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Curcumin supplementation likely attenuates delayed onset muscle soreness (DOMS)

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Oral curcumin decreases inflammatory cytokines and increases muscle regeneration in mice. To determine effects of curcumin on muscle damage, inflammation and delayed onset muscle soreness (DOMS) in humans. Seventeen men completed a double-blind randomized-controlled crossover trial to estimate the effects of oral curcumin supplementation (2.5 g twice daily) versus placebo on single-leg jump performance and DOMS following unaccustomed heavy eccentric exercise. Curcumin or placebo was taken 2 d before to 3 d after eccentric single-leg press exercise, separated by 14-d washout. Measurements were made at baseline, and 0, 24 and 48-h post-exercise comprising: (a) limb pain (1-10 cm visual analogue scale; VAS), (b) muscle swelling, (c) single-leg jump height, and (d) serum markers of muscle damage and inflammation. Standardized magnitude-based inference was used to define outcomes. At 24 and 48-h post-exercise, curcumin caused moderate-large reductions in pain during single-leg squat (VAS scale -1.4 to -1.7; 90 %CL: ±1.0), gluteal stretch (-1.0 to -1.9; ±0.9), squat jump (-1.5 to -1.1; ± 1.2) and small reductions in creatine kinase activity (-22-29 %; ±21-22 %). Associated with the pain reduction was a small increase in single-leg jump performance (15 %; 90 %CL ± 12 %). Curcumin increased interleukin-6 concentrations at 0-h (31 %; ±29 %) and 48-h (32 %; ±29 %) relative to baseline, but decreased IL-6 at 24-h relative to post-exercise (-20 %; ±18 %). Oral curcumin likely reduces pain associated with DOMS with some evidence for enhanced recovery of muscle performance. Further study is required on mechanisms and translational effects on sport or vocational performance.
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Eur J Appl Physiol (2015) 115:1769–1777
DOI 10.1007/s00421-015-3152-6
Curcumin supplementation likely attenuates delayed onset muscle
soreness (DOMS)
Lesley M. Nicol1 · David S. Rowlands2 · Ruth Fazakerly3 · John Kellett4
Received: 4 November 2014 / Accepted: 11 March 2015 / Published online: 21 March 2015
© Springer-Verlag Berlin Heidelberg 2015
(1.0 to 1.9; ±0.9), squat jump (1.5 to 1.1; ± 1.2)
and small reductions in creatine kinase activity (22–
29 %; ±21–22 %). Associated with the pain reduction was
a small increase in single-leg jump performance (15 %;
90 %CL ± 12 %). Curcumin increased interleukin-6 con-
centrations at 0-h (31 %; ±29 %) and 48-h (32 %; ±29 %)
relative to baseline, but decreased IL-6 at 24-h relative to
post-exercise (20 %; ±18 %).
Conclusions Oral curcumin likely reduces pain associ-
ated with DOMS with some evidence for enhanced recov-
ery of muscle performance. Further study is required on
mechanisms and translational effects on sport or vocational
Keywords Performance · Eccentric exercise ·
Inflammation · Recovery · Visual analogue scale
AP-1 Activator protein 1
AIS Australian Institute of Sport
CK Creatine kinase
COX-2 Cyclooxygenase 2
DOMS Delayed onset muscle soreness
DNA Deoxyribonucleic acid
NF kappa B Nuclear factor kappa beta
IL-6 Interleukin 6
1RM One repetition maximum
TNF-alpha Tumour necrosis factor alpha
VAS Visual analogue scale
DOMS is pain or discomfort that occurs after unaccus-
tomed or high intensity eccentric exercise (Cheung et al.
Introduction Oral curcumin decreases inflammatory
cytokines and increases muscle regeneration in mice.
Purpose To determine effects of curcumin on muscle
damage, inflammation and delayed onset muscle soreness
(DOMS) in humans.
Method Seventeen men completed a double-blind ran-
domized-controlled crossover trial to estimate the effects
of oral curcumin supplementation (2.5 g twice daily) ver-
sus placebo on single-leg jump performance and DOMS
following unaccustomed heavy eccentric exercise. Cur-
cumin or placebo was taken 2 d before to 3 d after eccen-
tric single-leg press exercise, separated by 14-d washout.
Measurements were made at baseline, and 0, 24 and 48-h
post-exercise comprising: (a) limb pain (1–10 cm visual
analogue scale; VAS), (b) muscle swelling, (c) single-leg
jump height, and (d) serum markers of muscle damage and
inflammation. Standardized magnitude-based inference
was used to define outcomes.
Results At 24 and 48-h post-exercise, curcumin caused
moderate-large reductions in pain during single-leg squat
(VAS scale 1.4 to 1.7; 90 %CL: ±1.0), gluteal stretch
Communicated by Michael Lindinger.
* David S. Rowlands
1 SportsMed Canterbury, 156 Bealey Avenue,
Christchurch, New Zealand
2 School of Sport and Exercise, Massey University,
63 Wallace St, Wellington, New Zealand
3 Department of Sports Medicine, Australian Institute of Sport,
Canberra, Australia
4 62 Springfield Drive, Hawker, ACT, Australia
1770 Eur J Appl Physiol (2015) 115:1769–1777
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2003; Connolly et al. 2003; Lund et al. 1998; MacIntyre
et al. 1995). DOMS is caused by muscle damage, which
has associated symptoms of muscle shortening, increased
passive stiffness, decreases in strength and power, localized
soreness and disturbed proprioception (Proske and Morgan
2001). Symptoms can present from post-exercise and typi-
cally subside after 3–4 days (Clarkson and Sayers 1999).
Reducing the negative effects of DOMS may maximise
training and performance gains as well as prevent injury
(Armstrong 1984; Eston and Peters 1999; Johansson et al.
1999; Sellwood et al. 2007).
Curcumin (diferuloylmethane) is an extract from the
root of the curcuma plant, commonly known as turmeric
root. Curcumin gives the spice turmeric its distinctive yel-
low colour. Previously used in Chinese (Itokawa et al.
2008) and Indian medicine, curcumin has documented
anti-inflammatory, anticarcinogenic and antioxidant prop-
erties (Maheshwari et al. 2006; Menon and Sudheer 2007;
Itokawa et al. 2008). It affects cytokine-mediated path-
ways by inhibiting NF kappa B, AP-1 binding to DNA and
decreasing the production of the enzyme COX-2, all of
which play a pivotal role in the inflammatory cascade (Tha-
loor et al. 1999; Davis et al. 2007).
Animal studies have shown that curcumin can increase
muscle regeneration and improve behaviours associated with
DOMS in mice (Davis et al. 2007). Systemic treatment with
curcumin led to faster restoration of normal muscle archi-
tecture when given to mice after local tissue injury (Thaloor
et al. 1999). In a study by Thaloor et al. (1999), mice mas-
seter muscles were subjected to freeze injury, and those mice
injected intraperitoneally with curcumin daily for 10 days,
until sections were removed, showed large centrally nucle-
ated recovering fibres in the site of damage; whereas the
controls were devoid of regenerating fibres. Davis et al.
(2007) treated mice with oral curcumin 3 days prior to
downhill running and the curcumin-treated mice were able
to run significantly longer before fatigue at 48 and 72 h and
exhibited more spontaneous activity than the mice on pla-
cebo. Curcumin-treated mice also had statistically significant
decreased IL-6, TNF-alpha concentrations at 24 and 72 h and
CK activity at 24 h, compared to those treated with placebo.
To our knowledge, no studies have quantified the effect
of curcumin on DOMS or measured muscle performance
in humans using a robust, adequately powered double-blind
placebo-controlled experimental design (Drobnic et al.
2014). The aim of this study was to evaluate the effect of
oral curcumin compared to placebo on DOMS, using a dou-
ble-blind randomized-controlled unilateral crossover trial.
Functional and physical symptoms of DOMS and the recov-
ery of performance were assessed in a cohort of healthy,
active men. It was hypothesised that curcumin would lead
to worthwhile effect size reductions in leg pain percep-
tion, swelling, systemic markers of muscle damage and
inflammation and maintain the vertical jump performance
after eccentric loading exercise designed to produce DOMS.
A total of 19 healthy men aged 18–39 y were recruited
into the study. Participants were undertaking light to mod-
erate regular physical activity including sports training
e.g. social football and basketball, but not doing lower
limb resisted exercise (mean ± SD endurance training
2.5 ± 2.2 h week1, team training 1.1 ± 1.6 h week1).
Two withdrew from the study following acceptance due to
the inability to attend testing commitments, and no replace-
ments were added due to resource constraints. The remain-
ing 17 subjects had an age 33.8 ± 5.4 year and weight
83.9 ± 10.0 kg (height not measured). Fifteen subjects had
a dominant right leg and two a dominant left leg.
Double-blind randomized-controlled unilateral-leg crosso-
ver trial was performed to compare the effects of taking
oral curcumin versus placebo on single-leg jump perfor-
mance and the levels of markers associated with DOMS
after a bout of unaccustomed leg press exercise (Fig. 1).
All subjects completed two experimental trials separated
by at least 14 days. Randomization was applied to both the
order of treatment or placebo and to the sequence of right
or left leg use within the unilateral crossover. Exclusion
criteria comprised regular leg weight training in the prior
3 months, current lower limb musculoskeletal injury, cur-
rent use of non-steroidal anti-inflammatory drugs and neu-
rological disease involving the lower limb. The AIS ethics
committee approved the study and all participants provided
written informed consent. All outcome assessments were
carried out at the AIS Sports Medicine Department.
Randomization and masking
The randomization sequence was generated using a random
numbers table ( Allocation
was concealed using sequentially numbered medication.
Investigators and participants were blinded by provision of
the medications by AIS nursing staff according to the rand-
omization protocol.
