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Effect of bench press exercise intensity on muscle soreness and inflammatory

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DOI: 10.1080/02640410802632144 · Source: PubMed

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Journal of Sports Sciences, Month 2009; 00(0): 1–9

60
Effect of bench press exercise intensity on muscle soreness and
5 inflammatory mediators

65
1 2 3 4
MARCO C. UCHIDA , KEN NOSAKA , CARLOS UGRINOWITSCH , ALEX YAMASHITA ,
10
EIVOR MARTINS JR5, ANSELMO S. MORISCOT4, & MARCELO S. AOKI6
1
Department of Biological Sciences and Health, UniFIEO, São Paulo, Brazil, 2School of Exercise, Biomedical and Health
70
Sciences, Edith Cowan University, Joondalup, WA, Australia, 3School of Physical Education and Sport, University of São
Paulo, São Paulo, Brazil, 4Department of Cell and Developmental Biology, University of São Paulo, São Paulo, Brazil,
15 5
Faculty of Physical Education, University of Mogi das Cruzes, Mogi das Cruzes, Brazil and 6School of Arts, Sciences and
Humanities, University of São Paulo, São Paulo, Brazil
75
(Accepted 18 November 2008)
20

Abstract
This study compared four different intensities of a bench press exercise for muscle soreness, creatine kinase activity, 80
interleukin (IL)-1b, IL-6, tumor necrosis factor-a (TNF-a), and prostaglandin E2 (PGE2) concentrations in the blood.
Thirty-five male Brazilian Army soldiers were randomly assigned to one of five groups: 50% one-repetition maximum
25 (1-RM), 75% 1-RM, 90% 1-RM, 110% 1-RM, and a control group that did not perform the exercise. The total volume
(sets 6 repetitions 6 load) of the exercise was matched among the exercise groups. Muscle soreness and plasma creatine
kinase activity increased markedly (P 5 0.05) after exercise, with no significant differences among the groups. Serum PGE2
concentration also increased markedly (P 5 0.05) after exercise, with a significantly (P 5 0.05) greater increase in the 110% 85
1-RM group compared with the other groups. A weak but significant (P 5 0.05) correlation was found between peak muscle
soreness and peak PGE2 concentration, but no significant correlation was evident between peak muscle soreness and peak
30 creatine kinase activity, or peak creatine kinase activity and peak PGE2 concentration. All groups showed no changes in
IL-1b, IL-6 or TNF-a. Our results suggest that the intensity of bench press exercise does not affect the magnitude of muscle
soreness and blood markers of muscle damage and inflammation.
90
Keywords: Delayed-onset muscle soreness, muscle damage, cytokines, creatine kinase, progtaglandin E2
35

