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Repeated high-force eccentric exercise: Effects on muscle pain and damage


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Five women and three men (aged 24-43 yr) performed maximal eccentric contractions of the elbow flexors (for 20 min) on three occasions, spaced 2 wk apart. Muscle pain, strength and contractile properties, and plasma creatine kinase (CK) were studied before and after each exercise bout. Muscle tenderness was greatest after the first bout and thereafter progressively decreased. Very high plasma CK levels (1,500-11,000 IU/l) occurred after the first bout, but the second and third bouts did not significantly affect the plasma CK. After each bout the strength was reduced by approximately 50% and after 2 wk had only recovered to 80% of preexercise values. Each exercise bout produced a marked shift of the force-frequency curve to the right which took approximately 2 wk to recover. The recovery rate of both strength and force-frequency characteristics was faster after the second and third bouts. Since the adaptation occurred after the performance of maximal contractions it cannot have been a result of changes in motor unit recruitment. The observed training effect of repeated exercise was not a consequence of the muscle becoming either stronger or more resistant to fatigue.
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Repeated high-force eccentric exercise:
effects on muscle pain and damage
Medicine, University College London and Middlesex Hospital Medical School,
The Rayne Institute, London WClE 6JJ, United Kingdom; and Department
Exercise Science,
Massachusetts, Amherst, Massachusetts 01003
peated high-force eccentric exercise: effects on muscle pain and
damage. J. Appl. Physiol. 63(4): 1381-1386,1987.-Five women
and three men (aged 24-43 yr) performed maximal eccentric
contractions of the elbow flexors (for 2Q min) on three occa-
sions, spaced 2 wk apart. Muscle pain, strength and contractile
properties, and plasma creatine kinase (CK) were studied before
and after each exercise bout. Muscle tenderness was greatest
after the first bout and thereafter progressively decreased. Very
high plasma CK levels (1,500-11,000 W/l) occurred after the
first bout, but the second and third bouts did not significantly
affect the plasma CK. After each bout the strength was reduced
by -50% and after 2 wk had only recovered to 80% of preex-
ercise values. Each exercise bout produced a marked shift of
the force-frequency curve to the right which took approximately
2 wk to recover. The recovery rate of both strength and force-
frequency characteristics was faster after the second and third
bouts. Since the adaptation occurred after the performance of
maximal contractions it cannot have been a result of changes
in motor unit recruitment. The observed training effect of
repeated exercise was not a consequence of the muscle becom-
ing either stronger or more resistant to fatigue.
training; fatigue; elbow flexors; creatine kinase
have shown that exercise involving
high-force eccentric muscle contractions can produce
temporary muscle pain and damage. Evidence of damage
includes disruption of muscle fibers (8,
circulating levels of muscle proteins (3,9,18,19), muscle
uptake of radionuclides
(17, 20,
25), and changes in
voluntary strength and contractile properties in the im-
mediate postexercise period (5, 22).
One interesting feature is the rapidity with which the
pain and muscle damage are reduced or abolished by
repeated exercise (2-4, 7, 11, 13). In our previous work
release of creatine kinase (CK) and muscle tender-
ness were measured after one bout of exercise involving
contractions at 50% maximum force. When the exercise
was repeated 1 wk later both pain and
release were
much reduced. This training effect was found to last -6
wk, indicating a considerable and long-lasting adaptation
(11). There are a number of possible explanations for the
training which include the following.
There may be a change in the pattern of motor unit
recruitment. Previous studies have used submaximal
contractions that allow the possibility that training may
cause a change in the order of motor unit recruitment
such that either susceptible fibers are spared on the
second and subsequent occasions or more fibers are
recruited and the force-fiber ratio is reduced. This can
be investigated by using maximal contractions.
2) There may be some adaptation in the muscle fibers
such that they become more resistant to the fatiguing
and damaging effects of eccentric exercise. This might
be evident as a change in th’e strength and contractile
properties of the muscle.
3) It has been suggested that eccentric exercise pref-
erentially damages a population of fibers that are nearing
the end of the cycle of growth and replacement
this case, a decrement in force generation would occur
after the first exercise which would be absent on subse-
quent occasions.
The purpose of the present investigation was to test
these possibilities. To this end we have compared the
changes in strength and contractile properties with the
pain and plasma CK response after three bouts of max-
imal eccentric contractions of the elbow flexors spaced
at two weekly intervals.
Eight subjects (5 females and 3 males) rang-
ing in age from 24 to 43 yr took part in the study. They
were healthy and active but none was participating in
any training programs, and they had not participated in
studies involving eccentric contractions for at least 3 mo.
Their physical characteristics are shown in Table
were fully informed of the nature and risks of the pro-
cedures to be used. The study had the approval of the
Committee for the Ethics of Human Procedures at Uni-
versity College Hospital.
