capillary density High Medium Low
(Adapted with permission from Garrett WE, Jr, Best TM: “Anatomy, Physiology, and Mechanics of Skeletal Muscle,” in Buckwalter JA,
Einhorn TA, Simon SR [eds]: Orthopaedic Basic Science: Biology and Biomechanics of the Musculoskeletal System, ed 2. American Academy of
Orthopaedic Surgeons, Rosemont, Ill: 2000, p. 692.)
but a subsequent loss in function
(Fig. 5). These data may have sig-
nificant implications for the use of
NSAIDs in pain treatment associated
with neuromuscular injury.
Skeletal Muscle Pain
Numerous studies have documented
the existence of pain after blunt trau-
ma, eccentric exercise, injection of
noxious agents, and peripheral nerve
disease in skeletal muscles. It is
clear, however, that muscle fiber
damage does not necessarily cause
pain. This statement is based on the
observation that muscle biopsies ob-
tained from patients with primary
muscle diseases such as Duchenne
muscular dystrophy reveal major
disruptions of the myofibrillar and
sarcotubular apparatus, yet the pa-
tients themselves remain pain free.
Thus, pain within muscle that occurs
after fiber injury probably results
from secondary events that occur
after the damage itself. Based on this
evidence and extrapolation of experi-
mental data obtained from muscles,
tendons, and joints, muscle pain is
thought to result from stimulation of
nociceptors within the muscle itself.
Skeletal Muscle Innervation
Muscles are supplied by a rich
and extensive network of receptors
that are innervated by small myelin-
ated (group III) and unmyelinated
(group IV) afferent nerve fibers.
These fibers conduct much more
slowly (Table 2) than do either the
α-motoneurons that project to the
muscle fibers (i.e., extrafusal muscle
fibers), the γ-motoneurons that pro-
ject to the muscle spindles (intra-
fusal muscle fibers), or even the Ia
afferents that feed back from muscle
spindles to the spinal cord.
Nociception in Skeletal Muscle
Although the bulk of the data on
the neurophysiology of pain has
been obtained from studies of cuta-
neous receptors, studies of muscle
and visceral pain are much more
clinically relevant. The extensive
studies by Mense et al18-20 provide a
wealth of understanding regarding
these nociceptive mechanisms in
muscle and viscera. They delineated
several important differences be-
tween muscle and visceral pain
compared with cutaneous pain.
First, cutaneous pain is localized
with great accuracy, and muscle
pain is difficult to localize. Second,
Delayed-Onset Muscle Soreness
Journal of the American Academy of Orthopaedic Surgeons
Figure 3 Longitudinal electron micrographs of rabbit tibialis anterior muscle after 30 min of
eccentric contractions. A, Sample from normal muscle showing clean alignment of myofi-
brils across the field. B, Sample from muscle showing smearing of the Z band material
(small arrowheads) and extension of the Z bands into adjacent A bands (circled regions).
Figure 2 Cross-sectional light micrographs of rabbit tibialis anterior muscle under different
staining conditions. Enlarged fiber, shown with arrows, is of the FG fiber type. A, Hema-
toxylin-eosin. B, Myofibrillar adenosine triphosphate following preincubation at pH = 9.4.
C, Succinate dehydrogenase. D, α-Glycerophosphate dehydrogenase.
2 µm
while increasing the activation inten-
sity of cutaneous receptors does not
change the size of the receptive field,
increasing muscular pain intensity
results in referral to remote sites such
as other muscles, fascia, tendons,
joints, or ligaments. Third, muscle
pain is associated with symptoms
mediated through the autonomic
nervous system, such as decreased
blood pressure, nausea, and sweat-
ing, whereas cutaneous pain is not.
In contrast to results produced
from analogous studies of the skin,
repetitive electrical stimulation of
muscle afferents results only in
painful sensations. Increasing the in-
tensity does not modify the subjec-
tive nature of the pain and serves
only to elicit the description of a
“cramp” as well as a decreased ability
to localize the site of pain source.21
Additionally, the magnitude of re-
ferred pain is positively correlated to
the stimulation frequency of deep
nociceptive fibers.