Eccentric exercise protocol
Participants performed a muscle damaging protocol con-
sisting of seven sets of ten eccentric single-leg press
1771Eur J Appl Physiol (2015) 115:1769–1777
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repetitions on a leg press machine (Vaile et al. 2008a).
A single episode of eccentric exercise can have an effect
on blood chemistry responses, muscle soreness and per-
formance if the exercise is repeated within a few weeks
(Brown et al. 1997; Byrnes and Clarkson 1986; Mair et al.
1995; Nosaka et al. 2001). Therefore, alternate legs were
used for placebo and treatment.
The 1RM weight lifted concentrically was determined
for each participant on protocol day 3 (Fig. 1). An eccentric
loading protocol developed previously was used to induce
DOMS (Vaile et al. 2007, 2008a). 120 % of the one rep-
etition maximum was calculated on day one of the study
and used for the weight lowered eccentrically. On proto-
col day 3 (Fig. 1), each participant performed 5 sets of 10
repetitions at 120 % 1RM and 2 sets of 10 repetitions at
100 % 1RM. 1RM was performed on each leg individually
and each participant completed all 7 sets. The same proto-
col has been used to induce DOMS previously (Vaile et al.
2007, 2008a). During each eccentric contraction the load
was resisted with the allocated leg from full knee extension
to 90° angle of knee flexion with the eccentric contraction
lasting for 3–5 s duration. After each eccentric contraction
the load was raised by the subject, using both legs concen-
trically. Participants had a 3 min rest between sets.
Participants swallowed with water 5 sealed identical
opaque capsules containing either 2.5 g curcumin or pla-
cebo (2.5 g Avicel 105, an inert plant cellulose) twice daily
for 2.5 days prior to exercise, then 5 capsules twice daily
for 2.5 days after exercise. The capsules were prepared by
a pharmacist using a specific protocol. The constituents of
the curcumin used were bisdemethoxycurcumin 29 mg tab-
let1; demethoxycurcumin 62.7 mg tablet1 and curcumin
964 mg tablet1, with total curcuminoids 1,060 mg tablet1
(Eurofins Scientific Inc, Petaluma, CA). The dose was cal-
culated from the previous mice experiments, taking human
size and safety into account (Davis et al. 2007). There is
no treatment related toxicity evident for daily doses of cur-
cumin of 8 g for 3 months (Hsu and Cheng 2007). Sub-
jects were advised not to carry out any leg weight training
during the testing periods but were asked to continue their
usual physical activity. Subjects were asked at the comple-
tion of the study whether they thought they could identify
if they were taking curcumin or placebo. The participants
reported that they could not distinguish between the treat-
ment and placebo.
Outcome measures
All outcome measures were recorded during familiarisation
and at baseline, immediately post the eccentric exercise, 24
and 48 h after the exercise (Fig. 1).
Muscle pain A VAS was used to measure quadriceps and
gluteal skeletal muscle pain before and after the eccentric
exercise. The VAS was a horizontal 10 cm line, marked
with 1–10 with the terminal descriptors no pain and severe
pain as used previously to monitor changes in perceived
pain following muscle damaging protocols (Vaile et al.
2007, 2008a; Sellwood et al. 2007; Johansson et al. 1999;
Cleak and Eston 1992; Harrison et al. 2001). Pain was rated
for single-leg squat, walking downstairs, passive stretch of
the quadriceps, passive stretch of the gluteals and single-
leg vertical jump. Muscle pain was assessed before muscle
1 2 3 4 5
~14 d Washout
1 2
Day number
1RM Tesng
3 4 5
Muscle damage
24 H 48 H
Baseline Post
Experimental Block 1
procedures: Curcumin Supplementaon
1 2 3 4 5
Experimental Block 2
Day number
Fig. 1 Experimental design
1772 Eur J Appl Physiol (2015) 115:1769–1777
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Muscle tenderness Tenderness was assessed using a
somedic pressure algometer (Somedic, Sollentuna, Swe-
den) at 4 standardized points. The quadriceps points were
marked on the anterior thigh along a line drawn from the
anterior superior iliac spine to the superior pole of the
patella. One point was at the midpoint of this line (mid
belly rectus femoris) and the other at 5 cm above the supe-
rior pole of the patella (musculotendinous junction). These
Quadriceps points have been used previously in DOMS
research (Sellwood et al. 2007). The first gluteal point was
at the midpoint of a line drawn from the posterior superior
iliac spine and greater trochanter and second at the mid-
point of a line drawn from the PSIS to the ischial tuber-
osity. The points were marked at baseline with an indel-
ible marker pen. Participants were asked to state when the
pressure became unbearable and a force reading was made
from the algometer. One measurement was made, due to
the increasing pain associated with repeated measurements.
Swelling A non-stretch anthropometric measuring tape
was used to measure swelling at three standardized points
on the upper leg. The first point was 5 cm above the supe-
rior pole of the patella, the second at the midpoint of a line
drawn between the proximal pole of the patella and anterior
superior iliac spine (Sellwood et al. 2007) and the third at
the sub gluteal line.
Jump performance Single-leg vertical squat jump was
used to assess the effect of curcumin on quadriceps and
gluteal function. The jump and reach method using Vertec
(Vertec, Vertec Sports Imports, Hilliard, OH) was used to
assess vertical jump performance. The maximum height
obtained from three jumps was recorded. Vertical jump per-
formance is an index of muscle power of the lower limbs.
Muscle damage and inflammation Serum samples were
obtained for CK activity, as a marker of muscle damage
(Vaile et al. 2007; Eston and Peters 1999), and for candi-
date curcumin-modulated inflammatory markers IL-6 and
TNF-alpha (Davis et al. 2007; Thaloor et al. 1999; Mahesh-
wari et al. 2006). Blood samples were collected in 9-ml
serum separator tubes, left to clot, then spun at 4500 RPM
for 5 min, with resulting serum aliquoted into four, 2 ml
cryotubes and frozen immediately at 80 °C until analy-
sis. TNF-alpha and IL-6 were analysed by chemilumines-
cent immunometric assay (Immulite 1, Siemens, Erlangen,
Germany). CK activity was by wet chemistry (Hitachi 911,
Roche, Boehringer, Germany).
Sample size Sample size was calculated using magnitude-
based clinical inference (Hopkins et al. 2009). In the
absence of empirical data, the smallest effect size of 0.2
times mean sample variation (SDbetween) in VAS of 16 on
a 0–100 scale (Gaston-Johansson and Gustafsson 1990)
was used as the value for the smallest meaningful change,
with test–retest reliability calculated from Pearson r = 0.88
(Gaston-Johansson and Gustafsson 1990), where test–retest
reliability equals the square root of (1 r) times SDbetween.
The calculations resulted in n = 19.
General method Estimates and uncertainty (90 % con-
fidence interval) for the effect of treatment on outcomes
were derived from a mixed model analysis of variance
(Proc mixed, SAS 9.0, Cary, NC). Fixed effects were time
and order of treatment within the crossover interacted with
treatment to account for possible systemic repeated bout
effect. The random effects were subject and the subject
treatment interaction. All data except VAS were log-trans-
formed prior to analysis to manage non-uniformity of error.
Subject descriptive and VAS outcome data in line graphs
are raw means and standard deviations. Unless otherwise
noted, mean effects derived from the analysis of log-trans-
formed variables are back log-transformed least-squares
means or geometric adjusted means. All data are rounded
to 2 significant figures.
Statistical inference The standardized effect sizes (cur-
cumin-placebo/appropriate reference value for placebo)
were interpreted using magnitude-based inference (Batter-
ham and Hopkins 2006). Statements about the mixed model
estimate of the true (large sample) value of effects were
qualified using a modified Cohen’s d effect size (trivial,
0.0–0.2; small, 0.2–0.6; moderate, 0.6–1.2; large, 1.2–2.0;
very large, >2.0); in this scheme, the threshold for small-
est substantial effect size was 0.2 (Hopkins et al. 2009).
Uncertainly around the estimated standardized effect sizes
was assigned a qualitative term for the following probabil-
ity bins: <0.5 %, almost certainly not; <5 %, very unlikely;
<25 %, unlikely; <75 %, possible; >75 %, likely; >95 %,
very likely; >99.5 %, almost certain (Hopkins et al. 2009).
An effect was unclear if the uncertainty (confidence inter-
val) included both substantial increases and decreases (i.e.
>5 %) (Hopkins et al. 2009). Readers are referred else-
where for published descriptions, examples, and statisti-
cal rationale for magnitude-based inference (Rowlands
et al. 2008a, 2014 ; Batterham and Hopkins 2006; Hopkins
Muscle pain and swelling
All pain outcome measures showed an increase in VAS
score from baseline at 24 and 48 h post indicating the exer-
cise loading protocol was effective at producing DOMS
(Fig. 2). Curcumin was associated with likely moderate
to large effect size reductions in single-leg squat and glu-
teal stretch pain at 24 and 48 h, relative to baseline and/
1773Eur J Appl Physiol (2015) 115:1769–1777
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or post-eccentric exercise; the effect size on gluteal stretch
pain at 48 h was moderate, relative to the change at 24 h.
Pain on walking down stairs was moderately reduced at
48 h (Table 1; Fig. 2). In contrast, pain upon stretching
quadriceps muscle was not clearly affected by curcumin
supplementation. At 24 and 48 h, curcumin generated mod-
erate reductions in pain during the vertical jump, relative to
post-eccentric exercise (Table 1; Fig. 2). The effect of cur-
cumin on swelling and pain-pressure algometry outcomes
were trivial or inconclusive (not shown for brevity).
Single‑leg jump performance
Curcumin increased first jump height by a likely
small magnitude from post-exercise to 24 h (15.4 %;
90 %CL ± 11.6 %) and 48 h (15.8 %; ±11.6 %), where
the threshold for smallest important effect was 9.3 %. How-
ever, all other jump contrasts were trivial (contrasts not
shown for brevity).