To exercise the elbow flexors the subject sat
in an adjustable chair with the upper arm supported on
a shelf, the height of which could be adjusted to bring
the upper arm to an angle of 90” with the body. An
inextensible cord passed from a wrist cuff to a pulley
attached to the wall in front of the subject and then to
the experimenter. The latter was able to forcibly extend
the elbow and overcome the maximal effort of the subject
by means of a winch with a mechanical advantage of
-1O:l. The signal from the strain gauge was amplified
and displayed on an ultraviolet recorder. Details of the
procedure have been given elsewhere (12).
0161-7567/87 $1.50 Copyright 0 1987 the American Physiological Society 1381
1. Physical characteristics
the subjects
Subj. No. Sex &e Ht, m W kg
1 M 43 1.76 71.9
2 M 41 1.68 73.4
3 F 37 1.67 68.4
4 F 35 1.76 65.3
5 M 39 1.64 69.9
6 F 24 1.56 47.7
7 F 26 1.60 48.3
8 F 40 1.58 49.6
The subjects performed one eccentric maximal volun-
tary contraction every
s for 20 min. Each contraction
lasted -2 s. The range of elbow movement was from full
flexion to full extension with care being taken not to
hyperextend the elbow. The exercise was repeated on
three occasions that were separated by an interval of 2
Force measurement. Isometric maximum voluntary
contraction (MVC) force was measured before and im-
mediately after each exercise period and repeated at daily
intervals thereafter. Three attempts were made on each
occasion, and the highest was taken as the maximal force.
When recording force from voluntary contractions of
painful muscles there is the possibility that the contrac-
tions are submaximal, even with well-motivated subjects.
To determine whether this was the case electrical stim-
ulation (at both
Hz) was superimposed on the
voluntary contractions. With this technique additional
force is generated by the electrical stimulation only if
the voluntary contractions are submaximal (23).
The force-frequency relationship was determined by
percutaneous electrical stimulation of the biceps at
(for 5 s) and
10, 20, 50,
10, and
Hz for 2 s each.
Damp electrodes (8, cm”) were bandaged onto the upper
arm, over the proximal and distal ends of the biceps.
Square-wave pulses of 50 pus and up to
V were used
(Digitimer dual high-voltage stimulator, Hertfordshire,
UK). The force at each frequency was expressed as a
percent of that generated by stimulation at 100 Hz (l/
lOO%, lO/lOO%,
etc.). Care was taken to ensure that at
least 25% of the elbow flexors were stimulated, compar-
ing the stimulated contractions with the MVC.
.For all the isometric measurements the wrist was tied
and the upper arm supported to prevent movement of
the arm in any direction. The shoulder was prevented
from forward movement by being clamped to the back of
the chair. In our experience daily testing in this way
neither causes muscle pain or damage nor does it modify
the response to eccentric exercise.
Plasma CK. Blood was collected from an antecubital
vein into heparinized tubes before and at daily intervals
after each exercise period. CK activity was determined
by the Department of Chemical Pathology, University
College Hospital, using a Boehringer Mannheim kit
method with N-acetylcysteine activation. The normal
range using this method is 60-190 IU/l.
Muscle tenderness. This was measured daily after the
exercise by recording the force required to elicit tender-
ness at fixed sites on the skin over the biceps and
brachioradialis (22). Twelve test sites were spaced -2 cm
apart over the muscle surface and marked with indelible
ink. At each site a gradually increasing force was applied
through a flat plastic disc of 2 cm diam attached to a
force transducer with digital readout (Penny & Giles
Transducers, Christchurch, Dorset, UK). The subject
was asked to indicate when the sensation of pressure
changed to discomfort, and the force at that point was
recorded. Tenderness was recorded as absent if not re-
ported before 30 N. The value of the force (N) has been
subtracted from 30 to give a tenderness score.
Statistics. Data were analyzed using repeated-measures
analysis of variance. Statistical significance was set at P
c 0.05.
A4aximal voluntary force. Superimposition of electrical
stimulation on the voluntary contractions demonstrated
that all subjects were able to fully activate their muscles
during the isometric contractions despite any discomfort.
The values for MVC, expressed as a percent of the
initial preexercise force, are presented in Fig.
was a large decrease in voluntary force (-50%) immedi-
ately after the three exercise periods. There was no
significant difference between the extent of force loss
after the three bouts. Recovery was slow and there were
differences between the rate of recovery from the first
compared with that from the second and third occasions.
After the first exercise force had hardly improved after
24 h (49% initial), whereas after exercise bouts 2 and 3
there was recovery to 66 and 69%, respectively. The
values for bouts 2 and 3 at this time differed significantly
from bout 1 but not from each other. After the first bout
of exercise the MVC remained significantly lower than
the initial force until
wk after the third and final
exercise. There was no evidence of an increase in strength
as a result of the exercise in any of the subjects.