Factors That Modulate
Nociception in Skeletal Muscle
The type III and IV nociceptors in
skeletal muscle have been studied
extensively in the cat hindlimb prep-
aration.18,19 The percentages of
motor and sensory nerves innervat-
ing the lateral gastrocnemius-soleus
muscles have been shown to be ap-
proximately 60% and 40%, respec-
tively. Of the sensory nerves, about
40% of them can be classified as
nociceptive, suggesting an overall
high sensibility within these mus-
cles (15% to 20% of the innervating
Experimental demonstration of
factors affecting nociception is ob-
tained by using single nociceptive
afferents from anesthetized cats
and experimentally perturbing the
system. For example, Mense and
Meyer18 measured the discharge
activity of these group III afferents
and saw almost no activity on light
touch with a painter’s brush (Fig. 6),
some activity on moderate touch,
and high activity with noxious touch
(pinching the muscle with forceps).
No activity was observed on pas-
sive stretch of the muscle within
the physiologic range (6 mm in this
case), but when the muscle was
stretched 9 or 12 mm, a moderate
level of activity was recorded. This
makes teleologic sense because
nociceptors are designed not only
Richard L. Lieber, PhD, and Jan Fridén, MD, PhD
Vol 10, No 1, January/February 2002 71
Figure 4 A, Cross-section of muscle fibers showing enlarged fiber (3) and two normal
fibers (1 and 2), and muscle spindle (ms). B, Longitudinal section of muscle along plane
shown in panel A(white dotted line) revealing the inflammatory process that leads to the
enlarged fiber type (3) and size variation observed (compare with Fig. 2). Enlarged fibers
thus represent “supercontracted” cells being digested by inflammatory cells close by.
(Reproduced with permission from Fridén J, Lieber RL: Segmental muscle fiber lesions
after repetitive eccentric contractions. Cell Tissue Res 1998;293:165-171.)
Day 3 Day 7 Day 28
Days after Exercise
TA Maximum Tension (g)
Figure 5 Maximum tetanic tension of tibialis anterior (TA) muscles from flurbiprofen-
treated versus untreated animals. The flurbiprofen-treated animals generated higher mus-
cle forces early in the treatment and lower muscle forces later in the treatment. (Adapted
with permission.17)
25 µm
to signal tissue damage but also to
prevent it.
Inflammatory Factors
Other factors that caused in-
creased output from nociceptors
were injection of factors presumed
to be involved in the inflammatory
response, such as bradykinin ([BK]
cleaved from precursor plasma pro-
teins), 5-hydroxytryptamine (re-
leased from platelets after vascular
damage), and prostaglandins ([PGs]
a byproduct of the cyclooxygenase
pathway). All receptors studied
showed clear signs of BK-induced
sensitization characterized by a low-
ered threshold to local pressure
stimulation. Because BK is known
to release PGE2from cells, it can
actually potentiate its own action.
This finding has led to the idea that
compounds that block the effect of
PG synthesis (e.g., acetylsalicylic
acid [ASA]) might reduce or abolish
the stimulatory action of BK. This
was, in fact, the case. There was a
complete lack of effect of BK within
15 minutes of injection of ASA,
demonstrating the peripheral effect
of ASA in that connections with the
central nervous system were cut in
this preparation.
Ischemia for prolonged periods
(up to about 15 minutes) is not
painful and does not evoke sympa-
thetic reflexes. However, if a muscle
contracts under ischemic conditions,
pain rapidly develops. Most likely
BK is involved in this response be-
cause kinin is released from plasma
proteins during ischemia. Mense
and Stahnke19 demonstrated activa-
tion of group IV muscle receptors
during ischemic contractions. Mus-
cle contraction alone did not elicit
the response, but afferent activity in-
creased fourfold when the same con-
traction was performed while oc-
cluding the nutrient artery.
Reflex-Mediated Pain
Reports in some of the older clin-
ical literature suggest that increased
activity or excitability of the γ-motor
system causes the painful spasms
that sometimes appear in skeletal
muscle. Increased activity of the γ-
motor system would then lead to
increased discharge frequency in
muscle spindle afferent fibers that
would, in turn, lead to increased
activation of α-motoneurons. By
this mechanism, a vicious cycle
could result that would be strong
enough to lead to ischemic contrac-
tions and pain by any one of a num-
ber of the mechanisms described
above. Unfortunately, experimental
evidence supporting this concept is
lacking.20 The main finding of these
studies was that resting activity of
the γ-motoneurons was significantly
reduced by inflammation and that
the reflex excitability of the neurons
was likewise inhibited. These re-
sults demonstrated that nociceptive
muscle afferents actually inhibit
homonymous γ-motoneurons, which
may represent an advantage to the
muscle in that it could reduce po-
tentially damaging forces on it.