Ratamess, 2004). It is also known that the total 95

Introduction
40 Resistance training is important not only for athletes
but also for members of the general population
(Hass, Feigenbaum, & Franklin, 2001; Kraemer
et al., 2002; Kraemer & Ratamess, 2004). When
prescribing resistance training, intensity is a key
45 factor, which is determined by the percentage of one-
repetition maximum (1-RM) and number of repeti-
tions (Hass et al., 2001; Kraemer et al., 2002;
Kraemer & Ratamess, 2004). It has been documen-
ted that 45–50% of 1-RM (e.g. 415 repetitions) is
50 effective for motor learning and muscular endurance,
70–80% of 1-RM (e.g. 6–12 RM) is appropriate for
muscle hypertrophy, and 80–85% of 1-RM or
beyond (e.g. 1–6 RM) is recommended to increase
maximum strength (Campos et al., 2002; Kraemer &
55
Correspondence: M. S. Aoki, School of Arts, Sciences and Humanities, University of São Paulo, Av. Lineu Prestes 1524, CEP 05508-900, São Paulo, SP,
Brazil. E-mail: saldanha.caf@usp.br
ISSN 0264-0414 print/ISSN 1466-447X online Ó 2009 Taylor & Francis
DOI: 10.1080/02640410802632144
volume of resistance training (sets 6 repetitions 6
load) determines the training stimulus (Kraemer &
Ratamess, 2004), and affects the responses of the
nervous, hormonal, and muscular systems (Kraemer
et al., 2002; Kraemer & Ratamess, 2004). 100
One of the consequences of resistance exercise,
especially in the initial stages of a training pro-
gramme, is delayed-onset muscle soreness (DOMS).
Delayed-onset muscle soreness is characterized by a
dull pain felt during movement or palpation of the 105
affected muscle (Cheung, Hume, & Maxwell, 2003),
and usually develops several to 24 h after exercise,
peaking after 1–3 days and disappearing 7–10 days
post-exercise (Nosaka, Newton, & Sacco, 2002a). It
has been reported that the severity of DOMS after 110
unaccustomed exercise is dependent on the intensity
 2 M. C. Uchida et al.
115 of eccentric contractions. For instance, Nosaka and
Newton (2002) showed that maximum eccentric
contractions induced significantly greater DOMS
than sub-maximal (50%) eccentric contractions of
the elbow flexors, when 30 contractions were
120 performed for both protocols. However, the total
volume was not considered by Nosaka and Newton
(2002), thus the difference in the volume of the two
exercises might have been the reason for the
difference in severity of DOMS. Indeed, Paschalis
125 and colleagues (Paschalis, Koutedakis, Jamurtas,
Mougios, & Baltzopoulos, 2005) compared 12 sets
of 10 maximal eccentric contractions and continuous
eccentric contractions at 50% of the maximal
eccentric torque of the knee extensors using an
130 isokinetic dynamometer, and found no significant
difference in DOMS between the conditions when
total work was calculated. However, no previous
studies have compared resistance exercise intensities
based on one-repetition maximum by matching the
135 total volume. The bench press is one of the most
popular exercises in resistance training, but few
previous studies have reported DOMS and muscle
damage following such exercise.
The underlying mechanisms of DOMS are not
140 completely understood; however, it is generally
accepted that DOMS is associated with muscle
and/or connective tissue damage and/or subsequent
inflammatory responses (Cheung et al., 2003). In the
inflammatory responses induced by exercise, macro-
145 phages produce prostaglandin E2 (PGE2) that
sensitizes muscle afferent nociceptors (Cheung
et al., 2003). Therefore, it is possible that PGE2 is
associated with DOMS. Tegeder and colleagues
(Tegeder, Zimmermann, Meller, & Geisslinger,