Muscle damage and inflammation
Curcumin had a likely small lowering impact on serum
CK activity at 24 h (22 %; 90 %CL ± 22 %) and 48 h
(29 %; ±21 %) post-exercise relative to baseline. Mean-
while, curcumin increased (likely small standardized dif-
ferences) serum IL-6 immediately post-exercise (31 %;
±29 %) and again at 48-h post-exercise (32 %; ±29 %)
relative to baseline, but decreased IL-6 at 24-h relative to
post-exercise (20 %; ±18 %). Curcumin had no impact
on TNF-alpha concentrations (Fig. 3).
The main finding from the current study was that cur-
cumin supplementation caused moderate to large-sized
reductions in DOMS-related leg–muscle pain symptoms at
several sites, which was associated with lower blood CK
and higher blood IL6. There was also some evidence for
improved muscle performance (measured by increased first
jump height) at 24–48 h post-eccentric exercise, but other
jumps were trivial so more work is required to clarify the
nature of the effect on performance. To the authors’ knowl-
edge, this is the first double-blind within-subject controlled
randomized trial to evaluate the effect of practical quanti-
ties of oral curcumin on DOMS in human subjects and pro-
vides new information on possible utility of the nutrient in
sports and rehabilitation.
The results suggest that curcumin has potential to be
part of the nutritional intake of individuals wishing to lower
post-exercise soreness, which may hasten return to effec-
tive training. In a recent single-blind pilot study on a novel
delivery method of curcumin, human subjects had signifi-
cantly less pain and less muscle damage on MRI than con-
trols (Drobnic et al. 2014). Other nutritional supplements
with antioxidant or anti-inflammatory properties have also
been shown to lower post-exercise muscle soreness and
damage markers. These supplements include: dairy protein
(Rowlands et al. 2008b; Saunders 2007; Cockburn et al.
2008; Cooke et al. 2010) and tart cherries (Howatson et al.
2009; Kuehl et al. 2010). Other supplements with antioxi-
dant or anti-inflammatory properties include exotic ber-
ries (acai, goji), quercetin, green tea and fish oils; however,
there appears to be reduced translation in benefits from
rodents to well-trained humans (Nieman et al. 2012). Com-
parably, variable results in reduction in DOMS have been
shown with massage (Cheung et al. 2003). No effect has
Walk downstairs
Single leg vercal jump
Stretch gluteal
Stretch quadriceps
Single leg squat
24 h 48 h 24 h 48 h
Baseline Post-
Baseline Post-
*** **
Fig. 2 Effect of curcumin supplementation on measures of leg pain
in the 48 h period following recovery from eccentric exercise. All
data are the mean change from baseline for VAS scale units with bars
representing the SD. The qualified threshold for smallest substantial
change in outcome in response to treatment is the 0.2 × baseline
SDbetween. A magnitude-based summary of statistical contrasts is in
Table 1. To assist with identification of likely effects of treatment,
the probability of substantial change is reproduced from Table 1 via
inclusion above the time point for the respective contrast denoted by
the unique symbol: relative to baseline +; relative to post-exercise,
*. Accordingly, qualified likelihood was shown as increased number
of symbols (*used for example): *possible, **likely, ***very likely,
****most likely
1774 Eur J Appl Physiol (2015) 115:1769–1777
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been shown with stretching, cryotherapy, electrical modali-
ties, homoeopathy and ultrasound (Cheung et al. 2003).
Curcumin was hypothesised to lower DOMS through
an anti-inflammatory mechanism. Unlike in the earlier ani-
mal studies referred to above, the effect of curcumin on
TNF-alpha was inconclusive and IL6 variable. The small
reduction in blood CK at 24 and 48 h post-exercise with
curcumin, however, is in keeping with our hypothesis for
lower muscle damage and suggests the effect of curcumin
may support restoration of membrane integrity as a compo-
nent of improved recovery from muscle damage. The small
possible changes in CK, inconclusive effect of TNF and
IL6 suggests that only minimal muscle damage was caused
by the eccentric protocol. The peak median CK increase of
200 % from baseline, increase in CK at 24 and 48 h in both
control and curcumin-treated subjects indicates that the
eccentric protocol may have caused muscle trauma, often
associated with DOMS (Vaile et al. 2008b); however, other
studies have shown peak increases up to 600 % (Byrne and
Eston 2002a, b). TNF-alpha was also selected for analy-
sis in the current study because of its inhibitory effect on
muscle tissue repair following injury (Moresi et al. 2008).
The blunting of CK with curcumin treatment is in keeping
with a prior animal study (Davis et al. 2007) and suggests
the effect of curcumin is transient and related to improved
membrane integrity due to an effect on inflammatory or
other regeneration processes. Non-steroidal anti-inflam-
matory drugs have not been shown to alter DOMS or CK
following ultramarathon competition (Nieman et al. 2006),
suggesting curcumin might work via a mechanism separate
from inflammatory-mediated responses.
The relative lowering of IL-6 at 24-h post-exercise sup-
port the proposed anti-inflammatory action of curcumin,
however, the small increases IL-6 immediately post-exer-
cise and 48 h post-exercise prevent firmer conclusions.
Large increases in inflammatory cytokines in the work-
ing muscle, blood and possibly the brain were proposed
by other researchers to trigger DOMS (Willoughby et al.
2003a, b). Curcumin has been reported to block the activ-
ity of transcription factor NF-kappaB, reduce AP-1 bind-
ing to DNA as well as decreasing the production of COX-
2, all of which play a role in the inflammatory cascade
(Singh and Aggarwal 1995); (Davis et al. 2007; Thaloor
et al. 1999). Curcumin appears to target NF- kappaB as
opposed to COX-2, indicating the potential for less seri-
ous side effects than NSAIDs. (Davis et al. 2007). NF-
kappaB was not measured but should be included in future
research. The analgesic effect of curcumin is related to the
desensitisation or inhibition of transient receptor potential
ion channels (Di Pierro et al. 2013a). This analgesic effect
may have played a role in the reduction in pain in our sub-
jects. All VAS measures showed a reduction in pain except
quads stretch, which can be accounted for by the eccen-
tric exercise preferentially targeting the gluteal muscles.
The analgesic mechanism may also account for the likely
small increase in first jump performance followed by trivial
Table 1 Effect of curcumin supplementation on leg-muscle pain during lower limb exercise
a Effect of curcumin vs control derived from the analysis of the raw VAS scale units
b ±90 %CL: add and subtract this number to the mean effect to obtain the 90 % confidence limits for the true difference
c Threshold for substantial is the smallest standardized difference =0.2 times baseline standard deviation
d Symbols for the probability of a substantial change follow the magnitude-based descriptor
e Likely (>75 %)
f Very likely (>95 %)
g Most likely (>99.5 %)
Mean effect comparisons (scale units)a with ±90 %CLb and Inferenced
Variable Post-exercise baseline 24 h-baseline 48 h-baseline 24 h-post-exercise 48 h-post-exercise Thresholdc
Single-leg 0.9 ± 1.0 0.5 ± 1.0 0.8 ± 1.2 1.4 ± 1.0 1.7 ± 1.0
Squat ModerateeUnclear ModerateeLargefLargef0.22
Walk 0.3 ± 0.9 0.3 ± 0.6 1.0 ± 1.2 0.6 ± 1.2 1.3 ± 1.2
Downstairs Unclear Unclear Unclear Unclear V. Largef0.12
Gluteal 0.6 ± 0.9 0.3 ± 0.9 1.3 ± 0.8 1.0 ± 0.9 1.9 ± 0.9
Stretch Unclear Unclear ModeratefModerateeLargeg0.25
Quadriceps 0.1 ± 1.1 0.2 ± 0.9 0.3 ± 1.0 0.1 ± 0.8 0.2 ± 1.0
Stretch Unclear Unclear Unclear Unclear Unclear 0.41
Vertical 0.7 ± 1.2 0.8 ± 1.2 0.3 ± 1.2 1.5 ± 1.2 1.1 ± 1.2
Jump Unclear Unclear Unclear ModeratefModeratee0.27
1775Eur J Appl Physiol (2015) 115:1769–1777
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second and third jump performance; or alternatively, cur-
cumin could affect performance by an as yet-to-be-defined
regulatory mechanism acting on phosphocreatine availabil-
ity or metabolism.
Additionally, curcumin-lowered IL-1 beta content in the
brain, and it has been hypothesised that curcumin is capa-
ble of enhancing a behavioural response due to CNS effect
(Davis et al. 2007). This could account for the reduction in
pain measured by VAS by reducing the perceived discom-
fort. An in vitro study of human tenocytes has shown cur-
cumin-modulated NF- kappa B signalling via inhibition of
IL-1 beta (Buhrmann et al. 2011).
Inflammatory processes, such as activation of IL-1 beta
networks, are central to successful skeletal muscle regener-
ation response to injury (Tidball and Villalta 2010); regen-
eration is both pro-inflammatory and anti-inflammatory.
Therefore, suppression of transient inflammation by nutri-
tional supplementation might, in fact, be negative for
recovery from exercise-induced muscle trauma. Chronic
application of some other nutritional supplements with
antioxidant and inflammatory properties (e.g. vitamin C
and E) during a period of training attenuated performance
gains (Braakhuis et al. 2014; Nikolaidis et al. 2012); how-
ever, negative effect on training adaptation may not be the
case for all micronutrients (Braakhuis et al. 2013). There-
fore, future work should examine not only the effect of
reduced soreness relating to short-term restoration of train-
ing capacity, but also the long-term supplement-interaction
effect on training adaptation mechanisms and phenotype. In
contrast, beneficial effects of supporting exercise adherence
in clinical populations (e.g. diabetes, peripheral arterial dis-
ease) who suffer muscle pain and soreness associated with
exercise (Hirsch et al. 2001) may outweigh dampening of
signalling for adaptive stimuli (Di Pierro et al. 2013b).