ContractiZe properties. After exercise there was a sig-
nificant decrease in force generation at low frequencies
of stimulation. A representative index of this is the force
generated by 20 Hz stimulation expressed as a percent
of that at 100 Hz (20/100%). These values are presented
in Fig. 2. A large decrease in the 2O/lOO% value to -40%
was seen immediately after each exercise bout, there
being no significant difference between the decrement
seen on the three occasions. As with the MVC measure-
ments (Fig. 1) there was a faster recovery after the second
and third exercise bouts compared with the first. The
2O/lOO% value was significantly less than the initial
value until the 9th day after the first exercise but was
not significantly different from preexercise values by the
4th and 3rd days after the second and third bouts of
Plasma CK. Although there was a large intersubject
variation in the CK response, all showed a substantial
increase after bout 1, the peak values ranging from 1,570
to 10,904 IU/l, which was much greater than the response
seen after bouts 2 and 3 (Fig. 3 and Table 2). The plasma
CK only showed a significant increase after the first
MuscZe tenderness. Muscle tenderness values are pre-
sented in Fig. 4. A significant difference in tenderness
was found among the three bouts, with each resulting in
80 [ -
.- + 60-
.- w
- 2 40 L
20 -
Mean & sem
1 I 1 1 1 I
2 3 4 5 6 7
Time (weeks)
FIG. 1. Maximal isometric strength during training period. Exercise was performed in lst, 3rd, and 5th wk. MVC,
maximum voluntary contraction.
Mean & sem
n -8
Time keks)
progressively less tenderness. The peak pain, which oc-
curred on day 2 after the first exercise and day 1 after
the second and third occasions, was significantly less on
the second compared with the first occasion and less
again on the third compared with the second occasion.
The sums of the pain scores over the 4 days after exercise
were reduced, being 43 and 35% of the initial response
after the second and third bouts, respectively.
There were no obvious relationships among the vari-
ables measured such as the extent of force loss and
subsequent pain or increase in plasma CK. Changes in
force and contractile properties were similar in all the
subjects (Figs. 1 and Z), but there was considerable
variation in the pain and release of CK. There was no
obvious relationship between the extent of the response
and parameters such as age, sex, or general level of
physical fitness of the subjects (Tables 1 and 3).
FIG. 2. Force-frequency relationship
during training period. Exercise was per-
formed in lst, 3rd, and 5th wk.
5 6
The training effects of repeated high-force, eccentric
exercise were very obvious both from subjective reports
and objective measurements of pain and muscle damage.
Muscle pain and stiffness were much reduced after the
second and third bouts of exercise compared with the
The most striking training response was seen in the
CK efflux. The enzyme release after the first exercise
was similar in magnitude and time course to those that
we have previously reported (14, 18, 19), being both very
large and characteristically delayed for several days after
eccentric exercise. Despite variation between individuals
in the extent of the release, the plasma levels were always
greatest, by up to two orders of magnitude, after the first
bout of exercise. Although the mechanism of the exercise-
mean & sem
3. Plasma creatine kinase (CK)
during training period. Note marked
training effect seen here in comparison
with force measurements. Exercise was
performed in lst, 3rd, and 5th wk.
Time hueeks)
2. Range of plasma CK values before and after the three exercise bouts
Exercise Postexercise, days
Bout Preexercise 1 2 3 4 5 6 7 8
57-250 8%1,133 81-3,074 177-7,978 735-10,904 1,854-6,074 1,402-4,535 709-3,313 365-2,222
2 90-208 97-328 64-327 49-250 52-237 65-175
3 36-185 36-230 31-137 31-167
CK, creatine kinase, in IU/l.
Mean & sem
n= 8
4. Muscle tenderness during
training period. Pain progressively de-
creased after each exercise bout. Exer-
cise was performed in lst, 3rd, and 5th
1 2 3 4 5 6
nrne (weeks)
induced enzyme efflux is unknown, it is generally as-
sumed to reflect some form of membrane damage.
Suprisingly, in view of the major changes in pain and
enzyme release, the training had no effect on the maxi-
mum isometric strength, the extent of force loss after
the exercise, or the changes in contractile properties of
the muscles. Other workers have reported similar reduc-
tions in the MVC immediately after a single bout of
submaximal eccentric contractions (5,
and it has
often been assumed that the apparent force loss was
largely due to the pain preventing subjects from fully
activating their muscles (7, 15,
In the present study
the strength measurements were shown to be from fully
activated muscles, and thus the force loss was the result
of changes in the contractile elements.
Although both the pain and CK release responded to
training, it is unlikely that these were causally related.