DOMS represents a time-varying
cascade of events that are uniquely
associated with eccentric training of
a skeletal muscle. Currently, there
is not an adequate explanation for
the relationship between muscle
damage observed and clinical symp-
toms of pain. Intramuscular pain,
similar to that observed after appli-
cation of inflammatory factors to
Delayed-Onset Muscle Soreness
Journal of the American Academy of Orthopaedic Surgeons
60 s
Thermosensitive unit (group IV)
Touch Mod.
36 9 12 2 46
Stretch (mm) Contraction (kP)
Force 500
Counts (2s)1
Impulses (2s)1
Figure 6 Recording from intramuscular type III afferents with pressure of different levels
(left portion of panel) and with stretch above and beyond the physiological range (6 mm in
this case). (Reproduced with permission.18)
Table 2
Properties of Afferent Fibers in Peripheral Nerve
Axon Average
Fiber Group Myelinated Diameter (µm) Conduction (m/s)
I Yes 15 90-100
II Yes 10 40-50
III Yes 5 20-30
IV No <1 1
muscle, is likely to account for some
of the DOMS observed. In addition,
it is possible that reflex-mediated
pain also contributes to DOMS. In
the future, investigators will estab-
lish objective human models for
DOMS and perform more sophisti-
cated neurophysiologic analysis and
noninvasive imaging of the neuro-
muscular system to define the mech-
anism and prevention of DOMS
after athletic endeavors.
Richard L. Lieber, PhD, and Jan Fridén, MD, PhD
Vol 10, No 1, January/February 2002 73
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... While the mechanisms underlying DOMS are incompletely understood, the most accepted purported causes involve reversible microscopic damage and associated inflammation of muscle fibers (7,9,(11)(12)(13). These micro-injuries lead to the recruitment of neutrophils and macrophages that release several inflammatory and growth factors. ...
Full-text available
Immediate exercise-induced pain (IEIP) and DOMS are two types of exercise-induced muscle pain and can act as barriers to exercise. The burning sensation of IEIP occurs during and immediately after intensive exercise, whereas the soreness of DOMS occurs later. Acid-sensing ion channels (ASICs) within muscle afferents are activated by H ⁺ and other chemicals and have been shown to play a role in various chronic muscle pain conditions. Here, we further defined the role of ASICs in IEIP, and also tested if ASIC3 is required for DOMS. After undergoing exhaustive treadmill exercise, exercise-induced muscle pain was assessed in wild-type (WT) and ASIC3 −/− mice at baseline via muscle withdrawal threshold (MWT), immediately, and 24 h after exercise. Locomotor movement, grip strength, and repeat exercise performance were tested at baseline and 24 h after exercise to evaluate DOMS. We found that ASIC3 −/− had similar baseline muscle pain, locomotor activity, grip strength, and exercise performance as WT mice. WT showed diminished MWT immediately after exercise indicating they developed IEIP, but ASIC3 −/− mice did not. At 24 h after baseline exercise, both ASIC3 −/− and WT had similarly lower MWT and grip strength, however, ASIC3 −/− displayed significantly lower locomotor activity and repeat exercise performance at 24 h time points compared to WT. In addition, ASIC3 −/− mice had higher muscle injury as measured by serum lactate dehydrogenase and creatine kinase levels at 24 h after exercise. These results show that ASIC3 is required for IEIP, but not DOMS, and in fact might play a protective role to prevent muscle injury associated with strenuous exercise.
... DOMS can cause muscle tissue damage, and make muscle fibers produce inflammatory reaction, thus increasing the content of inflammatory markers such as neutrophils and eosinophils [26,27]. Cytokines are mainly involved in immune response, immune cell differentiation, inflammatory response and tissue repair. ...