A strength of this study is that it is a rigorous double-
blinded randomized design with a crossover of alternate
legs between subjects, to counter carryover of the response
to curcumin affecting the results in the subsequent experi-
mental block. To gain further analytical power, the treat-
ment effect on pain, power and algometry outcomes was
compared within-subject between legs. Additionally, the
within-block pre- and post-analysis cancel out the potential
influence of dominant and non-dominant leg effects on out-
comes. The current study also allowed for the evaluation of
the utility of curcumin as a potential treatment and preven-
tion for muscle soreness. Accordingly, we observed no side
effects experienced by the subjects while taking curcumin
and blinding was successful. Therefore, we conclude there
were no negative or harmful effects evident by taking the
current dose of curcumin.
A limitation of the current study was the use of an
algometer which indicated levels to the subject, potentially
influencing the outcome and could account for the trivial
algometer results. Other limitations include sample time
points and inference to exercise mode. Including a meas-
urement at 72 h post-exercise would have added to the rig-
our of this research as muscle soreness following heavy
eccentric exercise can last up to 4 days. Prior studies on
treatment for DOMS have shown a drop-off in pain post-
exercise levels by 72 h (Vaile et al. 2008a; Sellwood et al.
2007) and this was the rationale for the last measurement
at 48 h. We chose a heavy eccentric exercise model shown
to induce muscle trauma inflammation (Vaile et al. 2007,
2008a) because it provided a proof-of-principle model.
However, we clearly acknowledge that not all sports or
physical activities have heavy eccentric contraction com-
ponents (e.g. cycling, swimming), and follow-up research
is required to verify if any benefits to lower muscle sore-
ness accrues in predominantly concentric-only exercise.
Serum CK (IU/L) TNF-alpha (mmol/L)
IL-6 (mmol/L)
11.5 Control
24 h
48 h
Baseline Post-
Fig. 3 Effect of curcumin supplementation on muscle damage and
inflammatory cytokines. Data are the mean change from baseline
with bars representing the SD. To assist with identification of likely
effects of treatment, the probability of substantial change is repro-
duced from Table 1 via inclusion above the time point for the respec-
tive contrast denoted by the unique symbol: relative to baseline +;
relative to post-exercise, *. Accordingly, qualified likelihood was
shown as increased number of symbols (*used for example): *pos-
sible, **likely, ***very likely, ****most likely
1776 Eur J Appl Physiol (2015) 115:1769–1777
1 3
Furthermore, well-trained individuals are less susceptible
to DOMS, warranting investigation in trained muscle to
determine if the magnitude of the pain reduction is also
of a worthwhile magnitude in the athlete cohort (Cheung
et al. 2003). The effect of curcumin on DOMS in females
should also be examined as oestrogen is thought to be mus-
cle protective (Dieli-Conwright et al. 2009; Enns and Tii-
dus 2010). The effect on military performance may also
be worthwhile, where soldiers are often exposed to heavy
eccentric loading during day-long activity (Cleak and Eston
1992). Finally, the use of various additives, for example,
biopirine and modified curcumin formulations to improve
absorption warrant investigation. Limited bioavailability is
seen in rats with a 2 g kg1 dose. The dose in the current
study is approximately 0.3 g kg1 calculated from previous
animal studies (Davis et al. 2007) and was shown to be well
tolerated, and therefore, practical. Nevertheless, it is pos-
sible that a larger effect size on DOMS and performance
recovery would be seen with a larger dose or using modi-
fied curcumin formulations to improve absorption.
In conclusion, 2.5 d of curcumin supplementation prior
to and following heavy eccentric exercise in healthy men
likely lowered subsequent pain associated with DOMS
and lowered a blood marker for muscle damage, but
with equivocal evidence for reduced systemic inflamma-
tion. These findings provide the first empirical evidence
to support the possibility of using curcumin to prevent
and combat DOMS associated with heavy exercise. Fur-
ther research is required to determine the mechanisms of
action, to quantify if the effect is great enough to provide
short-term worthwhile benefit to performance sports, mili-
tary and other activity causing skeletal muscle trauma, and
to assess curcumin’s effect on females and clinical popu-
lations. Other work should explore the effects of chronic
supplementation on training adaptation, to investigate the
possibility of attenuated exercise adaptation in sport and
clinical populations.
Acknowledgments Dr Greg Lovell, Bev Andersen, Jill Flanagan,
Dr Chris Rumball, Dr Kieran Fallon, and all staff at AIS Sports Medi-
cine Department. Funding from the Australian Institute of Sport. Dr
Lesley Nicol is a board member of Drug Free Sport New Zealand.
Other authors have no disclosures.
Armstrong RB (1984) Mechanisms of exercise-induced delayed
onset muscular soreness: a brief review. Med Sci Sports Exerc
Batterham AM, Hopkins WG (2006) Making meaningful inferences
about magnitudes. Int J Sport Physiol Perf 1(1):50–57
Braakhuis AJ, Hopkins WG, Lowe TE (2013) Effect of dietary
antioxidants, training, and performance correlates on antioxi-
dant status in competitive rowers. Int J Sports Physiol Perform
Braakhuis AJ, Hopkins WG, Lowe TE (2014) Effects of dietary anti-
oxidants on training and performance in female runners. Eur J
Sport Sci 14(2):160–168
Brown SJ, Child RB, Day SH, Donnelly AE (1997) Exercise-induced
skeletal muscle damage and adaptation following repeated bouts
of eccentric muscle contractions. J Sports Sci 15(2):215–222.
Buhrmann C, Mobasheri A, Busch F, Aldinger C, Stahlmann R,
Montaseri A, Shakibaei M (2011) Curcumin Modulates nuclear
factor κB (NF-κB)-mediated inflammation in human tenocytes
in vitro: role of the phosphatidylinositol 3-kinase/akt pathway. J
Biol Chem 286(32):28556–28566. doi:10.1074/jbc.M111.256180
Byrne C, Eston R (2002a) The effect of exercise-induced muscle
damage on isometric and dynamic knee extensor strength and
vertical jump performance. J Sports Sci 20(5):417–425
Byrne C, Eston R (2002b) Maximal-intensity isometric and dynamic
exercise performance after eccentric muscle actions. J Sports Sci
20(12):951–959. doi:10.1080/026404102321011706
Byrnes WC, Clarkson PM (1986) Delayed onset muscle soreness and
training. Clin Sports Med 5(3):605–614
Cheung K, Hume P, Maxwell L (2003) Delayed onset muscle sore-
ness: treatment strategies and performance factors. Sports Med
33(2):145–164. doi:10.2165/00007256-200333020-00005
Clarkson PM, Sayers SP (1999) Etiology of exercise-induced muscle
damage. Can J Appl Physiol 24(3):234–248
Cleak MJ, Eston RG (1992) Muscle soreness, swelling, stiffness and
strength loss after intense eccentric exercise. Br J Sports Med
Cockburn E, Hayes P, French D, Stevenson E (2008) St Clair Gib-
son A: acute milk-based protein-CHO supplementation attenu-
ates exercise-induced muscle damage. Appl Physiol Nutr Metab
Connolly DA, Sayers SP, McHugh MP (2003) Treatment and pre-
vention of delayed onset muscle soreness. J Strength Cond Res
Cooke M, Rybalka E, Stathis C, Cribb P, Hayes A (2010) Whey
protein isolate attenuates strength decline after eccentrically-
induced muscle damage in healthy individuals. J Int Soc Sports
Nutr 7(1):30
Davis JM, Murphy EA, Carmichael MD, Zielinski MR, Groschwitz
CM, Brown AS, Gangemi JD, Ghaffar A, Mayer EP (2007) Cur-
cumin effects on inflammation and performance recovery fol-
lowing eccentric exercise-induced muscle damage. Am J Physiol
Regul Integr Comp Physiol 292(6):R2168–R2173
Di Pierro F, Rapacioli G, Di Maio E, Appendino G, Franceschi F,
Togni S (2013a) Comparative evaluation of the pain-relieving
properties of a lecithinized formulation of curcumin (Meriva®),
nimesulide, and acetaminophen. J Pain Res 6:201–205
Di Pierro F, Rapacioli G, Di Maio EA, Appendino G, Franceschi F,
Togni S (2013b) Comparative evaluation of the pain-relieving
properties of a lecithinized formulation of curcumin (Meriva®),
nimesulide, and acetaminophen. J Pain Res 6:201–205.
Dieli-Conwright CM, Spektor TM, Rice JC, Sattler FR, Schroeder
ET (2009) Hormone therapy attenuates exercise-induced skel-
etal muscle damage in postmenopausal women. J Appl Physiol
Drobnic F, Riera J, Appendino G, Togni S, Franceschi F, Valle X,
Pons A, Tur J (2014) Reduction of delayed onset muscle sore-
ness by a novel curcumin delivery system (Meriva®): a ran-
domised, placebo-controlled trial. J Int Soc Sports Nutr 11:31
Enns DL, Tiidus PM (2010) The influence of estrogen on skeletal
muscle: sex matters. Sports Med 40(1):41–58
Eston R, Peters D (1999) Effects of cold water immersion on the
symptoms of exercise-induced muscle damage. J Sports Sci
1777Eur J Appl Physiol (2015) 115:1769–1777
1 3
Gaston-Johansson F, Gustafsson M (1990) Rheumatoid arthri-
tis: determination of pain characteristics and comparison
of RAI and VAS in its measurement. Pain 41(1):35–40.