Whereas the CK response was virtually eliminated after
the first bout of exercise, the discomfort was only reduced
in a stepwise manner. Furthermore, the CK release and
pain are always separated in time (see Figs. 3 and
are often dissociated in magnitude. Thus one individual
3. Relationship between muscle strength, fatigue,
damage, and pain after eccentric contractions
Subj. No. 20/100%, Peak CK, Peak Tenderness
n % initial % initial IU/l Score
1 310 47.8 53.7 5,586 12.6
2 263 43.9 72.9 1,854 9.0
3 186 57.8 75.2 6,074 14.0
4 167 51.4 71.6 5,464 10.2
5 152 56.3 52.0 9,426 17.9
6 129 57.1 58.9 1,570 15.0
7 115 55.9 56.5 10,904 10.6
8 103 60.7 74.6 2,494 14.9
Relationship between initial strength of subjects and changes in
force generation, plasma creatine kinase (CK), and muscle pain after
first bout of exercise. Force measurements are those before and im-
mediately after exercise period. MVC, maximum voluntary contraction;
ZO/lOO%, force generated by 20 Hz of stimulation expressed as percent
of that at 100 Hz (% initial).
might have considerable pain but little or no evidence of
muscle membrane damage.
There is evidence that the pain and stiffness experi-
enced after eccentric contractions are a consequence of
shortening of the noncontractile material that is ar-
ranged in parallel with the contractile material (10, 13).
This may be a response to some form of damage to the
connective tissue, and if so the training could have caused
some adaptation of this tissue.
We have previously studied the training effect using
eccentric contractions at 50% maximum (11) and found
results similar to those reported here. With submaximal
contractions it was possible that changes might have
occurred in the recruitment pattern so that, after train-
ing, less susceptible motor units were used. Alternatively,
more motor units could be recruited, thereby reducing
the force per fiber. The results of the present study, using
maximum contractions, show that neither of these pos-
sibilities can be the entire explanation since maximal
contractions require the activation of all motor units so
there is no possibility of change in the extent or order of
The training program did not increase the voluntary
strength of the muscle, nor did it prevent the loss of force
or change in contractile properties (shown by the 20/
100% value, Fig. 2) that occurred to a similar extent after
each bout of exercise. This demonstrates that the adap-
tation did not involve any change in the strength or
contractile properties of the muscle or its ability to
withstand fatigue.
The present results provide some evidence in favor of
the possibility, suggested by Armstrong (l), that the first
bout of exercise causes damage and destruction to a
population of susceptible fibers, possibly those near the
end of their life cycle. There was a notable difference in
the time course of recovery of force generation after the
first exercise bout compared with the second and third,
being slower after the first bout (Figs. 1 and 5). This
difference in rate of recovery was also evident with the
20/100% value (Fig. 2). The slow recovery of force and
contractile properties was associated with the release of
CK from the muscle. It is possible that the loss of force
and release of soluble constituents represent the removal
1 a 1 1 a 1 1 4
0 1 2 3 4 5 6 7
Days after exercise
FIG. 5. Changes in maximum voluntary contraction (MVC) force
(means -+ SE) after first (squares) and second (diamonds) exercise
bouts. Values after second exercise bout were significantly greater than
after first at all times shown with exception of those on day 4.
and replacement of irreparably damaged fibers that may
have been particularly susceptible to damage, possibly
being near the end of the natural cycle of cell turnover.
This could equally well apply to either the entire fiber or
a part of it. After the initial damage they may fail to
repair and subsequently undergo degeneration, recover-
ing slowly and releasing soluble enzymes in the process.
The more resilient fibers, or parts of fibers, remain and
these are able to withstand the effects of eccentric exer-
cise without undergoing a process of degeneration and
enzyme release.
This seems to be the first report in which the time
course of the recovery of both strength and contractile
properties has been followed for more than a few days.
The MVC was very slow to recover, only returning to
-80% of the initial value in 2 wk. Interestingly, the
subjects were aware of impaired muscle function only
after the first exercise bout in which most pain was
experienced. They therefore felt that the training had
improved their performance, yet objective testing showed
appreciable and long-lasting weakness.
This study does not identify the mechanism by which
the pain and damage are reduced by training. However,
it does suggest that the prevention of enzyme release
with training may be due to the removal of contractile
material that is particularly sensitive to damage.
Received 19 December 1986; accepted in final form 1 May 1987.
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... metabolic fatigue) can be up to 30-60% in both human and rodent skeletal muscle immediately after a bout of maximal, unaccustomed ECC (4,6,12,36,53,54). Although rodent studies report a RBE in immediate strength loss when muscle is stimulated at supraphysiological frequencies, little to no adaption occurs at physiological stimulation frequencies in rodent muscle (36) or during human MVCs (12,19,48,51,53,55). For instance, many anesthetized mouse model studies stimulate the muscle up to 300 Hz (5,36,42); however, firing rates during conscious locomotion in rat and mouse motor units have been reported to average less than 125 Hz (27,29). ...