Background: Delayed-onset muscle soreness (DOMS), also known as tenderness of touch, refers to the pain caused by muscle mechanical stimulation, such as contraction and stretching. Chinese massage has been widely used in the treatment of sports fatigue and sports injury, but there is controversy in the efficacy. In this experiment, we established DOMS model in rats to observe the prevention and treatment effect of massage, to find the best time for intervention, and to provide scientific basis for the prevention and treatment of exercise fatigue. Methods: 130 male SD(sprague-dawley, SD) healthy rats were randomly divided into blank group, control group and massage group. Except for blank group, the other rats received DOMS model. Professionals applied kneading and twisting methods on both lower limbs of rats. The expression of IL-2, IL-6 and IL-8 in skeletal muscle of rats were determined by western blot, PCR and ELISA, and the content of serum creatine kinase was determined by ELISA. In addition, we measured the concentration of Ca2+, Ca2+-ATPase in mitochondria of skeletal muscle. The changes of skeletal muscle structure were observed by scanning electron microscopy. Results: After massage, the expression of IL-2, IL-6, IL-8 and CK decreased compared with control group (P < 0.01), the expression of IL-2, IL-6 and IL-8 in post massage group was lower than that in front massage group (P < 0.01), and the content of CK in front massage group was lower than that in post massage group(P < 0.01). The content of Ca2+ in front massage 24, 48 and 72h group was lower than that in post massage (P < 0.01), the concentration of Ca2+-ATPase in front massage 24h and 72h group was lower than that in post massage group (P < 0.05). Conclusion: Massage can prevent the injury of muscle and reduce the inflammatory reaction of muscle after exercise. It can also improve the activity of Ca2+-ATPase, enhance the transport of Ca2+ by mitochondria and protect the skeletal muscle.
... In such cases, we observe decreased efficiency, faster muscle fatigue, a decrease in the range of motion (ROM), and the appearance of pain in places where they are overloaded [4,5]. This phenomenon is exacerbated especially with eccentric exercises (ECC) [6], in which intense exercise may cause Delayed Onset Muscle Soreness (DOMS) [7]. ...
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Background: It has been demonstrated that pressotherapy used post-exercise (Po-E) can influence training performance, recovery, and physiological properties. This study examined the effectiveness of pressotherapy on the following parameters. Methods: The systematic review and meta-analysis were performed according to PRISMA guidelines. A literature search of MEDLINE, PubMed, EBSCO, Web of Science, SPORTDiscus, and ClinicalTrials has been completed up to March 2021. Inclusion criteria were: randomized control trials (RCTs) or cross-over studies, mean participant age between 18 and 65 years, ≥1 exercise mechanical pressotherapy intervention. The risk of bias was assessed by the Cochrane risk-of-bias tool for RCT (RoB 2.0). Results: 12 studies comprised of 322 participants were selected. The mean sample size was n = 25. Pressotherapy significantly reduced muscle soreness (Standard Mean Difference; SMD = -0.33; CI = -0.49, -0.18; p < 0.0001; I2 = 7%). Pressotherapy did not significantly affect jump height (SMD = -0.04; CI = -0.36, -0.29; p = 0.82). Pressotherapy did not significantly affect creatine kinase level 24-96 h after DOMS induction (SMD = 0.41; CI = -0.07, 0.89; p = 0.09; I2 = 63%). Conclusions: Only moderate benefits of using pressotherapy as a recovery intervention were observed (mostly for reduced muscle soreness), although, pressotherapy did not significantly influence exercise performance. Results differed between the type of exercise, study population, and applied treatment protocol. Pressotherapy should only be incorporated as an additional component of a more comprehensive recovery strategy. Study PROSPERO registration number-CRD42020189382.
... The mechanisms underlying the cause of DOMS are not fully understood; however, it is generally accepted that DOMS is associated with muscle and/or connective tissue damage and/or subsequent inflammatory responses [4] . The muscle microscopic injury is induced by a mechanical disruption to sarcomeres, swelling results from the movement of immune cells and fluid from the bloodstream into the interstitial spaces which are accompanied by inflammation and pain [5] . Following the muscle injury, enzymatic reactions, and inflammatory mediators such as thromboxanes, prostaglandins, and leukotrienes from the cyclooxygenase and lipoxygenase pathways increase which is associated with enhancing vascular permeability. ...
... In such cases, we observe decreased efficiency, faster muscle fatigue, a decrease in the range of motion (ROM), and the appearance of pain in places where they are overloaded [5] [6]. This phenomenon is exacerbated especially with eccentric exercises (ECC) [7], in which intense exercise may cause Delayed Onset Muscle Soreness (DOMS) [8]. ...
