Eur J Appl Physiol (2012) 112:4135–4142
DOI 10.1007/s00421-012-2404-y
ORIGINAL ARTICLE
Exercise-induced muscle damage from bench press exercise
impairs arm cranking endurance performance
Gregory G. Doncaster • Craig Twist
Received: 5 November 2011 / Accepted: 4 April 2012 / Published online: 24 April 2012
Ó Springer-Verlag 2012
Abstract The effects of exercise-induced muscle damage
(EIMD) on the physiological, metabolic and perceptual
responses during upper body arm cranking exercise are
unknown. Nine physically active male participants per-
formed 6 min of arm cranking exercise at ventilatory
threshold (VT), followed by a time to exhaustion (TTE)
trial at a workload corresponding to 80 % of the difference
between VT and VO _ 2peak 48 h after bench pressing exercise
(10 9 6 repetitions at 70 % one repetition maximum) or
20 min sitting (control). Reductions in isokinetic strength
and increased muscle soreness of the elbow flexors and
extensors were evident at 24 and 48 h after bench pressing
exercise (P \ 0.05). Despite no change in VO _ 2 , V_E , HR
and blood lactate concentration ([Bla]) between conditions
(P [ 0.05), rating of perceived exertion (RPE) was higher
during the 6 min arm cranking after bench pressing exer-
cise compared to the control condition (P \ 0.05). TTE
was reduced in the treatment condition (207.2 ± 91.9 cf.
_ 2 (P \ 0.05)
293.4 ± 75.6 s; P \ 0.05), as were end VO
and [Bla] at 0, 5 and 10 min after exercise (P \ 0.05). RPE
during the TTE trial was higher after bench pressing
(P \ 0.05), although end RPE was not different between
conditions (P [ 0.05). This study provides evidence that
EIMD caused by bench pressing exercise increases the
sense of effort during arm cranking exercise that leads to a
reduced exercise tolerance. The findings have implications
Communicated by Arnold de Haan.
G. G. Doncaster
C. Twist (&)
Department of Sport and Exercise Sciences,
University of Chester, Chester CH1 4BJ, UK
e-mail: c.twist@chester.ac.uk
for individuals participating in concurrent endurance and
resistance training of the upper body.
Keywords Upper body
Muscle damage

Sub-maximal exercise
Time to exhaustion
Introduction
Exercise-induced muscle damage (EIMD) occurs after
unaccustomed, eccentric-biased exercise or from exercise
with a high intensity or volume (Byrne et al. 2004;
Proske and Morgan 2001). Sarcomere disruption and
dysfunction to the excitation–contraction mechanism are
accompanied by the inflammatory response and reduc-
tions in muscle force, increased muscle pain, swelling
and increases in circulating blood proteins (Byrne et al.
2004). After eccentric exercise of the same relative load,
muscle damage to the elbow flexors is greater and
recovery of muscular performance is slower when com-
pared to the knee extensors (Chen et al. 2011; Jamurtas
et al. 2005; Nosaka et al. 1991; Paschalis et al. 2010).
The different response is because of the greater volume
of daily activity of the lower limb muscles, as well as
differences between upper and lower limb muscle
architecture, structure and length-tension characteristics
(Chen et al. 2011).
Exercise-induced muscle damage causes changes in the
physiological, metabolic and perceptual responses to
endurance exercise (Davies et al. 2008; Hotta et al. 2006;
Davies et al. 2009; Twist and Eston 2009; Gleeson et al.
1998; Asp et al.1998; Marcora and Bosio 2007). Increases
in minute ventilation (Hotta et al. 2006; Davies et al. 2008,
2009, Twist and Eston 2009), reduced muscle glycogen
availability (Asp et al. 1998) and increased lactate
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concentration (Gleeson et al. 1998) have all been reported
after eccentric exercise. These changes might reflect
changes in the metabolic demand of exercise towards non-
oxidative metabolism, which leads to a reduction in
endurance capacity (Asp et al. 1998). Furthermore, changes
in effort perception, associated with EIMD, also plays a
key role in limiting exercise performance via a fatigue
mechanism that is more central in origin (Marcora and
Bosio 2007; Twist and Eston 2009; Davies et al. 2009).