Harrison BC, Robinson D, Davison BJ, Foley B, Seda E, Byrnes WC
(2001) Treatment of exercise-induced muscle injury via hyper-
baric oxygen therapy. Med Sci Sports Exerc 33(1):36–42
Hirsch AT, Criqui MH, Treat-Jacobson D, Regensteiner JG, Cre-
ager MA, Olin JW, Krook SH, Hunninghake DB, Comerota AJ,
Walsh ME, McDermott MM, Hiatt WR (2001) Peripheral arte-
rial disease detection, awareness, and treatment in primary care.
J Am Med Assoc 286(11):1317–1324
Hopkins WG (2006) Estimating sample size for magnitude-based
inferences. Sportscience 10:60–63
Hopkins WG, Marshall SW, Batterham AM, Hanin J (2009) Pro-
gressive statistics for studies in sports medicine and exer-
cise science. Med Sci Sports Exerc 41(1):3–13. doi:10.1249/
Howatson G, McHugh M, Hill J, Brouner J, Jewell A, van Someren
K, Shave R, Howatson S (2009) Influence of tart cherry juice on
indices of recovery following marathon running. Scand J Med
Sci Sports 20(6):843–852
Hsu CH, Cheng AL (2007) Clinical studies with curcumin. Adv Exp
Med Biol 595:471–480. doi:10.1007/978-0-387-46401-5_21
Itokawa H, Shi Q, Akiyama T, Morris-Natsche S, Lee K (2008)
Recent advances in the investigation of curcuminoids. Chin Med
Johansson PH, Lindstrom L, Sundelin G, Lindstrom B (1999) The
effects of preexercise stretching on muscular soreness, tender-
ness and force loss following heavy eccentric exercise. Scand J
Med Sci Sports 9(4):219–225
Kuehl K, Perrier E, Elliot D, Chesnutt J (2010) Efficacy of tart cherry
juice in reducing muscle pain during running: a randomized con-
trolled trial. J Int Soc Sports Nutr 7(1):17
Lund H, Vestergaard-Poulsen P, Kanstrup IL, Sejrsen P (1998) The
effect of passive stretching on delayed onset muscle soreness,
and other detrimental effects following eccentric exercise. Scand
J Med Sci Sports 8(4):216–221
MacIntyre DL, Reid WD, McKenzie DC (1995) Delayed muscle sore-
ness. The inflammatory response to muscle injury and its clinical
implications. Sports Med 20(1):24–40
Maheshwari RK, Singh AK, Gaddipati J, Srimal RC (2006) Mul-
tiple biological activities of curcumin: a short review. Life Sci
Mair J, Mayr M, Muller E, Koller A, Haid C, Artner-Dworzak E,
Calzolari C, Larue C, Puschendorf B (1995) Rapid adaptation
to eccentric exercise-induced muscle damage. Int J Sports Med
16(6):352–356. doi:10.1055/s-2007-973019
Menon VP, Sudheer AR (2007) Antioxidant and anti-inflammatory
properties of curcumin. Adv Exp Med Biol 595:105–125.
Moresi V, Pristera A, Scicchitano BM, Molinaro M, Teodori L, Sas-
soon D, Adamo S, Coletti D (2008) Tumor necrosis factor-alpha
inhibition of skeletal muscle regeneration is mediated by a cas-
pase-dependent stem cell response. Stem Cells 26(4):997–1008
Nieman DC, Henson DA, Dumke CL, Oley K, McAnulty SR, Davis
JM, Murphy EA, Utter AC, Lind RH, McAnulty LS, Morrow JD
(2006) Ibuprofen use, endotoxemia, inflammation, and plasma
cytokines during ultramarathon competition. Brain Behav
Immun 20(6):578–584
Nieman DC, Laupheimer MW, Ranchordas MK, Burke LM, Stear
SJ, Castell LM (2012) A–Z of nutritional supplements: dietary
supplements, sports nutrition foods and ergogenic aids for health
and performance—Part 33. Br J Sports Med 46(8):618–620
Nikolaidis MG, Kerksick CM, Lamprecht M, McAnulty SM (2012)
Does vitamin C and E supplementation impair the favora-
ble adaptations of regular exercise? Oxid Med Cell Longev.
2012:707941. doi:10.1155/2012/707941
Nosaka K, Sakamoto K, Newton M, Sacco P (2001) How long does
the protective effect on eccentric exercise-induced muscle dam-
age last? Med Sci Sports Exerc 33(9):1490–1495
Proske U, Morgan DL (2001) Muscle damage from eccentric exer-
cise: mechanism, mechanical signs, adaptation and clinical
applications. J Physiol 537(Pt 2):333–345
Rowlands DS, Rossler K, Thorp RM, Graham D, Timmons BW,
Stannard S, Tarnopolsky MA (2008a) Effect of dietary protein
content during recovery from high-intensity cycling on subse-
quent performance and markers of stress, inflammation, and
muscle damage in well-trained men. Appl Physiol Nutr Metabol
Rowlands DS, Rossler K, Thorp RM, Graham DF, Timmons DW,
Stannard SR, Tarnopolsky MA (2008b) Effect of dietary protein
content during recovery from high-intensity cycling on subse-
quent performance and markers of stress, inflammation, and
muscle damage in well-trained men. Appl Physiol Nutr Metabol
Rowlands DS, Nelson AR, Phillips SM, Faulkner JA, Clarke J, Burd
NA, Moore D (2014) Stellingwerff T (2014) Protein-leucine fed
dose effects on muscle protein synthesis after endurance exer-
cise. Med Sci Sports Exerc 46(5):98–99
Saunders MJ (2007) Coingestion of carbohydrate-protein during
endurance exercise: influence on performance and recovery. Int J
Sport Nutr Exerc Metab 17:S87–S103
Sellwood KL, Brukner P, Williams D, Nicol A, Hinman R (2007)
Ice-water immersion and delayed-onset muscle soreness: a ran-
domised controlled trial. Br J Sports Med 41(6):392–397
Singh S, Aggarwal B (1995) Activation of transcription factor NF-
kappa B is suppressed by curcumin (diferuloylmethane) [cor-
rected]. J Biol Chem 270:24995–25000
Thaloor D, Miller KJ, Gephart J, Mitchell PO, Pavlath GK (1999)
Systemic administration of the NF-kappaB inhibitor curcumin
stimulates muscle regeneration after traumatic injury. Am J
Physiol 277(2 Pt 1):C320–C329
Tidball JG, Villalta SA (2010) Regulatory interactions between
muscle and the immune system during muscle regeneration.
Am J Physiol Reg Int Comp Physiol 298(5):R1173–R1187.
Vaile JM, Gill ND, Blazevich AJ (2007) The effect of contrast water
therapy on symptoms of delayed onset muscle soreness. J
Strength Cond Res 21(3):697–702
Vaile J, Halson S, Gill N, Dawson B (2008a) Effect of hydro-
therapy on the signs and symptoms of delayed onset muscle
soreness. Eur J Appl Physiol 102(4):447–455. doi:10.1007/
Vaile J, Halson S, Gill N, Dawson B (2008b) Effect of hydro-
therapy on the signs and symptoms of delayed onset muscle
soreness. Eur J Appl Physiol 102(4):447–455. doi:10.1007/
Willoughby D, Taylor M, Taylor L (2003a) Glucocorticoid receptor
and ubiquitin expression after repeated eccentric exercise. Med
Sci Sports Exerc 35:2023–2031
Willoughby DS, McFarlin B, Bois C (2003b) Interleukin-6 expres-
sion after repeated bouts of eccentric exercise. Int J Sports Med
... The results of an animal-based study revealed that curcumin supplementation can increase muscle regeneration and improve symptoms of DOMS. Further, the effect of curcumin supplementation on reducing symptoms of EIMD has also been recently investigated in humans (Amalraj, Divya, & Gopi, 2020;Jäger, Purpura, & Kerksick, 2019;Ms et al., 2020;Nicol, Rowlands, Fazakerly, & Kellett, 2015;Tanabe, 2019;Tanabe et al., 2019;Tanabe et al., 2015). ...
... Ten trials, involving 316 subjects, were published from 2014 to 2020, in which five were conducted in Asia (Amalraj et al., 2020;Nakhostin-Roohi et al., 2016;Tanabe, 2019;Tanabe et al., 2019), three in USA (Jäger et al., 2019;McFarlin et al., 2016;Ms et al., 2020), one in Spain (Drobnic et al., 2014), and one in Australia (Nicol et al., 2015). The intervention duration lasted from 1 to 56 days, and the daily dose of curcumin varied from 150 to 5,000 mg/day. ...
... Dose and duration represent two important factors, which can affect the final result in RCT studies, and in the case of curcumin supplementation, duration seems to be more effective than dose. Two of the included studies in this meta-analysis, which used a moderate dose of Curcumin (1,500 mg/d and 1,000 mg/d) and a longer period of intervention (24 and 56 days) (Jäger et al., 2019;Ms et al., 2020), revealed a greater decrease in CK activity level and VAS score compared to a study which used a high dose of curcumin (5,000 mg/d) and a shorter period of intervention (4 days) (Nicol et al., 2015). Our included studies employed a variety of daily doses, from 150 to 5,000 mg/d of curcumin, but after dose-response analysis for CK and VAS scores, we found that there was no significant difference between low doses (150 mg/d) and high doses (5,000 mg/d). ...