150 2002) investigated PGE2 release from the calf
muscles by micro-dialysis, and found that PGE2
release increased in the leg experiencing DOMS. On
the other hand, Hirose et al. (2004) reported no
significant changes in plasma PGE2 concentration
155 following eccentric exercise of the elbow flexors
resulting in DOMS. It is possible that the muscle
mass involved in the exercise was not large enough,
or that the magnitude of muscle damage and
inflammation was not severe enough, to detect
160 possible changes in plasma PGE2 concentration in
the study by Hirose et al. (2004). No previous study
has examined changes in PGE2 in the blood
following a bench press, and the effect of resistance
exercise intensity on those changes.
165 Leukocytes produce pro-inflammatory cytokines
such as interleukin-1b (IL-1b), interleukin-6 (IL-6),
and tumor necrosis factor-a (TNF-a) (Cannon & St.
Pierre, 1998; Dinarello, 1997; Peake, Nosaka, &
Suzuki, 2005; Smith et al., 2000), which are up-
170 regulated at the onset of inflammation (Dinarello,
1997). Previous investigations showed significant
changes in pro-inflammatory cytokines in the blood
after endurance exercise (Bassit, Curi, & Costa Rosa,
2008; Santos, Bassit, Caperuto, & Costa Rosa, 2004;
Trappe, Fluckey, White, Lambert, & Evans, 2001), 175
but changes in cytokines following a bout of bench
press exercise and the effect of exercise intensity are
unclear. It was hypothesized that PGE2 and pro-
inflammatory cytokines would increase in the blood
with the development of DOMS, and the magnitude 180
of increase in PGE2 and cytokines would be
influenced by the exercise intensity. Therefore, the
main aim of the present study was to test
the hypothesis that the magnitude of muscle soreness
after a bench press exercise would not be dependent 185
on the intensity if the total volume of the exercise was
matched. A secondary aim of the present study was
to examine the effect of bench press exercise intensity
with the same total volume on creatine kinase
activity, PGE2, and pro-inflammatory cytokines 190
(IL-6, IL-1b, and TNF-a).
Methods
195
Experimental design and 1-RM determination
Participants were randomly assigned to one of five
groups: 50% one-repetition maximum (1-RM), 75%
1-RM, 90% 1-RM, and 110% 1-RM based on a
bench press exercise, and a control group that did 200
not perform the exercise. One-repetition maximum
of the bench press was determined 7 days before the
exercise bout for all participants. For the determina-
tion of 1-RM, participants were instructed to grip the
bar at a comfortable position, which was typically 10– 205
20 cm wider than shoulder width (Kim, Mayhew, &
Peterson, 2002), and performed a warm-up consist-
ing of 8–10 repetitions using a light weight, 3–5
repetitions using a moderate weight, and 1–3
repetitions using a heavy weight. After the warm- 210
up, each participant was tested for 1-RM strength by
increasing the resistance on subsequent attempts
until he was unable to complete an attempt. Each
attempt was separated by 3 min of rest (Shimano
et al., 2006) and two trained spotters were always 215
present. The criterion measures consisted of muscle
soreness, serum PGE2 concentration, plasma crea-
tine kinase activity, and plasma IL-1b, IL-6, and
TNF-a concentration. These measurements were
taken before exercise (baseline) and 24, 48, and 72 h 220
after exercise, and changes in the measures over time
were compared among the groups.
Participants
225
Forty male Brazilian Army soldiers (mean + s: age
19.1 + 1.8 years; height 1.77 + 0.07 m; body mass
70.9 + 8.1 kg) volunteered to participate in the