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Background: It has been demonstrated that pressotherapy used post-exercise (Po-E) can influence training performance, recovery, and physiological properties. This study examined the effec-tiveness of pressotherapy on these parameters. Methods: The systematic review and meta-analysis were performed according to PRISMA guidelines. A literature search of MEDLINE, PubMed, EBSCO, Web of Science, SPORTDiscus and ClinicalTrials has been done up to March 2021. Inclusion criteria were: randomized control trials (RCTs) or cross-over studies, mean participant age be-tween 18-65 yrs., ≥ 1 exercise mechanical pressotherapy intervention. The risk of bias was assessed by the Cochrane risk-of-bias tool for RCT (RoB 2.0). Results: 12 studies comprised of 322 partici-pants have been selected. The mean sample size was n = 25. Pressotherapy significantly reduce muscle soreness(Standard Mean Difference;SMD= -0.33; CI = -0.49, -0.18; p < 0.0001; I2 = 7%). Pres-sotherapy did not significantly affect jump height (SMD = -0.04; CI =-0.36, -0.29; p = 0.82). Presso-therapy did not significantly affect creatine kinase level 24-96h after DOMS induction (SMD = 0.41; CI = -0.07, 0.89; p = 0.09; I2 = 63%). Conclusions: Only moderate benefits of using pressotherapy as a recovery intervention have been observed. Results varied between the type of exercise and used protocol. Pressotherapy should only be applied as an additional component of a more compre-hensive recovery strategy. Study PROSPERO registration number- CRD42020189382.
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Background Branched-chain amino acid (BCAA) supplementation is one of the most popular strategies used by the general population and athletes to reduce muscle soreness and accelerate the recovery process of muscle damage biomarkers after an intense exercise or training session. Objectives This systematic review and meta-analysis investigated the effects of BCAA supplementation on muscle damage biomarkers and muscle soreness after exercise-induced muscle damage (EIMD). Methods The systematic literature search for randomized controlled trials was conducted using seven databases, up to September 13th, 2022. The eligibility criteria for selecting studies were as follows: studies performed on healthy active participants, using BCAA at least once, controlled with a placebo or control group, performing resistance or endurance exercises, and followed up at least once post-EIMD. The methodological quality of the studies was assessed using the “SIGN RCT checklist”. Random-effects meta-analyses were processed to compute the standardized mean difference (Hedges’ g). Meta-regression analyses were completed with daily and total dosage and supplementation as continuous moderator variables. Results Of the 18 studies included in this study, 13 were of high quality and five were of acceptable quality. Our results revealed BCAA supplementation elicits a significant effect on reducing creatine kinase (CK) levels immediately (g=-0.44; p = 0.006) and 72 h (g=-0.99; p = 0.002), but not 24 h, 48 h, and 96 h post-EIMD. Additionally, a significant effect on delayed onset of muscle soreness (DOMS) was identified at 24 h (g=-1.34; p < 0.001), 48 h (g=-1.75; p < 0.001), 72 h (g=-1.82; p < 0.001), and 96 h (g=-0.82; p = 0.008), but not immediately post-EIMD. No significant effect was found on lactate dehydrogenase (LDH) levels at any time point. Meta-regression indicated higher daily and total dosages of BCAA, and longer supplementation periods were related to the largest beneficial effects on CK (total dosage and supplementation period) at 48 h, and on DOMS at 24 h (only daily dosage). Conclusion The overall effects of BCAA supplementation could be considered useful for lowering CK and DOMS after EIMD, but not LDH. The longer supplementation period prior to the EIMD could be more effective for CK and DOMS reduction.
Background: Delayed-onset muscle soreness (DOMS) is common after unaccustomed exercises and can restrict performance if intense physical activities are performed while the muscle is still sore. This study aimed to evaluate the recovery process following exercise-induced DOMS over a seven-day period by evaluating sensory, functional, and electromyographic parameters. Methods: Twenty-four healthy males participated in four experimental sessions (Day-0, Day-2, Day-4, Day-7). Pain perception, pressure pain sensitivity, active range of motion, maximal isometric strength, and muscle activity of the hamstrings during the maximal isometric contraction were assessed bilaterally at each session. A single-leg deadlift eccentric exercise (5-sets of 20-reps) was performed at the end of Day-0 to induce DOMS in the dominant leg. Findings: At Day-2, the DOMS-side showed increased pain sensitivity and decreased active range of motion, strength and muscle activity compared to Day-0 (P < 0.015). Muscle activity on the DOMS-side reached similar values than at baseline on Day-4, whereas pain perception, pressure pain sensitivity, maximal isometric strength, and active range of motion had returned to the baseline state on Day-7. No changes over time were observed on the control-side, showing all variables an excellent reliability between values at Day-0 and Day-7 (Intraclass Correlation Coefficient > 0.90). Interpretation: Surface electromyographic values during a maximal isometric contraction recover faster than the other parameters. Given the heterogeneous path of altered variables towards DOMS recovery, trainers and clinicians should consider a multimodal assessment, including quantitative sensory and functional measures in addition to the subjective perception of recovery.