Alterations in time-trial performance (Marcora and Bosio
2007; Twist and Eston 2009) and time to exhaustion (TTE)
trials (Marcora et al. 2008; Davies et al. 2009) after
eccentric exercise are mediated by alterations in rating of
perceived exertion (RPE). Marcora et al. (2008) demon-
strated that inhibitory effects of afferent neural feedback or
leg discomfort (peripheral factors) did not determine the
TTE during cycling. Rather, Marcora et al. (2008) sug-
gested that an increased central motor command (central
factors) to the fatiguing locomotor muscles simultaneously
increased RPE, causing ‘task disengagement’, as opposed
to ‘task failure’, to occur. Interestingly, Marcora et al.
(2008) evaluated performance 30–40 min after eccentric
exercise when muscle soreness was not present, meaning
the authors were able to exclude the effect of afferent
feedback from sore muscles on perception of effort.
Marcora et al. (2009) also demonstrated that mental fatigue
caused an earlier disengagement from the physical task due
to an increased perception of effort. Studies in mice have
also reported a relationship between elevated inflammatory
cytokines within the brain and reduced TTE during tread-
mill running (Carmichael et al. 2006). However, it remains
unclear whether the detrimental effects of EIMD on
endurance performance are influenced by mechanisms of
fatigue that are mediated peripherally, centrally or a com-
bination of both.
While the effects of EIMD on lower body exercise
endurance performance are well documented, the effects
of EIMD on upper body endurance performance have yet
to be elucidated. Indeed, should the upper limb muscu-
lature be more susceptible to EIMD than the lower limb
(Chen et al. 2011), the effects of eccentric exercise on
upper body endurance performance may well be more
severe than previously reported for cycling or running.
Studying arm-only exercise might also have implications
for sports where propulsion of the body is reliant on
upper body function, such as wheelchair sports, rowing
and swimming. Indeed, individuals engaging in concur-
rent upper body resistance and endurance exercise should
be aware of the potential impact of EIMD on perfor-
mance. Therefore, the purpose of this study was to
examine EIMD after bench press exercise and the effects
on physiological, metabolic, perceptual and performance
responses during arm cranking exercise.
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Eur J Appl Physiol (2012) 112:4135–4142
Methods
Participants and study design
After institutional ethical approval, nine physically active
(trained at least three times per week for a minimum of
30 min) male student participants were recruited for the
study (mean age 21.8 ± 1.7 years, body mass 80.9 ±
10.3 kg, stature 1.82 ± 0.09 m, upper body VO _ 2peak
-1 -1
30.1 ± 3.6 ml kg min ). The number of participants
was based on sample sizes of previous studies that have
observed an effect of EIMD on endurance performance
(Davies et al. 2008, Davies et al. 2009; Twist and Eston
2009). Participants had not taken part in any systematic
resistance training of the upper body six months prior to
the study. All participants completed a written informed
consent and a medical health questionnaire prior to com-
mencing the study. Participants were also asked to refrain
from any additional exercise and maintain a normal diet
during their participation in the study. In order to reduce
any time of day effects, all testing was completed at the
same time of day (±1 h).
All participants completed the treatment and control
condition with 7–10 days between conditions. Participants
were randomly allocated to two groups; the first comprised
five participants performing the treatment followed by
control condition, while the second group comprised four
participants performing the control followed by the treat-
ment condition.
The initial visit involved the assessment of one repeti-
tion maximum (1-RM) bench press, along with a habitua-
tion to the isokinetic dynamometer and arm crank
procedures. Thereafter, participants performed an incre-
mental arm cranking test to determine ventilatory threshold
(VT) and VO _ 2peak , which were subsequently used to
determine exercise intensities for the 6 min arm cranking
protocol and TTE trials. In the treatment condition, par-
ticipants performed muscle-damaging exercise using bench
pressing exercise and then returned 48 h later to perform a
6 min arm cranking protocol at a power output corre-
sponding to VT followed by a TTE trail at a workload
corresponding to 80 % of the difference between VT and
_ 2peak . In the control condition, participants were asked
VO
to remain seated for approximately 20 min and 48 h after
the 6 min arm cranking protocol and TTE trials were
performed. The decision to repeat arm cranking exercise at
48 h only was consistent with previous studies (Marcora
and Bosio 2007; Davies et al. 2008, 2009; Twist and Eston
2009) in an attempt to coincide with the peak in perceived
muscle soreness after muscle-damaging exercise. Mea-
surements of isokinetic force, creatine kinase (CK) and
perceived muscle soreness were also measured prior to the
Eur J Appl Physiol (2012) 112:4135–4142
sub-maximal exercise and then at 24 and 48 h after each
condition.