study. The participants were randomly assigned to
230 one of the four experimental groups or the control
group. Five soldiers dropped out during the study,
thus the number of participants for each group was as
follows: 50% 1-RM (n ¼ 8), 75% 1-RM (n ¼ 7), 90%
1-RM (n ¼ 7), 110% 1-RM (n ¼ 7), and control
235 (n ¼ 6). No significant differences in the age, height,
body mass or 1-RM strength were observed among
the groups (Table I). The participants had been
undertaking military physical training (running for
60 min and circuit training with body weight
240 exercises for 30 min, three sessions per week) for at
least one year before the present study. They also had
experience of resistance training including a bench
press exercise for a minimum of one year. However,
the participants had not been involved in resistance
245 training since starting their military training.
The participants were free from any musculoske-
letal or neurological problems. All participants were
instructed to refrain from any strenuous activities in
the 72 h before and during the experimental period.
250 The study was approved by the institutional ethics
committee (Protocol #679/05). All participants were
informed of the purpose and risks of the study before
signing an informed consent form.
255
Exercise protocol
The participants in the 50% 1-RM, 75% 1-RM, 90%
1-RM, and 110% 1-RM groups performed a bench
press warm-up routine (twp sets of 12 repetitions at
260 30% 1-RM, resting for 2 min between sets) before
the exercise bout. In the bench press exercise bout,
the 50% 1-RM group performed four sets of *20
repetitions maximum, the 75% 1-RM group per-
formed five sets of *11 repetitions maximum, the
265 90% 1-RM group performed ten sets of *4
repetitions maximum, and the 110% 1-RM group
performed eight sets of *4 repetitions maximum,
based on the 1-RM determined previously. The
participants performed each set with maximal effort
270 until they were unable to perform the repetition with
proper technique, which was judged by the investi-
gator. Thus the number of repetitions was not
exactly the number shown above. In the 110%
1-RM condition, participants performed the ec-
275 centric phase only with the load, whereas during
the concentric phase two spotters raised the weight to
Table I. Age, height, body mass, and 1-RM of the control, 50% 1-RM, 75% 1-RM, 90% 1-RM, and 110 % 1-RM groups (mean + s).
280 Control (n ¼ 6) 50% 1-RM (n ¼ 8)
Age (years) 18.6 + 0.6 19.4 + 1.6
Height (m) 1.78 + 0.07 1.78 + 0.07
Body mass (kg) 70.4 + 5.1 76.0 + 5.7
1-RM (kg) 55.8 + 6.9 59.5 + 11.2
285
Intensity of load and delayed-onset muscle soreness 3
the starting position. The rest between sets was
2 min for all conditions. The participants in the 50%
1-RM, 75% 1-RM, and 90% 1-RM groups were
instructed to move the bar for 2 s during the
eccentric phase and for 1 s during the concentric 290
phase, and to lower the bar to the point where it
touched the chest immediately followed by a full arm
extension. The participants in the 110% 1-RM group
were asked to devote 3 s to the eccentric contraction
for each repetition. The total volume of each 295
participant was calculated using the following for-
mula: total volume (kg) ¼ number of sets 6 number
of repetitions 6 load (kg) (Ahtiainen, Pakarinen,
Alen, Kraemer, & Hakkinen, 2005).
300
Muscle soreness
Muscle soreness of the pectoralis major muscle was
assessed using a visual analog scale (VAS), with ‘‘no
pain’’ at one end of a 100-mm line and ‘‘extremely 305
sore’’ at the other, when the muscle was palpated. In
the palpation assessment, the investigator applied
pressure to the medial part of the pectoralis major
with the tips of three fingers (II, III, and IV) for
approximately 3 s (Nosaka et al., 2002a), while the 310
participant was standing. To standardize the pressure
applied, the same investigator repeated the assess-
ment each day.
315
Blood sampling and analyses
Blood samples (*10 ml) were obtained from the an
antecubital vein in the morning (07:00–09:00 h)
after a 12-h overnight fast before and 24, 48, and
72 h after exercise. The blood was placed immedi- 320
ately into two 5-ml vacutainer tubes (Becton Dick-
insonÓ, NJ, USA), one containing EDTA for plasma
separation and the other for serum separation. Both
tubes were centrifuged at 2500 rev  min71 for
15 min at 48C, and plasma and serum samples were 325
stored at 7808C until analysis. Plasma samples were
used for the analysis of creatine kinase activity,
IL-1b, IL-6, and TNF-a, and serum samples
for PGE2.
Plasma creatine kinase activity was measured by a 330