... Greater reductions in low-frequency isometric torque compared with highfrequency isometric torque have traditionally been used as an indicator of excitation-contraction uncoupling (25,36,37). Several studies using indirect methods report that excitation-contraction uncoupling plays a significant role in immediate strength loss over repeated injuries in both human and rodent skeletal muscle (28,36,48). We suggest that the persistent loss in muscle strength associated with the performance of ECC reflects an intrinsic muscle protective mechanism. ...
... Despite not being directly measured, it seems that excitationcontraction uncoupling persists with repeated bouts of ECC (28,36,48). Thus, the ability of the muscle to recover excitationcontraction coupling and thereafter strength becomes critical for sustained training and performance improvement. ...
Full-text available
Lindsay, A, Abbott, G, Ingalls, CP, and Baumann, CW. Muscle strength does not adapt from a second to third bout of eccentric contractions: A systematic review and meta-analysis of the repeated bout effect. J Strength Cond Res 35(2): 576-584, 2021-The greatest muscle strength adaptations to repeated bouts of eccentric contractions (ECC) occur after the initial injury, with little to no change in subsequent bouts. However, because of the disparity in injury models, it is unknown whether three or more bouts provide further adaptation. Therefore, we performed a systematic review of the literature to evaluate whether a third bout of skeletal muscle ECC impacts immediate strength loss and rate of strength recovery compared with a second bout. A search of the literature in Web of Science, SCOPUS, Medline, and the American College of Sports Medicine database was conducted between May and September 2019 using the keywords eccentric contraction or lengthening contraction and muscle and repeated or multiple, and bout. Eleven studies with 12 experimental groups, using 72 human subjects, 48 mice, and 11 rabbits, met the inclusion criteria. A meta-analysis using a random effects model and effect sizes (ESs; Hedges' g) calculated from the standardized mean differences was completed. Calculated ESs for immediate strength loss provided no evidence that a third bout of ECC results in greater loss of strength compared with a second bout (ES = -0.12, 95% confidence interval [CI] = -0.41 to 0.17). Furthermore, the rate of strength recovery was not different between a second and third bout (ES = -0.15, 95% CI = -1.01 to 0.70). These results indicate a third bout of skeletal muscle ECC does not improve indices of strength loss or rate of strength recovery compared with a second bout. Therefore, coaches and athletes should expect some level of persistent weakness after each of their initial training sessions involving ECC, and the faster recovery of strength deficits in the second bout documented by previous research is not different from a third bout.
... However, there is evidence to suggest that the prophylactic influence of training may be brought about by the performance of a single exercise bout . Furthermore, the work of Newham et al (1987) suggests that an episode of eccentric exercise may protect against some aspects of muscle damage resulting from repeated exercise, but not others. ...
... This focal necrosis does not result in the regeneration of new fibres per se, but the repair of damaged segments. Newham et al (1987) suggested that the protective mechanism of eccentric exercise is more likely to be associated with changes in the connective tissue of the parallel elastic elements. Thus, the effect of the initial bout of exercise might be to act as a stimulus for new collagen synthesis resulting in a strengthening of the connective tissue matrix of the parallel elastic component of muscle. ...
... ThusSchwane and Armstrong (1983) studying the effects of eccentric work on the vastus intermedius muscle of rats found that whereas 90 min of downhill running caused appreciable delayed-onset fibre necrosis, if the downhill run was preceded by a similar 30 min run 3 days earlier, then no damage ensued.Intriguingly, the 30 min run did not prove to be damaging to the muscle, which suggests that the protective effect of exercise need not depend on initial damage to muscle fibres. In an investigation into the effects of repeated bouts of eccentric exercise of the human elbow flexors,Newham et al (1987) reported that whilst both muscle soreness and CK release were protected after the first exercise bout, the maximal voluntary force and stimulated low/high frequency force ratio were equally affected by subsequent bouts of exercise. Newham et al's findings appear to contrast with the results of the present study which suggest an almost complete protection against force loss after exercise where the recovery period is not greater than 21 days after the first exercise bout. ...