_ 2peak
Assessment of ventilatory threshold (VT) and VO
Participants were required to complete a 3-min warm-up at
30 W on an arm ergometer (Lode Angio, Groningen, The
Netherlands), after which the test commenced immediately
with a 15 W min-1 increment until volitional exhaustion.
Participants maintained a self-selected cadence between 60
and 80 rpm throughout, with exhaustion defined as the
point at which the participant could no longer continue as
instructed. Expired air was measured continuously using an
online metabolic system (Cosmed Quark b2, Cosmed S.r.I.,
Rome, Italy), which was calibrated according to the man-
ufacturer’s instructions before each test using ambient air
and a gas of known O2 and CO2 concentrations. Partici-
pants verbally reported a rating of perceived exhaustion
(RPE; Borg 1998) to the researcher and HR (Polar S210i,
Polar Electro, Oy, Finland) was recorded in the final 15 s
of each stage. Participants were instructed that RPE
referred to feelings of ‘effort’ expended during the partic-
ular task, and were asked to provide ratings accordingly
(Marcora 2009). VO _ 2peak was determined as the highest
value recorded over 30 s. The ventilatory threshold was
calculated using the ventilatory equivalent method (Amann
et al. 2006) from which the corresponding power output
was then calculated.
The 6 min arm cranking protocol and TTE trial
Participants completed a 6 min arm cranking protocol at
the power output corresponding to VT. Expired air was
measured continuously throughout (Cosmed Quark b2,
Cosmed S.r.I., Rome, Italy) to determine V_E , respiratory
exchange ratio (RER) and VO _ 2 . RPE, HR and a blood
lactate concentration ([Bla]; Arkray Lactate Pro, Arkray,
Kyoto, Japan) from an earlobe capillary were recorded in
the final minute. After a 3-min passive rest, participants
then worked to their limit of tolerance at a power output
corresponding to 80 % of the difference between their VT
and VO_ 2peak . This workload ensured that participants were
exercising in the severe exercise intensity domain (Jones
et al. 2009). Participants were encouraged to maintain this
workload for as long as possible and the test was termi-
nated when, despite verbal encouragement, the cadence
dropped below 60 rpm for greater than 5 s. Participants
received only visual feedback on their arm cranking
cadence, which they were asked to maintain for all trials.
Expired air was measured continuously throughout to
determine V_E , RER and VO _ 2 , with HR and RPE recorded
every 60 s during the TTE trial. [Bla] was recorded from
4137
an earlobe capillary immediately, 5 and 10 min after the
TTE trial.
Indirect markers of EIMD
Perceived muscle soreness in the upper body (elbow flexors
and extensors, pectoralis major and the trapezius) was
recorded after a single press-up using a 0–100 cm visual
analogue scale, with 0 representing no muscle soreness and
100 cm representing the worst soreness possible. Starting in
a prone position with hands and knees on the floor and
elbows fully extended, participants performed a single
press-up that involved flexion at the elbows until the chest
touched the floor followed by a return to the start position.
The use of the visual analogue scale for establishing per-
ceived muscle soreness has been used successfully in pre-
vious studies (Davies et al. 2008; Twist and Eston 2009).
Reciprocal measurements of upper body isokinetic
pushing and pulling force at 90° s-1 were measured using
an isokinetic dynamometer (Biodex 3, Biodex Medical
Systems, Shirley, NY). These movements were selected as
they best represented the muscle actions during the arm
cranking and muscle damaging protocol. Prior to testing
participants were asked to perform a 2-min warm-up at
30 W using the arm ergometer described above, followed
by static stretches of the elbow flexors and extensors,
shoulders and pectoral muscle groups. Participants were
seated in an upright position on the dynamometer, with
straps placed across the shoulders and the abdomen so as to
avoid any extraneous movement. The participant’s range of
motion was manually determined by the investigator to
ensure that the range was consistent between trials and
participants. In addition, the limb mass recorded to enable
gravity correction of peak torque values. The participant
performed five maximal efforts at 90° s-1 on the dominant
arm, with the highest recordings for pushing and pulling
used for analysis. Constant encouragement to provide
maximal voluntary effort was given verbally by the
investigator and visually via displaying real-time force.