Beckman DU 640 spectrophotometer using a com-
mercial kit (LabtestÓ, SP, Brazil). The normal
reference range of creatine kinase for this method is
335
75% 1-RM (n ¼ 7) 90% 1-RM (n ¼ 7) 110% 1-RM (n ¼ 7)
19.2 + 2.0 19.5 + 1.9 19.4 + 2.5
1.78 + 0.07 1.75 + 0.07 1.75 + 0.07 340
69.7 + 6.9 72.6 + 8.5 69.0 + 11.6
55.9 + 9.0 57.9 + 7.2 61.1 + 11.1
 4 M. C. Uchida et al.
30–200 IU  l71. Serum PGE2 concentration was
measured using a commercially available ELISA kit
345 (Assay DesignsÓ, MI, USA), and the sensitivity of
the assay was 13.4 pg  ml71. The coefficients of
intra-assay and inter-assay variation of the PGE2
assay were 8.9% and 3.0%, respectively. IL-1b, IL-6,
and TNF-a in plasma were measured by a Luminex-
350 based bead array method (LINCOplex simultaneous
multianalyte detection system; Linco ResearchÓ,
MO, USA). The cytokine assays were conducted
simultaneously from the same blood sample (25 ml).
The sensitivity limit of the measure for IL-1b, IL-6,
355 and TNF-a was 0.19, 0.79, and 0.22 pg  ml71,
respectively. The coefficients of intra-assay and inter-
assay variation for IL-1b, IL-6, and TNF-a were
13.5% and 13.3%, 13.6% and 12.7%, and 12.0%
and 13.0%, respectively.
360
Statistical analyses
Mixed models with group (50% 1-RM, 75% 1-RM,
90% 1-RM, 110% 1-RM, control) and time (base-
365 line, 24 h, 48 h, and 72 h post-exercise) as fixed
factors and participants as a random factor were
performed for changes in the criterion measures.
When a significant group or group 6 time interac-
tion effect was obtained, a Tukey post-hoc test was
370 performed for multiple comparison purposes. Cor-
relation analyses were performed using Pearson’s
product–moment correlation coefficient for peak
muscle soreness and peak creatine kinase activity or
peak PGE2 concentration, and peak creatine kinase
375 activity and peak PGE2 concentration by combining
all participants in the exercise groups (n ¼ 29).
Statistical significance was set at P 5 0.05.
The results are reported as means + standard devia-
tions (s).
380
Results
Exercise
385 All participants in the exercise group performed
maximal repetitions for each set as instructed, and
the number of repetitions was close to the expected
number for each intensity (*20 for 50% 1-RM;
*11 for 75% 1-RM; *4 for 90% 1-RM; *4 for
390 110% 1-RM), although the number of repetitions
decreased with increasing number of sets. There was
no significant difference (F ¼ 2.32, P ¼ 0.1) in the
395 Table II. Total volume of bench press exercise for the 50% 1-RM, 75% 1-RM, 90% 1-RM, and 110 % 1-RM groups (mean + s).
50% 1-RM
Total volume (kg) 2201.3 + 386.9
total volume of the exercise among the groups 400
(Table II).
Delayed-onset muscle soreness
A group 6 time interaction was observed for DOMS 405
(F ¼ 2.22, P ¼ 0.03). No muscle soreness was ob-
served at any time point for the control group
(P ¼ 0.3). Muscle soreness was significant (P 5 0.03)
and peaked 24–48 h after the bench press exercise
for all exercise groups, but no significant difference 410
was evident among the groups (P ¼ 0.39) (Figure 1).
Peak plasma creatine kinase activity
The magnitude of increase in plasma creatine kinase 415
activity from baseline to the highest value (at 24, 48
or 72 h post-exercise) varied among participants
(Table III). All exercise groups showed a significant
increase in post-exercise peak creatine kinase activity
(F ¼ 2.40, P 5 0.03). No significant (P ¼ 0.2) differ- 420
ence in the increase of peak creatine kinase was
evident among the exercise groups.
Serum PGE2 concentration
425
A group 6 time interaction was also observed for
PGE2 (F ¼ 4.24, P 5 0.0001). No significant
(P ¼ 1.0) changes in PGE2 were observed for the
control group, but all exercise groups showed
significant (P 5 0.05) increases from baseline to 24, 430
48, and 72 h post-exercise (Figure 2). The 110%
1-RM group had a significantly (P 5 0.05) greater
serum PGE2 concentration than the other exercise
groups at 24 and 48 h post-exercise.
435
IL-1b, IL-6, and TNF-a
Plasma concentrations of IL-1b, IL-6, and TNF-a
were not detectable for some participants even after
the exercise (Table IV). No marked changes in any of 440
the cytokines from baseline were observed, and no
differences among the groups were evident.
Correlations
445
As shown in Figure 3, there were no significant
correlations between peak muscle soreness and peak
creatine kinase activity (r ¼ 0.27, P ¼ 0.09), and
between peak PGE2 concentration and peak creatine
450
75% 1-RM 90% 1-RM 110% 1-RM
455
1988.0 + 349.7 1892.8 + 218.9 2153.9 + 390.6
 Intensity of load and delayed-onset muscle soreness 5