To quantify the effects of curcumin supplementation on exercise‐induced muscle damage, muscle soreness, inflammatory biomarkers, muscle strength, and joint flexibility via assessment of creatine kinase (CK), visual analogue scale (VAS) score, maximal voluntary contraction (MVC), and range of motion (ROM), respectively. Online databases, including PubMed, Google Scholar, and Scopus, were searched up to February 2021. RevMan® software (version 5.3) was used for assessing the risk of bias to assess the quality of studies. The mean differences (MD) and confidence intervals (95% CI) of CK activity (IU/L), VAS score, tumor necrosis factor (TNF‐α) (pg/ml), interleukin‐6 (IL‐6) (pg/ml), IL‐8 (pg/ml), MVC (nm) and ROM (degree) were pooled using a random‐ or fixed‐effect model. Between‐study heterogeneity was assessed using χ‐square or I2 statistic. Ten trials met the eligibility criteria and were included in the pooled analysis. Meta‐analysis showed that curcumin supplementation significantly reduced serum CK activity [WMD = −65.98 IU/L, 95% CI (−99.53 to −32.44)], muscle soreness [WMD = −0.56, 95% CI (−0.84 to −0.27)], and TNF‐α concentration [WMD = −0.22 pg/ml, 95% CI (−0.33 to −0.10)]. Also, curcumin supplementation elicited significant improvements in MVC [WMD = 3.10 nm, 95% CI (1.45–4.75)] and ROM [WMD = 6.49°, 95% CI (3.91–9.07)], although no significant changes in IL‐6 and IL‐8 levels were found. Dose–response analysis indicated that there is a significant non‐linear association between the daily dose and the final effect size regarding TNF‐α. Curcumin supplementation may improve some aspects of DOMS, including muscle damage, muscle soreness, inflammation, muscle strength, and joint flexibility. Further, well‐designed and high‐quality studies with larger sample sizes are needed to ascertain the long‐term effects and safety of curcumin supplementation.
... Nicol et al. (2015) reported that curcumin ingestion (5 days, 5 g/day) decreased CK and IL-6 concentrations after leg press resistance exercise relative to the placebo ingested condition [36]. In this study, curcumin ingestion resulted in reductions in pain and an improvement in muscle performance, as assessed by an increase in jump height during single-leg squats 24 and 48 h after eccentric single-leg press exercise in physically active individuals. ...
... Irrespective of paralleled [33][34][35] or crossover [30,31,36,37] design, previous studies demonstrated that curcumin ingestion attenuates some inflammatory responses, as assessed by IL-6, IL-8, TNF-α, and/or IL-10, regardless of exercise modalities (e.g., aerobic or resistance exercise) [33,[35][36][37]. Based on previous studies (Table 1), starting curcumin intake at least 2 days prior to exercise appears to be necessary for reducing inflammatory responses, regardless of the type of exercise. ...
... Irrespective of paralleled [33][34][35] or crossover [30,31,36,37] design, previous studies demonstrated that curcumin ingestion attenuates some inflammatory responses, as assessed by IL-6, IL-8, TNF-α, and/or IL-10, regardless of exercise modalities (e.g., aerobic or resistance exercise) [33,[35][36][37]. Based on previous studies (Table 1), starting curcumin intake at least 2 days prior to exercise appears to be necessary for reducing inflammatory responses, regardless of the type of exercise. ...
Full-text available
Dietary supplements are widely used as a nutritional strategy to improve and maintain performance and achieve faster recovery in sports and exercise. Exercise-induced muscle damage (EIMD) is caused by mechanical stress and subsequent inflammatory responses including reactive oxygen species and cytokine production. Therefore, dietary supplements with anti-inflammatory and antioxidant properties have the potential to prevent and reduce muscle damage and symptoms characterized by loss of muscle strength and delayed-onset muscle soreness (DOMS). However, only a few supplements are considered to be effective at present. This review focuses on the effects of dietary supplements derived from phytochemicals and listed in the International Olympic Committee consensus statement on muscle damage evaluated by blood myofiber damage markers, muscle soreness, performance, and inflammatory and oxidative stress markers. In this review, the effects of dietary supplements are also discussed in terms of study design (i.e., parallel and crossover studies), exercise model, and such subject characteristics as physical fitness level. Future perspectives and considerations for the use of dietary supplements to alleviate EIMD and DOMS are also discussed.
... The men from the group using curcumin reported less pain, and they had significantly less injury in their thighs 48 hours after the exercise test (Drobnic et al., 2014). A double-blind randomizedcontrolled study on 17 healthy men, who were given 2.5 g curcumin or placebo (two times a day for 2.5 days prior to sets of eccentric exercises, and 2.5 days after the exercises), showed that curcumin lowered subsequent pain associated with delayed onset muscle soreness, and lowered a blood marker for muscle damage (Nicol, Rowlands, Fazakerly, & Kellett, 2015). ...
... According to Tanabe et al. ingesting curcumin prior to exercise and sporting events could facilitate faster recovery and attenuate muscle damage through the decrease in creatine kinase (Tanabe, Chino, Ohnishi, et al., 2019). The ingestion of 2.5 g of curcumin supplementation capsules taken 48 hours before and 72 hours after eccentric exercise yield significant reduction in muscle pain according to Nicol et al. (Nicol et al., 2015). Tanabe et al. conducted two studies (Tanabe, Chino, Ohnishi, et al., 2019; wherein a significant reduction in muscle soreness and pain were noted by the effect of a 180 mg curcumin supplementation protocol, administered in 90 mg twice daily. ...
Full-text available
Dietary supplements are used to enrich the diet of athletes, and contribute to better adaptation on the part of athletes to their training, as well as quicker recovery from physical exercises. One such substance is turmeric, which has received widespread interest from medical, scientific and sports specialists due to its numerous benefits to human health and recovery. Curcumin is the most widely researched bioactive component of turmeric, but even curcumin-free turmeric is believed to be as effective as curcumin, and, therefore, this review concentrates on the effect of turmeric as a whole. Turmeric, also known as the 'golden spice', may help in the treatment of exercise-induced inflammation and muscle soreness, and, therefore, turmeric can enhance recovery in athletes. This current review focuses on the benefits of turmeric for athletes, including anti-inflammatory, antioxidant and muscle recovery activities exhibited by turmeric.
... ↑↑ strength after 48 and 72 h of exercise No effects regarding serum markers of inflammation and muscle damage were observed [176] Hesperetin Effects of 4-week supplementation (500 mg/day) in trained male athletes subjected to cycling time-trial performance ↑↑ absolute power (+5% than placebo) ↓↓ oxygen consumption/power ratio [177] Caffeic acid phenethyl ester Effects of 1, 2, and 4 µg/mL exposure in peripheral blood mononuclear cells of competitive cyclists against hyperthermal stress ↓↓ hyperthermia-induced survival inhibition, necrosis, superoxide levels, glutathione depletion [196] Curcumin Effects of supplementation (5 g/day) in men 2 days before and to 3 days after eccentric single-leg press exercise ↓↓ in pain during a single-leg squat, gluteal stretch, squat jump, IL-6 levels, and CK activity ↑↑ single-leg jump performance [234] Effects of 8-week supplementation (200 mg/day) in physically active men and women after completion of a downhill running bout ↓↓ peak extension torque values after 1 and 24 h of muscle-damaging exercise [193] Effects of 7-day supplementation (180 mg/day) in healthy men subjected to eccentric exercise ↓↓ IL-8, muscle soreness, and CK activity [106] Effects of 400 mg/day supplementation in 2 days before and 4 days after exercise ↓↓ exercise-induced muscle damage, by lowering CK, TNF-α, and IL-8 (-48, -25, and -21% than placebo) No significant differences regarding IL-6 and IL-10 levels and quadriceps muscle soreness were observed [235] Effects of 3-day supplementation (500 mg/day) in non-heat acclimated male and female ↓↓ indicators of cellular energy status SIRT1 and p-AMPK (-47.8 and -48.5% than placebo), and mediators of cellular heat shock response HSP70 protein (-11.0% than placebo) [236] participants subjected to treadmill runs ...
Full-text available
In recent years, many efforts have been made to identify micronutrients or nutritional strategies capable of preventing, or at least, attenuating, exercise-induced muscle damage and oxidative stress, and improving athlete performance. The reason is that most exercises induce various changes in mitochondria and cellular cytosol that lead to the generation of reactive species and free radicals whose accumulation can be harmful to human health. Among them, supplementation with phenolic compounds seems to be a promising approach since their chemical structure, composed of catechol, pyrogallol, and methoxy groups, gives them remarkable health-promoting properties, such as the ability to suppress inflammatory processes, counteract oxidative damage, boost the immune system, and thus, reduce muscle soreness and accelerate recovery. Phenolic compounds have also already been shown to be effective in improving temporal performance and reducing psychological stress and fatigue. Therefore, the aim of this review is to summarize and discuss the current knowledge on the effects of dietary phenolics on physical performance and recovery in athletes and sports practitioners. Overall, the reports show that phenolics exert important benefits on exercise-induced muscle damage as well as play a biological/physiological role in improving physical performance.
... Previous studies have shown that intense exercise and muscle contraction increase ROS production. The damage and modification of cell proteins, lipids, and DNA can lead to skeletal muscle fatigue and injury [7][8][9][10][11][12][13]. Therefore, antioxidant supplements are often used as prescriptions to resist the adverse reactions of exercise [14][15][16][17]. However, there are increasing evidence to show that exogenous antioxidant supplements have adverse reactions to some acute and chronic responses of skeletal muscles to exercise [18][19][20][21][22][23][24][25][26], as well as weaken the normal redox signaling pathway in muscles [13], weakening the adaptive response to endurance training [19][20][21]. ...
Full-text available
The mitochondrial unfolded protein response (UPRmt) can repair and remove misfolded or unfolded proteins in mitochondria and enhance mitochondrial protein homeostasis. Reactive oxygen species (ROS) produced by regular exercise is a crucial signal for promoting health, and skeletal muscle mitochondria are the primary source of ROS during exercise. To verify whether UPRmt is related to ROS produced by mitochondria in skeletal muscle during regular exercise, we adapted MitoTEMPO, mitochondrially targeted antioxidants, and ROS production by mitochondria. Our results showed that mitochondrial ROS is the key factor for activating UPRmt in different pathways.