Plasma blood CK activity was assessed by taking a
30 ll fingertip capillary sample of blood, which was then
analyzed using a colorimetric assay procedure (Reflotron,
Boehringer, Mannheim, Germany).
Muscle-damaging protocol
Bench press exercise was selected as it has been used to
improve arm cranking endurance performance (Jacobs
2009) and because both modes of exercise activate similar
musculature of the upper body (Smith et al. 2008; Saeter-
bakken et al. 2011).
One-repetition maximum (1-RM) bench press was
measured after a warm-up consisting of 10 repetitions at
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27.5 kg and 10 press-ups against the participant’s own
body mass. Thereafter, participants performed progressive
attempts until a 1-RM was obtained. This was completed
within 3–5 repetitions, allowing the participant several
minutes to recover between each attempt. A complete rep-
etition required the participant to lower the bar quickly to
the chest so that the elbow joint reached 90° and then lift the
bar off the chest so that the elbow joint was fully extended.
To induce symptoms of EIMD, participants performed
ten sets of six repetitions of bench pressing exercise against
a load corresponding to 70 % of their previously estab-
lished 1-RM (Uchida et al. 2009). Participants were
instructed to perform a 3 s eccentric phase followed by a
1 s concentric phase, with a 60 s passive recovery provided
between each set. The mean load lifted in the treatment
condition was 67.5 ± 7.2 kg.
Statistical analysis
Changes in isokinetic peak torque, CK and perceived
muscle soreness were evaluated using separate two-factor
(condition 9 time) repeated measures analysis of variance
(ANOVA). RPE during the TTE trial was evaluated using a
two-factor (condition 9 time) repeated measures ANOVA.
Assumptions of sphericity were evaluated using Mauchly’s
test, and where sphericity was violated (P \ 0.05) the
Greenhouse-Geisser correction factor was applied. Where
appropriate Bonferroni adjusted t tests were used to
investigate any significant results. Differences between
conditions in VO _ 2 , V_E , RER, HR, RPE and post [Bla]
during the 6 min arm cranking protocol and TTE perfor-
mance were analyzed using paired samples t tests. To
further analyze the effects of RPE on arm cranking per-
formance, each individual’s RPE during the TTE trial were
regressed against time in both the control and treatment
conditions. Paired samples t tests were then implemented to
identify whether the slope of the line (b-coefficients; b) and
the intercept (a) were significantly different between the
treatment and control conditions. Data are presented as
mean ± SD. The alpha level was set at P B 0.05 and all
statistics were calculated using SPSS for Windows (version
18.0) software.
Results
Perceived muscle soreness, isokinetic peak force
and CK
Baseline values for perceived muscle soreness, isokinetic
peak force and CK were not different at baseline between
the treatment and control conditions (all P [ 0.05). An
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Eur J Appl Physiol (2012) 112:4135–4142
increase in muscle soreness was observed in the treatment
condition at both time points after muscle-damaging
exercise, with the highest values reported at 48 h
(P \ 0.05). Conversely, muscle soreness remained
unchanged in the control condition (P [ 0.05). Peak is-
okinetic pushing force in the treatment condition was
decreased to 72.7 ± 12.9 and 78.1 ± 11.8 % of baseline
values at 24 and 48 h, respectively (P \ 0.05). Peak is-
okinetic pulling force in the treatment condition was
88.1 ± 12.3 and 93.8 ± 15.2 % of baseline values at 24
and 48 h, respectively, with values only reduced at 24 h
when compared to baseline measurements (P \ 0.05).