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Egzersize bağlı iskelet kası hipertrofisinin doğası, günümüzde hâlâ tartışmalı bir olgu olarak karşımıza çıkmaktadır. Kas hipertrofisi ölçüm yöntemleri ve kullanılan antrenman metotları gibi sürecin merkezinde yer alan çeşitli faktör ve limitasyonlar, geçmişte hipertrofik adaptasyon ve mekanizmaların doğru bir şekilde tanımlanmasına engel olmuştur. Spor biliminde yaşanan yenilik ve gelişmelerle birlikte çeşitli antrenman yöntemlerinin farklı ölçüm teknikleriyle karşılaştırıldığı uzun vadeli çalışmalar, önceki kaynaklarda yer alan hipertrofi tanımlamalarının doğruluğu konusunda şüphe uyandırmaktadır. Bu tanımlamalarla ilgili dikkat çeken en büyük eksiklik ise serial hipertrofi olgusuyla ilgilidir. Bu açıdan bu derleme, iskelet kası hipertrofisini etkileyen birçok faktörü inceleyerek bu faktörlerin serial hipertrofi üzerindeki etkilerini derlemeyi amaçlamaktadır. Bu derleme ile, hipertrofi tanımı ve hipertrofik adaptasyonlara literatür eşliğinde yeni ve güncel bir yaklaşım getirilmeye çalışılmıştır. Bu doğrultuda, 1969 ve 2020 yıları arasında yapılmış 62 çalışma ve kaynak taranmıştır. Sonuç olarak, tam hareket açıklığı, eksantrik antrenmanlar ve hızlı eksantrik antrenmanların, lif ve fasikül uzunluğundaki artışlar kapsamında daha fazla serial hipertrofiye neden olduğu, kısmi hareket açıklığı, konsantrik antrenmanlar ve yavaş eksantrik antrenmanların ise lif çapında daha fazla artışlar ortaya koyduğu vurgulanmıştır. Araştırmalar, direnç eğitimi dönemlerinde kas lifi hipertrofisi ile farklı morfolojik adaptasyonların ortaya çıkabileceğini göstermektedir.
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The effects of one 45-min bout of high-intensity eccentric exercise (250 W) were studied in four male runners and five untrained men. Plasma creatine kinase (CK) activity in these runners was higher (P less than 0.001) than in the untrained men before exercise and peaked at 207 IU/ml 1 day after exercise, whereas in untrained men the maximum was 2,143 IU/ml 5 days after exercise. Plasma interleukin-1 (IL-1) in the trained men was also higher (P less than 0.001) than in the untrained men before exercise but did not significantly increase after exercise. In the untrained men, IL-1 was significantly elevated 3 h after exercise (P less than 0.001). In the untrained group only, 24-h urines were collected before and after exercise while the men consumed a meat-free diet. Urinary 3-methylhistidine/creatinine in the untrained group rose significantly from 127 mumol/g before exercise to 180 mumol/g 10 days after exercise. The results suggest that in untrained men eccentric exercise leads to a metabolic response indicative of delayed muscle damage. Regularly performed long distance running was associated with chronically elevated plasma IL-1 levels and serum CK activities without acute increases after an eccentric exercise bout.
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Elevated serum creatine kinase MB isoenzyme (CK-MB) activity in marathon runners after competition may arise from injury to skeletal muscle, myocardium, or a combined tissue source. Normal radionuclide myocardial scintigraphy and the selective increase in skeletal muscle CK-MB reported in such runners strongly suggest a peripheral source. To understand this biochemical finding, the authors examined gastrocnemius muscles by electron microscopy from 40 male marathon runners at intervals after competition and from 12 male nonrunners. Muscle from runners showed post-race ultrastructural changes of focal fiber injury and repair: intra- and extracellular edema with endothelial injury; myofibrillar lysis, dilation and disruption of the T-tubule system, and focal mitochondrial degeneration without inflammatory infiltrate (1-3 days). The mitochondrial and myofibrillar damage showed progressive repair by 3-4 weeks. Late biopsies showed central nuclei and satellite cells characteristic of the regenerative response (8-12 weeks). Muscle from veteran runners showed intercellular collagen deposition suggestive of a fibrotic response to repetitive injury. Control tissue from nonrunners showed none of these findings. The sequential morphologic changes in runners suggest that the increase in skeletal muscle CK-MB is a marker of cellular regeneration.