Supplementation with cannabidiol (CBD) may expedite recovery when consumed after exercise. The purpose of this study was to determine if supplementation with CBD reduces inflammation and enhances performance following strenuous eccentric exercise in collegiate athletes. Twenty-four well-trained females (age = 21.2 ± 1.8 years, height = 166.4 ± 8 cm, weight = 64.9 ± 9.1 kg) completed 100 repetitions of unilateral eccentric leg extension to induce muscle damage. In this crossover design, participants were randomized to receive 5 mg/kg of CBD in pill form or a placebo 2 h prior to, immediately following, and 10 h following muscle damage. Blood was collected, and performance and fatigue were measured prior to, and 4 h, 24 h, and 48 h following the muscle damage. Approximately 28 days separated treatment administration to control for the menstrual cycle. No significant differences were observed between the treatments for inflammation, muscle damage, or subjective fatigue. Peak torque at 60°/s (p = 0.001) and peak isometric torque (p = 0.02) were significantly lower 24 h following muscle damage, but no difference in performance was observed between treatments at any timepoint. Cannabidiol supplementation was unable to reduce fatigue, limit inflammation, or restore performance in well-trained female athletes.
Physical activity results in a series of proinflammatory reactions and innate immune responses, which occur postexercise. This is followed by antiinflammatory reactions that are critical for regeneration and healing. The severity of inflammation following exercise depends on the type, duration, and intensity of the exercise bout, as well as the training status of the individual. Interventions designed to reduce the inflammatory response following exercise may, in fact, be detrimental to adaptation, though they may positively impact performance and competition with short turnaround times. Although acute inflammation is critical for recovery, chronic inflammation—even low-grade systemic and tissue-specific simmering inflammation—appears to be a mechanism associated with the aging process and is related to many chronic diseases. It appears that regular, sustained physical activity, including endurance and resistance-type exercise, may provide a protective impact on chronic low-grade inflammatory conditions. General patterns of dietary intake and specific nutrients and other dietary constituents or supplements demonstrate promise for positively impacting this relationship. Many of the same cytokine and chemokine actors that are modulated by physical activity also are affected by diet. Many of the intercellular signaling systems modulated by physical activity are also regulated by various aspects of nutrition, including carbohydrate and fatty acid metabolism and oxidation. While much of the focus of this chapter is on exercise training among people at optimal ages for fitness, there are important and obvious implications for nonathletes across the lifespan, especially during childhood and among the elderly. Research into non-steroidal anti-inflammatory drugs also has implications for exploring the effect of diet in modulating inflammatory and immune responses in context of physical activity.
In recent years, the increase in public awareness of sports has greatly promoted the development of the sports food industry. Sports food provides nutrition to meet the metabolic and energy needs of sports people. The nutritional components of sports food can be divided into basic nutrients and functional factors. Basic nutrients refer to the nutrients or metabolites required by the human body. Functional factors are bioactive ingredients that have potential effects in improving functions of the human body, such as protection of articular cartilage and improving muscle quality. Currently, there are various forms of sports foods in the market, including sports drinks, solid sports foods, semi-solid sports foods, and sports nutrition supplements. The sports food industry has seen many opportunities such as the expanding market, manufacturing technology development, and increasing funds investment. However, it also faces many challenges, such as lack of innovation, insufficient in-depth research, risks, and safety issues. This review would provide theoretical guidance for current sports food manufacture to meet the needs of increasing sports people worldwide.
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Delayed post-exercise muscle pain is a type of pain that is felt within the first 24 hours after exercise, peaks between 1 and 3 days, compared to acute muscle pain, and its effect decreases completely after 5-7 days. There is increasing interest and research into delayed muscle pain. Although there are different formation mecha- nisms on delayed muscle pain, the formation mechanisms have not been fully exp- lained. Nutritional interventions are one of the preventive and/or therapeutic ways to reduce delayed muscle soreness. Studies have reported that nutritional interven- tions can reduce delayed muscle soreness. Many studies have reported the effect of caffeine, omega-3 fatty acids, taurine, polyphenols, and curcumin on delayed muscle soreness. Consistent data have not been reported from minor interventions with supplements such as antioxidants, L-carnitine, BCAA, allicin. Delayed musc- le soreness is an area that needs more study in athletes. There is a need for more studies examining these factors by considering more factors such as the severity of the damage, individual response, the dose-response relationship used, the duration of intake and the markers they are affected by. The aim of this review is to address nutritional interventions that are thought to be effective in the treatment and pre- vention of delayed muscle pain and to discuss the relationship between delayed muscle pain and nutrition. Keywords: Nutrition, doms, delayed muscle soreness
Objectives High intensity exercise causes muscle damage, oxidative stress and inflammation. The purpose of this study was to investigate the effect of Curcumin supplementation on muscle damage, antioxidant status and inflammatory factors after successive simulated taekwondo competitions. Equipment and methods Eighteen healthy taekwondo men with mean age of 22.27 (0.94) years and Taekwondo experience of 6.47 (1.79) years were recruited based on the inclusion and exclusion criteria and randomly divided into two groups: Curcumin (4 g/day) and placebo (rice flour) groups. Subjects were supplemented 3 days before up to 2 days after the taekwondo competition. Creatine kinase (CK), lactate dehydrogenase (LDH), total antioxidant capacity (TAC), Malondialdehyde (MDA) and IL-6 were measured before the start of the supplementation (Baseline), before the start of the taekwondo competition (Pre), immediately (t0), 24 h (t1) and 48 h (t2) after the competition. Comparisons were performed by repeated measures ANOVA and P˂ 0.05 was considered as significant. Results CK, LDH and MDA increased significantly after the competition in placebo group compared to Curcumin supplemented group (P < 0.05). TAC significantly increased in Curcumin supplemented compared to placebo group after the competition (P < 0.05). No between group differences were observed in serum levels of IL-6 after the competition (P > 0.05). The effect of time on CK, LDH, TAC, MDA and IL-6 changes was significant (P < 0.05). Also, the changes of the variables (Ck, LDH, TAC and MDA) in all of the times were significant between groups (P < 0.05). Based on the results of this study, Curcumin supplementation has positive effects on reducing muscle damage and oxidative stress. Further larger scale trials are needed to confirm these findings.
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Skeletal muscle is often the site of tissue injury due to trauma, disease, developmental defects or surgery. Yet, to date, no effective treatment is available to stimulate the repair of skeletal muscle. We show that the kinetics and extent of muscle regeneration in vivo after trauma are greatly enhanced following systemic administration of curcumin, a pharmacological inhibitor of the transcription factor NF-κB. Biochemical and histological analyses indicate an effect of curcumin after only 4 days of daily intraperitoneal injection compared with controls that require >2 wk to restore normal tissue architecture. Curcumin can act directly on cultured muscle precursor cells to stimulate both cell proliferation and differentiation under appropriate conditions. Other pharmacological and genetic inhibitors of NF-κB also stimulate muscle differentiation in vitro. Inhibition of NF-κB-mediated transcription was confirmed using reporter gene assays. We conclude that NF-κB exerts a role in regulating myogenesis and that modulation of NF-κB activity within muscle tissue is beneficial for muscle repair. The striking effects of curcumin on myogenesis suggest therapeutic applications for treating muscle injuries.
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Inflammatory processes play essential roles in the pathogenesis of tendinitis and tendinopathy. These events are accompanied by catabolic processes initiated by pro-inflammatory cytokines such as interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). Pharmacological treatments for tendinitis are restricted to the use of non-steroidal anti-inflammatory drugs. Recent studies in various cell models have demonstrated that curcumin targets the NF-κB signaling pathway. However, its potential for the treatment of tendinitis has not been explored. Herein, we used an in vitro model of human tenocytes to study the mechanism of curcumin action on IL-1β-mediated inflammatory signaling. Curcumin at concentrations of 5-20 μm inhibited IL-1β-induced inflammation and apoptosis in cultures of human tenocytes. The anti-inflammatory effects of curcumin included down-regulation of gene products that mediate matrix degradation (matrix metalloproteinase-1, -9, and -13), prostanoid production (cyclooxygenase-2), apoptosis (Bax and activated caspase-3), and stimulation of cell survival (Bcl-2), all known to be regulated by NF-κB. Furthermore, curcumin suppressed IL-1β-induced NF-κB activation via inhibition of phosphorylation and degradation of inhibitor of κBα, inhibition of inhibitor of κB-kinase activity, and inhibition of nuclear translocation of NF-κB. Furthermore, the effects of IL-1β were abrogated by wortmannin, suggesting a role for the phosphatidylinositol 3-kinase (PI-3K) pathway in IL-1β signaling. Curcumin suppressed IL-1β-induced PI-3K p85/Akt activation and its association with IKK. These results demonstrate, for the first time, a potential role for curcumin in treating tendon inflammation through modulation of NF-κB signaling, which involves PI-3K/Akt and the tendon-specific transcription factor scleraxis in tenocytes.
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Eccentric exercise continues to receive attention as a productive means of exercise. Coupled with this has been the heightened study of the damage that occurs in early stages of exposure to eccentric exercise. This is commonly referred to as delayed onset muscle soreness (DOMS). To date, a sound and consistent treatment for DOMS has not been established. Although multiple practices exist for the treatment of DOMS, few have scientific support. Suggested treatments for DOMS are numerous and include pharmaceuticals, herbal remedies, stretching, massage, nutritional supplements, and many more. DOMS is particularly prevalent in resistance training; hence, this article may be of particular interest to the coach, trainer, or physical therapist to aid in selection of efficient treatments. First, we briefly review eccentric exercise and its characteristics and then proceed to a scientific and systematic overview and evaluation of treatments for DOMS. We have classified treatments into 3 sections, namely, pharmacological, conventional rehabilitation approaches, and a third section that collectively evaluates multiple additional practiced treatments. Literature that addresses most directly the question regarding the effectiveness of a particular treatment has been selected. The reader will note that selected treatments such as anti-inflammatory drugs and antioxidants appear to have a potential in the treatment of DOMS. Other conventional approaches, such as massage, ultrasound, and stretching appear less promising.