groups. Second, the increases in plasma creatine

kinase activity after exercise were not significantly 515
different among the exercise groups. Third, PGE2
460 increased markedly after exercise, and the 110%
1-RM group showed a significantly greater increase
than the other three exercise groups. Fourth, no
significant changes in pro-inflammatory cytokines 520
were observed after exercise regardless of the
465 intensity. It is important to note that the variability
among participants in each exercise group was large
Figure 1. Muscle soreness (mean + s) at baseline (pre) and 24, 48, for all measures, especially for plasma creatine kinase
and 72 h after bench press exercise for the control, 50% 1-RM, activity. It has been reported that plasma creatine 525
75% 1-RM, 90% 1-RM, and 110% 1-RM groups.
kinase activity shows great variability (Clarkson,
470 Nosaka, & Braun, 1992; Nosaka & Clarkson,
1996). Nosaka and Clarkson (1996) reported a large
Table III. Mean (range in parentheses) plasma creatine kinase
variability in peak creatine kinase response (236–
activity at baseline and peak values after exercise for the control,
50% 1-RM, 75% 1-RM, 90% 1-RM, and 110 % 1-RM groups. 25244 IU  l71) among participants after eccentric 530
exercise. Because of the small number of participants
475 Baseline (IU  l71) Peak (IU  l71) in each group in the present study, the power to
detect a potential difference among groups might
CONTROL 187 (117–210) 238 (153–356)
50% 1-RM 213 (43–200) 535 (109–919)* have been limited. However, it appears that the
75% 1-RM 157 (91–201) 668 (192–1353)* results of the present study support the hypothesis 535
90% 1-RM 178 (118–241) 311 (240–518)* that the magnitude of muscle soreness after a bench
480 110% 1-RM 151 (49–205) 623 (317–3110)* press exercise is not dependent on the intensity when
*Significant (P 5 0.05) difference from baseline value.
total volume is matched.
Nosaka and Newton (2002) reported that muscle
soreness with extension of the elbow joint was 540
approximately 50% greater for maximal intensity
485 compared with sub-maximal (50% of the maximal)
eccentric exercise of the elbow flexors, but no
significant difference in muscle soreness with palpa-
tion was evident between conditions. In the present 545
study, muscle soreness with extension was not
490 assessed, but the palpation assessment did not show
any significant difference among the exercise groups,
which is in line with the findings of Nosdaka and
Newton (2002). Paschalis et al. (2005) reported no 550
significant difference in DOMS between high-in-
495 Figure 2. Serum PGE2 concentration (mean + s) at baseline (pre) tensity (12 sets of 10 maximal eccentric contractions)
and 24, 48, and 72 h after bench press exercise for the control, and low-intensity (continuous eccentric contractions
50% 1-RM, 75% 1-RM, 90% 1-RM, and 110% 1-RM groups.
*Significantly (P 4 0.05) higher values for the 110% 1-RM group
at 50% of the maximal eccentric torque) quadriceps
compared with the other exercise groups. eccentric exercise, where the total work of the two 555
exercise protocols was the same. This was supported
500 by the present study, which confirmed that the
intensity of muscle contractions was not a main
kinase activity (r ¼ 0.28, P ¼ 0.08). However, a weak factor determining the magnitude of DOMS. There-
but significant (P ¼ 0.03) correlation was found fore, it can be assumed that the total volume rather 560
between peak muscle soreness and peak PGE2 than the intensity determines the magnitude of
505 concentration (r ¼ 0.41). DOMS. It should be noted that an exercise with
repetitive low-intensity contractions also results in
DOMS, as shown in endurance events such as the
Discussion
marathon (Nieman et al., 2005; Vickers, 2001). This 565
The main findings of the present study were as also suggests that intensity of exercise is not a
510 follows: First, DOMS developed significantly after primary factor determining the magnitude of
bench press exercise, but no marked difference in the DOMS.
magnitude of DOMS was evident among the 50% It has been documented that the magnitude of
1-RM, 75% 1-RM, 90% 1-RM, and 110% 1-RM muscle soreness does not necessarily reflect the 570
 6 M. C. Uchida et al.

Table IV. The numbers of participants (n) with detectable concentrations of IL-1b, IL-6, and TNF-a, and the mean (and range)
concentrations of cytokines at baseline and 24, 48, and 72 h after exercise for the control, 50% 1-RM, 75% 1-RM, 90% 1-RM, and 110 % 1-
RM groups.
630
Baseline 24 h 48 h 72 h
575 mean (range); n mean (range); n mean (range); n mean (range); n