This thesis examines the nature of fatigue and damage as it affects healthy and dystrophic skeletal muscle. Initial fatigue studies were carried out using isolated mouse muscles. After 3 min of repeated maximal stimulation, extensor digitorum longus muscle force was reduced to 26% of the fresh value but this could be reversed by the addition of caffeine to the incubation medium, suggesting that acute fatigue is primarily due to failure of the processes of activation. In the human tibialis anterior (TA) muscle it was found that fatigue resulting from stimulated isometric contractions were affected by muscle length. Exercise at short lengths resulted in less force loss at the resting length, whereas exercise at long muscle lengths caused a greater force loss than normal at the resting length. There was a preferential force loss at sub-maximal stimulation frequencies, and this was exacerbated when muscles were exercised in a lengthened positon. Similar changes were observed using isolated mouse soleus muscles. Because of uncertainties about the adequate diffusion of metabolites in isolated muscles the properties of dystrophin-deficient (mdx) mouse muscles were investigated using an in vivo preparation of the TA. The mdx TA was, on average, 30% stronger than that of control mice but had a reduced force/cross-sectional area and a smaller low/high frequency force ratio due to a faster activation time, mdx muscle also displayed a greater fatigue resistance when exercised at a low frequency, but this was not the case with stimulation at maximal frequency. In order to test whether the altered contractile properties of mdx muscle were due to the presence of degenerating and regenerating fibres, the contractile characteristics of normal muscle were investigated during damage and recovery. Damage was induced by stimulated lengthening 1 contractions of the foot dorsiflexor muscles of mice. Maximum force, force-frequency characteristics, and morphology were measured for up to 20 days after exercise. Although the properties of normal/damaged and mdx muscles displayed a number of superficial similarities, it is unlikely that the altered contractile characteristics of mdx muscles are due to the presence of damaged fibres. The possibility that dystrophin-deficient muscles are more susceptible to exercise induced muscle damage was examined by comparing the responses of mdx and muscles to an episode of eccentric work. The findings were unequivocal, normal and mdx TA muscles displayed similar degrees of force loss 3 days after exercise (55% and 52% respectively) and comparable rates of force recovery after 12 days (76% and 80% of control in normal and mdx muscles respectively). The protective effect afforded by a bout of eccentric exercise against subsequent muscle injury from a similar exercise was characterised. Re-exercising a muscle after 10 days recovery had little effect on the immediate consequences of exercise, but reduced the degree of delayed onset force loss and fibre necrosis. Animals re-exercised after 12 weeks recovery displayed no apparent protection against delayed onset muscle damage when the exercise was repeated. These findings me in general agreement with work carried out in humans, but the time course of recovery post exercise is at least three times faster in the mouse, which has made a study of the long-term effects of eccentric exercise more practical. Six weeks after exercise, increases in muscle mass and force were evident, with a proportion of fibres displaying internal nuclei and signs of fibre splitting. Surprisingly, greater forces and fibre hypertrophy also occurred after 12 weeks recovery from an episode of eccentric work.
... Acute onset muscle soreness occurs during exercise and may lastup to 4 to 6 hours before subsiding [1][2][3][4][5][6][7]. Delayed Onset Muscle Soreness (DOMS) has onset 8 to 24 hours postexercise, with soreness peaking 24 to 48 hours postexercise [8][9][10][11][12][13]. The etiology of DOMS has been the topic of numerous studies, from which several theories have evolved Despite differences in theories, the following factors have been documented: 1. Strenuous activity especially eccentric exercise causes injury or traumato the muscle, its musculotendinous junction, or both [8][9][10][11]14,15]. 2. Injury and/or trauma initiates an inflammatory response resulting in muscles feeling painful and swollen 3. Pain before the exercise, right after the exercise and at the 24 th , 48 th , 72 nd and 96 th hours. ...
... Delayed Onset Muscle Soreness (DOMS) has onset 8 to 24 hours postexercise, with soreness peaking 24 to 48 hours postexercise [8][9][10][11][12][13]. The etiology of DOMS has been the topic of numerous studies, from which several theories have evolved Despite differences in theories, the following factors have been documented: 1. Strenuous activity especially eccentric exercise causes injury or traumato the muscle, its musculotendinous junction, or both [8][9][10][11]14,15]. 2. Injury and/or trauma initiates an inflammatory response resulting in muscles feeling painful and swollen 3. Pain before the exercise, right after the exercise and at the 24 th , 48 th , 72 nd and 96 th hours. ...
... DOMS associated with a reduction of muscle strength production is a result of tissue damage, which is caused by high eccentric force production during eccentric actions [22]. Growing evidence from human studies shows that appropriate pre-training using eccentric exercise prevents muscle damage and soreness, also known as an acclimatization or adaptation eff ect [21,23,24]. ...
... Prostaglandins as well as histamine, kinins and others, sensitize nociceptors [24,27]. Macrophages are thought to begin synthesizing and releasing prostaglandins within 30 minutes of injury and to continue for a minimum of 24 hours [16]. ...