Compared to baseline, values at 24 and 48 h for peak
isokinetic pushing (100.9 ± 10.3 and 101.6 ± 8.6 %, res-
pectively) and pulling force (98.6 ± 6.8 and 102.8 ±
7.8 %, respectively) were not different in the control
condition (P [ 0.05). There was no main effect for time
(P [ 0.05) or time by group interaction on CK (P [ 0.05)
suggesting that plasma blood CK activity remained
unchanged over the 48-h period for both conditions.
Table 1 displays changes in muscle soreness, peak isoki-
netic force (pushing and pulling) and CK.
Six-min arm cranking protocol
No differences were observed for VO _ 2 , V_E , RER, HR and
[Bla] between conditions (all P [ 0.05) However, RPE
was higher after muscle-damaging exercise when com-
pared to the control condition (t = 3.507, P \ 0.05). Data
from the 6 min arm cranking protocol for both conditions
are shown in Table 2.
TTE trial
Table 3 shows the data from the TTE trial for both the
control and treatment conditions. Paired sampled t tests
revealed that muscle-damaging exercise resulted in a
decrease in TTE (t = -2.520, P \ 0.05), end VO _ 2 (t =
-3.367, P \ 0.05) and [Bla] immediately (t = -2.756,
P \ 0.05) and at 5 (t = -2.449, P \ 0.05) and 10 min
(t = -2.835, P \ 0.05) post exercise. Despite approaching
significance, HR and V_E were not statistically different
between conditions (P [ 0.05).
Repeated measures ANOVA revealed main effects of
time (F = 116.47, P \ 0.05) and condition (F = 7.47,
P \ 0.05) for RPE during the TTE trial. However, RPE at
the point of exhaustion was not different between condi-
tions (t = 0.17, P [ 0.05; Fig. 1). Comparisons of within-
subjects slopes (b) between conditions revealed that
there was a trend (t = 2.195, P = 0.06) for an accelerated
rate of increase in RPE in the treatment condition
(b = 0.04 ± 0.02) when compared to the control condition
Eur J Appl Physiol (2012) 112:4135–4142 4139

Table 1 Indirect markers of exercise-induced muscle damage at Table 3 Comparisons of VO _ 2 , V_E , RER, HR, RPE and immediate, 5
baseline, 24 and 48 h in the treatment and control conditions and 10 min post [Bla] between the treatment and control conditions at
48 h
Baseline 24 h 48 h
Treatment Control P value
Muscle soreness (cm)
Treatment 5 ± 13 54 ± 20* 65 ± 27* Time (s) 207.2 ± 91.9* 293.4 ± 75.6 0.036
Control 5 ± 11 5±9 3±7 _ 2
End VO 29.3 ± 2.4* 33.8 ± 4.2 0.010
Peak isokinetic pulling force (N) (ml kg-1 min-1)
Treatment 413.2 ± 71.2 362.5 ± 76.6* 389.2 ± 105.1 HR (b min-1) 170 ± 17 177 ± 13 0.067
Control 414.0 ± 60.8 408.9 ± 70.5 425.5 ± 66.6 V_E 86.5 ± 19.6 101.0 ± 20.5 0.063
Peak isokinetic pushing force (N) (l min-1)
Treatment 497.5 ± 78.5 357.1 ± 58.2* 388.6 ± 82.3* RPE 19.6 ± 0.7 19.4 ± 1.3 0.559
Control 452.0 ± 71.1 454.0 ± 69.8 456.7 ± 76.1 Post [Bla] (mmol l-1) 7.5 ± 1.3* 8.7 ± 1.1 0.025
CK (U l-1) 5 min [Bla] (mmol 1-1) 7.6 ± 1.6* 8.4 ± 1.2 0.040
Treatment 63.7 ± 88.2 82.4 ± 76.5 78.9 ± 50.8 10 min [Bla] (mmol l-1) 5.9 ± 1.9* 7.1 ± 1.7 0.044
Control 36.9 ± 33.8 50.5 ± 53.9 62.9 ± 57.6
Corresponding P values are provided
* Significantly different from baseline value (P \ 0.05) * Significantly different from control condition (P \ 0.05)

Table 2 Comparisons of VO _ 2 , V_E , RER, HR, RPE and post [Bla] 20

between the treatment and control conditions at 48 h during the 6 min
18
sub-maximal exercise trial
16
Treatment Control P value
RPE

14
Treatment
_ 2
VO 21.4 ± 3.5 21.2 ± 4.6 0.833 12

(ml kg-1 min-1) 10 Control

V_E 48.3 ± 11.9 44.5 ± 17.0 0.303 8

(l min-1)
RER 1.01 ± 0.03 0.99 ± 0.04
HR (b min-1) 139 ± 19 140 ± 14
RPE 14.4 ± 1.0* 12.5 ± 1.1
Post [Bla] (mmol l-1) 3.7 ± 1.0 3.8 ± 1.3
Corresponding P values are provided
* Significantly different from control condition (P \ 0.05)
(b = -0.02 ± 0.01). However, there was no difference in
the intercept of RPE against time (t = 0.559, P [ 0.05)
between the treatment and control conditions (a = 13.9 ±
2.1 cf. a = 13.5 ± 2.0, respectively).