IL-1b (pg  ml71) Control 1.7 (0.1–3.5); 6 1.0 (0.1–2.0); 6 2.1 (0.3–3.2); 5 1.6 (0.5–2.9); 6
50% 1-RM 1.1 (0.1–3.0); 6 1.3 (0.4–4.1); 6 0.5 (0.1–0.7); 6 0.7 (0.1–1.7); 6
75% 1-RM 1.1 (0.2–3.4); 5 1.8 (0.8–3.9); 3 1.4 (0.3–2.6); 2 1.4 (0.7–3.2); 4 635
90% 1-RM 1.6 (0.5–0.9); 3 1.5 (0.8–2.0); 4 0.4 (0.1–0.6); 4 1.4 (0.5–2.7); 4
580 110% 1-RM 0.7 (0.6–0.7); 2 0.7 (0.7–0.9); 5 1.2 (0.9–1.5); 2 0.5 (0.1–0.8); 4
IL-6 (pg  ml71) Control 2.8 (1.1–6.0); 3 2.2 (0.1–6.5); 4 2.1 (0.8–3.2); 4 2.3 (0.7 –6.1); 4
50% 1-RM 2.2 (0.3–4.1); 3 1.5 (0.1–4.0); 3 4.0 (4.0); 1 2.0 (2.0); 1
75% 1-RM 2.8 (1.0–7.0); 6 2.2 (0.6–6.2); 6 1.8 (0.1–3.6); 6 2.6 (1.4–4.5); 6 640
90% 1-RM 1.5 (0.4–3.3); 5 1.9 (0.1–4.6); 4 1.6 (0.1–5.5); 5 1.4 (0.1–4.3); 5
110% 1-RM 1.9 (0.6–5.6); 5 2.0 (0.1–5.7); 5 1.8 (0.5–3.5); 4 1.4 (0.1–3.1); 5
585
TNF-a (pg  ml71) Control 2.6 (0.9–5.3); 6 1.7 (0.1–4.3); 6 2.0 (0.8–4.5); 6 1.8 (0.1–4.0); 6
50% 1-RM 2.1 (0.2–4.3); 8 1.5 (0.6–4.7); 7 1.6 (0.5–4.0); 7 1.5 (0.1–2.7); 8
75% 1-RM 1.3 (0.4–2.4); 7 1.0 (0.4–2.0); 7 1.3 (0.9–2.0); 7 1.7 (0.5–3.8); 7
90% 1-RM 1.4 (0.1–4.6); 6 1.7 (0.4–4.2); 6 1.4 (0.2–3.4); 6 1.3 (0.4–2.2); 6 645
110% 1-RM 2.0 (0.7–3.6); 5 2.3 (0.3–5.6); 6 2.6 (0.2–6.4); 6 1.5 (0.3–2.8); 6
590

650

595

655

600

660

605

665

610

670

615

675
Figure 3. Correlation between peak muscle soreness and peak creatine kinase (CK) activity (3A), peak muscle soreness and peak PGE2
620 concentration (3B), and peak PGE2 concentration and peak CK activity for the exercise groups (3C) (n ¼ 29).

magnitude of muscle damage (Nosaka et al., 2002a;
Warren, Lowe, & Armstrong, 1999). In the present
625 study, only plasma creatine kinase activity was used
as a marker of muscle damage, and it has been
questioned whether creatine kinase activity in the
blood can be used as a quantitative marker of 680
muscle damage, mainly because of a large variability
in the creatine kinase response (Clarkson et al.,
1992). In the present study, we also found a large
variability in changes in plasma creatine kinase