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Objective: The purpose of this study is to review mechanisms for Delayed Onset Muscle Soreness (DOMS) and the pharmacological treatment options with Non-Steroidal Anti-Inflammatory Drugs (NSAIDs). Method: Our review of published research literature was based on an appropriate number of subjects included in the study with a statistical power of .80 or higher and an effect size of .30 or higher. In the case of review articles, two cited references from each article where significant data were used to establish the conclusion were examined for type II error using the criteria mentioned above. Our review also includes inflammation, tissue damage, and the treatment of DOMS with both selective and non-selective NSAIDs. Results: Frequently cited mechanisms of DOMS are "mechanical strain" and "metabolic overload" within the muscle structure. The inflammation associated with DOMS is caused by eccentric exercise-induced muscle damage. NSAIDs inhibit prostaglandin synthesis and/or block cyclooxygenase and there by reduce the pain and swelling associated with inflammation. There are both selective and non-selective NSAIDs, the former being the COX-2 inhibitors (e.g., celecoxib) and the later (e.g., ibuprofen, naproxen, and aspirin). Conclusion: For the treatment of DOMS, naproxen taken at anti­inflammation levels for at least 3 days shows the most consistent results for improving the recovery rate of affected muscle.
... Green et al. [33] observed greater recovery of MVDC in the caffeine group, although the pain perception was not different between the caffeine and placebo groups. Therefore, it remains only speculative that pain may interfere with the ability to produce force and some evidence suggests that damaged muscles could be fully active regardless of the muscle pain existence [51,73]. ...
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The effect of caffeine on mitigating exercise-induced muscle damage (EIMD) is still poorly understood, but it was hypothesized that caffeine could contribute to decreasing delayed onset muscle soreness, attenuating temporary loss of strength, and reducing circulating levels of blood markers of muscle damage. However, evidence is not conclusive and beneficial effects of caffeine ingestion on EIMD are not always observed. Factors, such as the type of exercise that induces muscle damage, supplementation protocol, and type of marker analyzed contribute to the differences between the studies. To expand knowledge on the role of caffeine supplementation in EIMD, this systematic review aimed to investigate the effect of caffeine supplementation on different markers of muscle damage. Fourteen studies were included, evaluating the effect of caffeine on indirect muscle damage markers, including blood markers (nine studies), pain perception (six studies), and MVC maximal voluntary contraction force (four studies). It was observed in four studies that repeated administration of caffeine between 24 and 72 h after muscle damage can attenuate the perception of pain in magnitudes ranging from 3.9% to 26%. The use of a single dose of caffeine pre-exercise (five studies) or post-exercise (one study) did not alter the circulating blood levels of creatine kinase (CK). Caffeine supplementation appears to attenuate pain perception, but this does not appear to be related to an attenuation of EIMD, per se. Furthermore, the effect of caffeine supplementation after muscle damage on strength recovery remains inconclusive due to the low number of studies found (four studies) and controversial results for both dynamic and isometric strength tests.
... DOMS severity is decreased following a similar second eccentric exercise bout, the "repeat bout effect" [51][52][53], with the repeated bout (3 weeks later) vs first bout effect reducing blood oxidative stress in humans, indicated by a 1.8-fold increase in reduced glutathione (GSH) coupled with a 6.1-fold decrease in the lipid peroxidation byproduct, thiobarbituric acid reactive substances (TBARS) levels. These second bout effects may indicate tissue adaptations that lessen subsequent exercise-induced muscle damage [52], which may be reflective of first bout ROS-driven plasticity. ...
The mechanistic interactions among redox status of leukocytes, muscle, and exercise in pain regulation are still poorly understood and limits targeted treatment. Exercise benefits are numerous, including the treatment of chronic pain. However, unaccustomed exercise may be reported as undesirable as it may contribute to pain. The aim of the present review is to evaluate the relationship between oxidative metabolism and acute exercise-induced pain, and as to whether improved antioxidant capacity underpins the analgesic effects of regular exercise. Preclinical and clinical studies addressing relevant topics on mechanisms by which exercise modulates nociceptive activity and how redox status can outline pain and analgesia are discussed, in sense of translating into refined outcomes. Emerging evidence points to the role of oxidative stress-induced signaling in sensitizing nociceptor sensory neurons. In response to acute exercise, there is an increase in oxidative metabolism, and consequently, pain. Instead, regular exercise can modulate redox status in favor of antioxidant capacity and repair mechanisms, which have consequently increased resistance to oxidative stress, damage, and pain. Data indicate that acute sessions of unaccustomed prolonged and/or intense exercise increase oxidative metabolism and regulates exercise-induced pain in the post-exercise recovery period. Further, evidence demonstrates regular exercise improves antioxidant status, indicating its therapeutic utility for chronic pain disorders. An improved comprehension of the role of redox status in exercise can provide helpful insights into immune-muscle communication during pain modulatory effects of exercise and support new therapeutic efforts and rationale for the promotion of exercise.