W was found to produce low specific contact resistance (ρ c ∼8.0×10<sup>-5</sup> Ω cm<sup>2</sup>) ohmic contacts to n<sup>+</sup>‐GaN (n=1.5×10<sup>19</sup> cm<sup>-3</sup>) with limited reaction between the metal and semiconductor up to 1000 °C. The formation of the β–W 2 N and W–N interfacial phases were deemed responsible for the electrical integrity observed at these annealing temperatures. No Ga out‐diffusion was observed on the surface of thin (500 Å) W contacts even after 1000 °C, 1 min anneals. Thus, W appears to be a stable contact to n<sup>+</sup>‐GaN for high temperature applications. © 1996 American Institute of Physics.
The study was undertaken to test the widely held hypothesis that a painful lesion of the skeleto-motor system leads to an increase in the neuromuscular component of muscle tone by activating gamma-motoneurones in the affected region. In chloralose-anaesthetized cats, artificial myositis was induced in the lateral gastrocnemius-soleus (LGS) muscle and several hours later the impulse activity was recorded from single gamma-motoaxons supplying the medial gastrocnemius (MG) muscle. Under the conditions of the study, the majority of the fusimotor neurones had a resting activity and could be readily excited by natural stimuli. In contrast to the assumptions of the working hypothesis, the gamma-motoneurones in the myositis animals were not activated but showed a strong inhibition; both resting activity and excitability by electrical and natural stimuli were decreased. Additional recordings from fusimotor neurones of a flexor muscle (tibialis anterior, TA) demonstrated that in the preparation used, the behaviour of the flexor gamma-motoneurones was different from extensor ones in that the former usually had no resting activity and did not respond to natural stimuli. The only discernible effect of a myositis of the LGS muscle on the TA gamma-motoneurones was a decrease in their electrical reflex threshold. The results of the study do not support the assumption that a painful muscle lesion is followed by an activation of the gamma-loop that leads to an increase in muscle tone. Instead, the data may offer an explanation for the weakness and--in chronic cases--the reflex atrophy of lesioned muscles.
Several host defense responses and metabolic reactions that occur during infection have been observed after exercise. We hypothesized that these reactions, known as the "acute phase response," contribute to the breakdown and clearance of damaged tissue after exercise. This hypothesis was tested with 21 male volunteers representing two ranges of age (22-29 and 55-74 yr), who ran downhill on an inclined treadmill to accentuate damaging eccentric muscular contractions. The subject groups were further divided in a double-blind placebo-controlled protocol, which examined the influence of 48 days of dietary vitamin E supplementation before the exercise. All subjects were monitored for 12 days after exercise for changes in circulating leukocytes, superoxide release from neutrophils, lipid peroxidation, and efflux of the intramuscular enzyme creatine kinase (CK) into the circulation. Among those receiving placebo, the less than 30-yr-old subjects responded to exercise with a significantly greater neutrophilia and higher plasma CK concentrations than the greater than 55-yr-old subjects. Dietary supplementation with vitamin E tended to eliminate the differences between the two age groups, primarily by increasing the responses of the greater than 55-yr-old subjects. At the time of peak concentrations in the plasma, CK correlated significantly with superoxide release from neutrophils. The association of enzyme efflux with neutrophil mobilization and function supports the concept that neutrophils are involved in the delayed increase in muscle membrane permeability after damaging exercise.