685 activity following exercise. As mentioned earlier, the
small number of participants in each group is a
limitation of the present study. However, it is
important to note that the magnitude of increase
in plasma creatine kinase activity after the bench
690 press exercise was not large, and no significant
difference in the changes was evident among the
exercise groups (Table III). This might indicate that
the magnitude of muscle damage was not different
among the four intensities, even if creatine kinase
695 was not sensitive enough to reflect a difference in
the magnitude of muscle damage. Furthermore, a
weak correlation between peak muscle soreness
and peak creatine kinase activity was observed
(Figure 3A). This supports the work of Nosaka
700 et al. (2002a), who reported a weak correlation
between muscle soreness and plasma creatine kinase
activity after eccentric exercise of the elbow flexors.
Even if the magnitude of damage to contractile
properties is dependent on the intensity of exercise,
705 it is unlikely that the magnitude of muscle soreness
is dependent on the magnitude of muscle fibre
damage. Malm et al. (2000) have documented that
DOMS may not be directly associated with damage
and inflammation of muscle fibres, but is due to
710 inflammation of connective tissue. It may be that
damage to connective tissue was not substantially
different among the intensities of bench press
exercise. Further studies are necessary to address
such speculation.
715 It has been proposed that the inflammatory
process contributes to the development of DOMS
(Cheung et al., 2003). Prostaglandin E2 is one of the
key molecules in the inflammatory responses, acting
as a potent vasodilator and synergistically with other
720 mediators such as histamine and bradykinin to
increase vascular permeability (Davies, Bailey, Gold-
enberg, & Ford-Hutchinson, 1984) and as a hyper-
algesic substance (Dinarello, Gatti, & Bartfai, 1999).
Tegeder et al. (2002) showed that the release of
725 PGE2 was associated with DOMS using a micro-
dialysis technique. Trappe and colleagues (Trappe,
Fluckey, White, Lambert, & Evans, 2001) demon-
strated that muscle PGE2 content was augmented
(*60%) after eccentric exercise of the knee exten-
730 sors. These findings suggest that PGE2 released
locally in the muscle is associated with DOMS;
however, previous studies (Croisier et al., 1996;
Hirose et al., 2004; Peake et al., 2005) failed to
demonstrate increases in PGE2 in the blood after
735 eccentric exercise resulting in muscle damage. In
contrast, the present study found a significant
increase in plasma PGE2 concentration after the
bench press exercise (Figure 2), and a weak but
significant correlation between peak DOMS and
740 peak PGE2 concentration (Figure 3B). This discre-
pancy might be related to the type of exercise
Intensity of load and delayed-onset muscle soreness 7
performed in the studies involving different muscle
mass and exercise volume.
It should be noted that the increase in serum PGE2
concentration was significantly greater for the 110% 745
1-RM group compared with the other groups
(Figure 2). The PGE2 response observed in the
110% 1-RM group might be related to the greater
mechanical stress induced by the protocol. The
110% 1-RM group performed only eccentric actions, 750
thus it is possible to speculate that the greater
mechanical stress was associated with the greater
increase in PGE2. In fact, previous in vitro studies
demonstrated that mechanical stress induced by
stretching increased PGE2 production in tendon 755
fibroblasts (Wang et al., 2003; Yang, Im, & Wang,
2005).
The present study did not detect any changes in
IL-1b, IL-6 or TNF-a, which supports the results of
previous studies (Hirose et al., 2004; Peake, Nosaka, 760
Muthalib, & Suzuki, 2006) reporting no significant
changes in these cytokines after eccentric exercise of
the elbow flexors. In addition, plasma concentrations
of IL-1b, IL-6, and TNF-a were not detectable for
some participants even after exercise. It appears that 765
muscle damage and inflammation induced by
resistance exercise do not result in large increases
in pro-inflammatory cytokines as endurance exercise
does (Bassit et al., 2008; Santos, Bassit, Caperuto, &
Costa Rosa, 2004; Trappe et al., 2001). It is 770
reasonable to assume that factors other than muscle
damage, such as duration of exercise, energy
requirement, and oxidative stress, determine the
magnitude of the cytokine response (Peake et al.,
2005). Peake and colleagues (2005) reported that 775
increases in anti-inflammatory cytokines (e.g. IL-1ra,
IL-10, IL-12p40) were markedly greater after high-
intensity running than either low-intensity running
or downhill running, and concluded that exercise
intensity rather than exercise-induced muscle da- 780
mage appears to be responsible for inflammatory
cytokine production. In a recent study, Prokopchuk
et al. (2007) showed that muscle gene expression of 1
cytokines (IL-4, IL-13, IL-4Ra and IL-13Ra) is up-
regulated after resistance exercise, and a higher 785
intensity protocol results in greater cytokine re-
sponses than a sub-maximal intensity one. In the
present study, no increases in the cytokines were
observed even after the highest intensity exercise
(110% 1-RM) (Table IV). It is likely that cytokine 790
responses to exercise in the muscles are not
necessarily detected in the blood.
In conclusion, the results of the present study
suggest that the bench press exercise intensity per se
did not influence the magnitude of DOMS and 795
blood markers of muscle damage and inflammation
when the total volume was equal. Therefore, even
low-intensity resistance exercise might induce
 8 M. C. Uchida et al.
DOMS and muscle damage when total volume is
800 matched to a high-intensity resistance exercise.
Besides exercise intensity, the design of resistance
training programmes should also consider total
volume as a potential cause of muscle damage and
DOMS. No muscle function measure was used in
805 the present study to assess muscle damage. Future
research should include a muscle function measure,
and increase the number of participants to confirm
the results of the present study.
810
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