Discussion
Decreases in isokinetic force and increases in perceived
muscle soreness confirm that the bench pressing protocol
caused EIMD in the upper body. These changes were
similar to those previously reported in studies examining
EIMD after bench press (Uchida et al. 2009) and eccentric
exercise using a isokinetic dynamometer (Chen et al. 2011;
Paschalis et al. 2010). CK values were lower at all times
points in both conditions and is probably a result of the
different measurement methods used between this study
6
0 60 120 180 240 300
0.303
Time (s)
0.906
0.008 Fig. 1 Changes in RPE during time to exhaustion trial for treatment
and control conditions.  Significant main effect of time (P \ 0.05).
0.864
*Significant main effect of condition (P \ 0.05)
and those of Uchida et al. (2009), who used a similar
procedure to evoke EIMD. Furthermore, while CK showed
small increases after bench pressing exercise, these values
did not reach significance. These findings are consistent
with previous studies that have observed no change in CK
after eccentric exercise (Kuipers et al. 1985; Walsh et al.
2001) and support the poor correlation between CK and
muscle function after muscle-damaging exercise (Fridén
and Lieber 2001; Warren et al. 1999).
To the authors’ knowledge, this is the first study to
investigate the effects of EIMD on upper body endurance
performance using arm crank ergometry. Despite the
presence of muscle damage, exercise metabolism during
submaximal arm cranking remained unchanged. These
findings support previous work that has observed similar
responses during cycling after eccentric exercise (Walsh
et al. 2001; Davies et al. 2008; Twist and Eston 2009).
Studies that have reported changes in oxidative metabolism
after eccentric exercise have tended to occur in studies

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examining running, where changes in limb kinematics have
explained an increased oxygen demand (Braun and Dutto
2003). Therefore, that body position and limb kinematics
were unchanged between conditions, coupled with no dis-
ruption to the oxygen delivery at the active muscle,
explains why arm cranking during the 6 min protocol was
not impaired.
Although VO_ 2 , HR, RER and [Bla] remained unchanged
in the treatment condition, participants’ RPE increased for
the same relative workload during the 6 min arm cranking
protocol. Such observations are consistent with those
findings previously reported for fixed intensity cycling after
EIMD of the lower body (Davies et al. 2009; Twist and
Eston 2009). An increased RPE response after muscle-
damaging exercise has been attributed to an increased
ventilatory response (Davies et al. 2009; Twist and Eston
2009), which transcends from stimulation of III and IV
nerve afferents located in and around the blood vessels of
exercising muscle that control ventilation (Hotta et al.
2006; Haouzi et al. 2004). However, in contrast to findings
reporting the effects of EIMD on sub-maximal cycling
(Davies et al. 2009; Twist and Eston 2009), increases in
perceived effort did not accompany a contemporaneous
increase in the ventilatory response during arm cranking
exercise, as V_E remained unaltered during the treatment
condition. The dependency of RPE on feedback from the
skeletal muscle, heart and lungs has been challenged by
Marcora (2009), who proposes that an increase in RPE
during exercise is likely to be centrally governed from the
brain. And while Amann et al. (2010) reported that
blocking of afferent feedback response from the lower limb
muscles lead to a concomitant reduction in V_E and RPE
response, this was not the case when upper body exercise
was performed under the same conditions. Amann et al.