Novel, unaccustomed exercise has been shown to result in temporary, repairable skeletal muscle damage. After exhaustive endurance exercise, muscle damage can be produced by metabolic disturbances associated with ischaemia. Extensive disruption of muscle fibres also occurs after relatively short term eccentric exercise where high mechanical forces are generated. Biopsies taken after repetitive eccentric muscle actions have revealed broadening, streaming and, at times, total disruption of Z-discs. Muscles that develop active tension eccentrically also become sore, lose inherent force-producing capability, and show a marked release of muscle proteins into the circulation. Because creatine kinase (CK) is found almost exclusively in muscle tissue, it is the most common plasma marker of muscle damage. Despite the universal use of CK as a marker, several factors with regard to efflux and clearance remain unexplained. Also the large intersubject variability in response to exercise complicates its interpretation. Damage progresses in the postexercise period before tissues are repaired. However, the mechanism to explain exercise-induced muscle damage and repair is not well defined. Among the factors that may influence the damage and repair processes are calcium, lysosomes, connective tissue, free radicals, energy sources, and cytoskeletal and myofibrillar proteins. Physical conditioning results in an adaptation such that all indicators of damage are reduced following repeated bouts of exercise. Recently, investigators have suggested that the prophylactic effect of training may be due to performance of a single initial exercise bout. Following a second bout of exercise performed 1 to 6 weeks after the first bout, there is a reduction in morphological alterations and performance decrements and a profoundly reduced elevation in plasma CK levels. Several hypotheses have been presented to explain the repeated bout or rapid training effect. Stress-susceptible fibres may be eliminated or susceptible areas within a fibre may undergo necrosis and then regenerate. These regenerated fibres, along with adaptations in the connective tissue, may provide greater resistance to further insult.
In chloralose-anaesthetized cats, the impulse activity of single afferent units conducting at less than 30 m s-1 and having receptive fields in the triceps surae muscle or the calcaneal tendon, was recorded from thin filaments of the dorsal roots L7 and S1. The receptive fields of the units were tested with a variety of graded natural stimuli (local pressure, stretch, contractions, temperature changes). In addition, the algesic agent bradykinin was injected into the receptive fields, but the sensitivity of the receptors to this substance was not used for classification purposes. Four types of receptors could be distinguished using the strongest response to innocuous natural stimulation as the criterion for characterizing a given ending: (a) nociceptors showing no response to innocuous forms of stimulation and requiring noxious (tissue-threatening) stimuli to be clearly activated; (b) low-threshold pressure-sensitive receptors responding to innocuous indentation of the tissue but being relatively insensitive to stretch and contractions; (c) contraction-sensitive receptors reaching high discharge frequencies during active contractions of moderate force and innocuous stretch, but being relatively insensitive to local pressure stimulation; (d) thermosensitive receptors responding strongly to small changes in temperature without reacting to innocuous mechanical stimulation. The possible involvement of the different receptor types in central nervous functions (nociception, mechanoreception, ergoreception, thermoregulation) is discussed.
The aim of the study was to find out to what extent muscle receptors with slowly conducting afferent fibres (group III and IV) are activated by muscular contractions of moderate force, and what kind of muscle afferents could mediate the pain of ischaemic exercise. In chloralose-anaesthetized cats, the impulse activity of single afferent units from the triceps surae muscle was recorded from dorsal root filaments during muscular contractions with intact blood supply and after occlusion of the muscle artery. Two types of responses were observed to contractions without muscular ischaemia. One was characterized by sudden onset and a graded response amplitude to contractions of increasing force. In most cases stretching the muscle was also an effective stimulus. Units showing this response behaviour were labelled c.s.m (contraction-sensitive with mechanical mechanism of activation). The other response type had a more delayed onset and often outlasted the exercise period; because of the unknown mechanism of activation, units of this kind were labelled c.s.x. The proportion of c.s.m receptors was significantly higher amongst group III than amongst group IV units. During ischaemic contractions of comparable force the c.s.m and c.s.x receptors exhibited an unchanged or a decreased response amplitude. Under these conditions another receptor type (N, for nociceptive) was activated which did not respond to contractions with intact blood supply. Vigorous activations during ischaemic work were only observed in group IV receptors. The majority of the 131 group III and IV units tested did not respond to contractions at all. These contraction-insensitive (c.i.) endings probably comprised different receptor populations (nociceptors, thermoreceptors, low-threshold mechanoreceptors). It is concluded that the various central nervous effects of muscular exercise without ischaemia which are known to be due to raised activity in thin muscle afferents (e.g. cardiopulmonary adjustments, spinal locomotor reflexes) are probably produced by the c.s.m and c.s.x types. The pain of ischaemic contractions is most likely mediated by the N receptors most of which possess non-myelinated afferent fibres.