... Using a more "relevant" aerobic task causing EIMD, Sherman and colleagues (1984) reported a ~ 50% reduction in knee extensor torque in trained male runners following a marathon in addition to significant elevations in markers of muscle damage. This is in contrast to a high-intensity strength/resistance exercise bout where repeated movements of arm flexion or leg extension could reduce muscle strength by as much as 50-70% from baseline values, albeit these values were demonstrated in novice, and not trained, individuals (Newham et al. 1987;Clarkson and Dedrick 1988;Sayers and Clarkson 2001). Yet, the time course for strength loss following either resistance or aerobic exercise is relatively similar, with a return of strength to baseline values by ~ 7 days, at least when initial reduction was < 50% (Paulsen et al. 2012). ...
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There have been a multitude of reviews written on exercise-induced muscle damage (EIMD) and recovery. EIMD is a complex area of study as there are a host of factors such as sex, age, nutrition, fitness level, genetics and familiarity with exercise task, which influence the magnitude of performance decrement and the time course of recovery following EIMD. In addition, many reviews on recovery from exercise have ranged from the impact of nutritional strategies and recovery modalities, to complex mechanistic examination of various immune and endocrine signaling molecules. No one review can adequately address this broad array of study. Thus, in this present review, we aim to examine EIMD emanating from both endurance exercise and resistance exercise training in recreational and competitive athletes and shed light on nutritional strategies that can enhance and accelerate recovery following EIMD. In addition, the evaluation of EIMD and recovery from exercise is often complicated and conclusions often depend of the specific mode of assessment. As such, the focus of this review is also directed at the available techniques used to assess EIMD.
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Occupational disease is an important public health problem of the 21st century. Occupational disease still accounts for many preventable illnesses and injuries in the workplace. It is important to incorporate modern knowledge of disease epidemiology and cutting-edge diagnostic methods and treatment with the most recent developments in the management and prevention methods to better control work-related diseases and injuries. This book covers a selection of the common occupational diseases and injuries. It offers accurate, current information on the history, causes, diagnosis, management and prevention of several occupational diseases. Key features: - 14 chapters contributed by more than 30 experts in occupational and preventive medicine - Comprehensive treatment of the history, causes, diagnosis, management and prevention of many important occupational diseases (including asbestosis, silicosis, work-related asthma, occupational cancer, mesothelioma, arsenic, and other diseases.). - Each chapter highlights the latest research findings and cutting-edge technologies - References for further reading Modern Occupational Diseases: Diagnosis, Epidemiology, Management and Prevention serves as a useful guide for all readers interested in occupational diseases. The suggested readership includes trainees in occupational medicine, general practitioners, medical students, graduate students in public health programs, occupational health nurses, and professionals involved in occupational health and safety roles at public and private levels.
The purpose of the study was to determine if repeated exertional heat injuries (EHIs) worsen the inflammatory response and subsequent organ damage. We assessed the impact of a single EHI bout (EHI0) or 2 separate EHI episodes separated by 1 (EHI1), 3 (EHI3), and 7 (EHI7) days in male C57BL/6J mice (N = 236). To induce EHI, mice underwent a forced running protocol until loss of consciousness or core temperature reached ≥ 42.7°C. Blood and tissue samples were obtained 30 minutes, 3 hours, 1 day or 7 days after the EHI. We observed that mice undergoing repeated EHI events (EHI1, EHI3, and EHI7) had longer running distances prior to collapse (~ 528 meters), tolerated higher core temperatures (~0.18°C) prior to collapse, and had higher minimum core temperature (indicative of injury severity) during recovery relative to EHI0 group (~2.18°C; all P < .05). Heat resilience was most pronounced when latency was shortest between EHI episodes (i.e., thermal load and running duration highest in EHI1), suggesting the response diminishes with longer recoveries between EHI events. Furthermore, mice experiencing a second EHI exhibited increased serum & liver HSP70, and lower corticosterone, FABP2, MIP-1β, MIP-2, and IP-10 relative to mice experiencing a single EHI at specific points during the recovery period (typically 30-min to 3-hr after the EHI). Our findings indicate that an EHI event may initiate some adaptive processes that provide acute heat resilience to subsequent EHI conditions. Data and code are available at Open Science Framework repository:
Mechanisms of exercise induced delayed onset muscle soreness: a brief review
  • R B Armstrong
  • W C Byrnes
  • P M Clarkson
  • J S White
  • S S Hsich
  • P N Frykman
  • Repeated Exercise
ARMSTRONG, R. B. Mechanisms of exercise induced delayed onset muscle soreness: a brief review. Med. Sci. Sports Exercise 16: 529-538,1984. BYRNES, W. C., P. M. CLARKSON, J. S. WHITE, S. S. HSICH, P. N. FRYKMAN, REPEATED EXERCISE: MUSCLE PAIN AND DAMAGE