(2010) attributed no change in ventilation to attenuated
afferent feedback at the thoracic or cervical spinal level
from various trunk muscles involved in upper body exer-
cise, which may explain the results observed in our study.
That is to say, despite demonstrating symptoms of EIMD
after bench pressing exercise, there was little impact of this
muscle damage in stimulating the ventilatory response to
arm cranking exercise.
The role of muscle pain on effort perception is unclear.
Increased perception of effort is associated with an increase
in muscle pain after eccentric exercise, which is known to
heighten the sense of effort during force matching tasks
(Proske et al. 2003; Weerakkody et al. 2003). However,
using a different methodological approach, Khan et al.
(2011) have suggested that evoked muscle pain has a no
effect on the sense of effort and motor output during vol-
untary muscle actions. Furthermore, Marcora et al. (2008)
have demonstrated that 30–40 min after eccentric exercise,
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Eur J Appl Physiol (2012) 112:4135–4142
when muscles were weaker but increases in perceived
muscle soreness were yet to appear, participants reported
an increased RPE during cycling exercise. Therefore, these
studies suggest that an increase in central motor command
is more important than muscle pain in determining RPE.
Unfortunately, we are not able to confirm the mechanism
that caused an increase in RPE, but propose that reductions
in force and increases in muscle soreness contributed to an
increased sense of effort in the presence of EIMD.
The TTE during arm cranking was reduced in eight of
the nine participants after muscle-damaging exercise and
supports previous findings of a reduced exercise tolerance
during cycling TTE trials (Davies et al. 2008, 2009).
However, TTE was *27 % shorter in the presence of
EIMD for arm cranking exercise compared to *18 %
reduction observed in studies that have studied the effects
of EIMD on lower body exercise (Davies et al. 2008,
2009). The large reductions in endurance capacity observed
in our study are consistent with a greater magnitude of
functional impairment in upper limbs after eccentric
exercise (Chen et al. 2011; Jamurtas et al. 2005; Nosaka
et al. 1991; Paschalis et al. 2010).
A reduced limit of tolerance was also accompanied by a
lower end VO _ 2 and lower [Bla] compared to the control
condition. An altered sense of effort imposed by muscle-
damaging exercise is the most likely explanation for these
findings. Despite the RPE remaining unchanged at the start
and end-point, RPE was higher during the TTE test and had
a higher rate of increase in the treatment condition. This
resulted in participants exercising for a shorter time after
EIMD and explains the lower metabolic response. Such
impediments to performance have previously been reported
to result in a shorter TTE in mice (Carmichael et al. 2006)
and a reduced time-trial running distance in humans
(Marcora and Bosio 2007). Furthermore, the dispropor-
tionate increase in RPE compared to the reduction in end
_ 2 , [Bla] and V_E in the treatment condition suggests
VO
dissociation between metabolic stress and perceived exer-
tion. These findings support those presented by Marcora
et al. (2008) who suggests that the sense of effort is cen-
trally generated by forwarding neural signals, termed cor-
ollary discharges, from motor to sensory areas of the
cerebral cortex. This results in an increase in central motor
command in order to exercise at the same relative workload
under conditions of EIMD, the result of which a shorter
TTE. Participants therefore engaged with the exercise task
until a point at which they no longer felt able to continue; a
decision that was influenced by their perception of effort
and not by peripheral fatigue. Indeed, that the rate of
increase in RPE was faster in the treatment condition
despite no difference in the y-intercept and a lower meta-
bolic response supports our argument.
Eur J Appl Physiol (2012) 112:4135–4142
Conclusion
This is the first study to examine the impact of EIMD on
upper body endurance performance. Increases in perceived
exertion during sub-maximal exercise are likely to be
mediated by the increased central motor command neces-
sary to compensate for the muscle weakness caused by
eccentric exercise and sensations of pain resulting from the
eccentric exercise. Our findings also indicated that a
reduction in exercise tolerance was accompanied by a
reduced metabolic response at exhaustion in the presence
of EIMD. However, the disproportionate increase in RPE
compared to the metabolic response during a shorter TTE
trial indicates that an individual’s perception of effort is
fundamental in determining exercise tolerance. These
findings have implications for individuals participating in
concurrent endurance and resistance training of the upper
body.
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