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Background Delayed onset muscle soreness (DOMS) due to eccentric muscle activity is associated with inflammatory responses and production of reactive oxygen species (ROS) that sustain both inflammation and oxidative stress. Curcumin, a powerful promoter of anti-oxidant response, is one of the best-investigated natural products, and is now commercially available as a lecithin delivery system (Meriva®, Indena SpA, Milan) with improved bio-availability. The aim of this study was to test whether curcumin could attenuate damage from oxidative stress and inflammation related to acute muscle injury induced by eccentric continuous exercise Methods This was a randomised, placebo-controlled, single-blind pilot trial. Twenty male healthy, moderately active volunteers were randomised to curcumin given as the Phytosome® delivery system 1 g twice daily (200 mg curcumin b.i.d.) or matching placebo. Supplementation was initiated 48 hours prior to a downhill running test and was continued for 24 hours after the test (4 days in total). Muscle damage was quantified by magnetic resonance imaging, laboratory tests and histological analyses on muscle samples obtained 48 hours after the test. Patient-reported pain intensity was also recorded. Results Subjects in the curcumin group reported less pain in the lower limb as compared with subjects in the placebo group, although significant differences were observed only for the right and left anterior thighs. Significantly fewer subjects in the curcumin group had MRI evidence of muscle injury in the posterior or medial compartment of both thighs. Increases in markers of muscle damage and inflammation tended to be lower in the curcumin group, but significant differences were only observed for interleukin-8 at 2 h after exercise. No differences in markers of oxidative stress and muscle histology were observed Conclusions Curcumin has the potential for preventing DOMS, as suggested by its effects on pain intensity and muscle injury. Larger studies are needed to confirm these results and further clarify the mechanism of action of curcumin.
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Delayed onset muscle soreness (DOMS) is a familiar experience for the elite or novice athlete. Symptoms can range from muscle tenderness to severe debilitating pain. The mechanisms, treatment strategies, and impact on athletic performance remain uncertain, despite the high incidence of DOMS. DOMS is most prevalent at the beginning of the sporting season when athletes are returning to training following a period of reduced activity. DOMS is also common when athletes are first introduced to certain types of activities regardless of the time of year. Eccentric activities induce micro-injury at a greater frequency and severity than other types of muscle actions. The intensity and duration of exercise are also important factors in DOMS onset. Up to six hypothesised theories have been proposed for the mechanism of DOMS, namely: lactic acid, muscle spasm, connective tissue damage, muscle damage, inflammation and the enzyme efflux theories. However, an integration of two or more theories is likely to explain muscle soreness. DOMS can affect athletic performance by causing a reduction in joint range of motion, shock attenuation and peak torque. Alterations in muscle sequencing and recruitment patterns may also occur, causing unaccustomed stress to be placed on muscle ligaments and tendons. These compensatory mechanisms may increase the risk of further injury if a premature return to sport is attempted. A number of treatment strategies have been introduced to help alleviate the severity of DOMS and to restore the maximal function of the muscles as rapidly as possible. Nonsteroidal anti-inflammatory drugs have demonstrated dosage-dependent effects that may also be influenced by the time of administration. Similarly, massage has shown varying results that may be attributed to the time of massage application and the type of massage technique used. Cryotherapy, stretching, homeopathy, ultrasound and electrical current modalities have demonstrated no effect on the alleviation of muscle soreness or other DOMS symptoms. Exercise is the most effective means of alleviating pain during DOMS, however the analgesic effect is also temporary. Athletes who must train on a daily basis should be encouraged to reduce the intensity and duration of exercise for 1–2 days following intense DOMS-inducing exercise. Alternatively, exercises targeting less affected body parts should be encouraged in order to allow the most affected muscle groups to recover. Eccentric exercises or novel activities should be introduced progressively over a period of 1 or 2 weeks at the beginning of, or during, the sporting season in order to reduce the level of physical impairment and/or training disruption. There are still many unanswered questions relating to DOMS, and many potential areas for future research.
HARRISON, B. C., D. ROBINSON, B. J. DAVISON, B. FOLEY, E. SEDA, and W. C. BYRNES. Treatment of exercise-induced muscle injury via hyperbaric oxygen therapy. Med. Sci. Sports Exerc., Vol. 33, No. 1, 2001, pp. 36–42. Purpose: This study examined the role of hyperbaric oxygen therapy (HBO) in the treatment of exercise-induced muscle injury. Methods: 21 college-aged male volunteers were assigned to three groups: control, immediate HBO (iHBO), and delayed HBO (dHBO). All subjects performed 6 sets (10 repetitions per set) of eccentric repetitions with a load equivalent to 120% of their concentric maximum. HBO treatments consisted of 100-min exposure to 2.5 ATA and 100% oxygen with intermittent breathing of ambient air (30 min at 100% O2, 5 min at 20.93% O2). HBO treatments began either 2 (iHBO) or 24 h (dHBO) postexercise and were administered daily through day 4 postexercise. Forearm flexor cross-sectional area (CSA) and T2 relaxation time via magnetic resonance imaging (MRI) were assessed at baseline, 2, 7, and 15 d postinjury. Isometric strength and rating of perceived soreness of the forearm flexors were assessed at baseline, 1, 2, 3, 4, 7, and 15 d postinjury. Serum creatine kinase (CK) was assessed on day 0 and on days 1, 2, 7, and 15 postinjury. Results: Mean baseline CSA values were: 2016.3, 1888.5, and 1972.2 mm2 for control, iHBO, and dHBO, respectively. All groups showed significant increases in CSA in response to injury (21% at 2 d, 18% at 7 d) (P < 0.0001), but there were no significant differences between groups (P = 0.438). Mean baseline T2 relaxation times were: 26.18, 26.28, and 27.43 msec for control, iHBO, and dHBO, respectively. Significant increases in T2 relaxation time were observed for all groups (64% at 2 d, 66% at 7 d, and 28% at 15 d) (P < 0.0001), but there were no significant differences between groups (P = 0.692). Isometric strength (P < 0.0001), serum CK levels (P = 0.0007), and rating of perceived soreness (P < 0.0001) also indicated significant muscle injury for all groups, but there were no differences between groups (P = 0.459, P = 0.943, and P = 0.448, respectively). Conclusion: These results suggest that hyperbaric oxygen therapy was not effective in the treatment of exercise-induced muscle injury as indicated by the markers evaluated.
Delayed onset muscle soreness (DOMS) is a sensation of discomfort that occurs 1 to 2 days after exercise. The soreness has been reported to be most evident at the muscle/tendon junction initially, and then spreading throughout the muscle. The muscle activity which causes the most soreness and injury to the muscle is eccentric activity. The injury to the muscle has been well described but the mechanism underlying the injury is not fully understood. Some recent studies have focused on the role of the cytoskeleton and its contribution to the sarcomere injury. Although little has been confirmed regarding the mechanisms involved in the production of delayed muscle soreness, it has been suggested that the soreness may occur as a result of mechanical factors or it may be biochemical in nature. To date, there appears to be no relationship between the development of soreness and the loss of muscle strength, in that the timing of the two events is different. Loss of muscle force has been observed immediately after the exercise. However, by collecting data at more frequent intervals a second loss of force has been reported in mice 1 to 3 days post-exercise. Future studies with humans may find this second loss of force to be related to DOMS. The role of inflammation during exercise-induced muscle injury has not been clearly defined. It is possible that the inflammatory response may be responsible for initiating, amplifying, and/or resolving skeletal muscle injury. Evidence from the literature of the involvement of cytokines, complement, neutrophils, monocytes and macrophages in the acute phase response are presented in this review. Clinically, DOMS is a common but self-limiting condition that usually requires no treatment. Most exercise enthusiasts are familiar with its symptoms. However, where a muscle has been immobilised or debilitated, it is not known how that muscle will respond to exercise, especially eccentric activity.
Unlabelled: Protein-leucine ingestion after strenuous endurance exercise accentuates muscle protein synthesis and improves recovery of muscle performance. Purpose: The objective of this study is to determine whether a low-dose protein-leucine blend ingested after endurance exercise enhances skeletal muscle myofibrillar protein fractional synthetic rate (FSR). Method: In a crossover design, 12 trained men completed 100 min of high-intensity cycling, then ingested either 70/15/180/30 g of protein/leucine/carbohydrate/fat (15LEU), 23/5/180/30 g of 5LEU, or 0/0/274/30 g of CON beverages in randomized order in four servings during the first 90 min of a 240-min recovery period. Muscle biopsies were collected at 30 and 240 min into recovery with FSR determined by L-[ring-13C6]phenylalanine incorporation and mTORC1 pathway phosphorylation by Western blot. Results: The 33% (90% CL, ±12%) increase in FSR with 5LEU (mean, SD: 0.080, 0.014%·h(-1)) versus CON (0.060, 0.012%·h(-1)) represented near-maximal FSR stimulation. Tripling protein-leucine dose (15LEU: 0.090, 0.11%·h(-1)) negligibly increased FSR (13%, ±12% vs 5LEU). Despite similar FSR, mTORC1(Ser2448) phosphorylation only increased with 15LEU at 30 min, whereas p70S6K(Thr389), rpS6(Ser240/244), and 4E-BP1γ(Ser112) phosphorylation increased with protein-leucine quantity at one or both time points. Plasma leucine and essential amino acid concentrations decreased during recovery in CON but increased with protein-leucine dose. Serum insulin was increased in 15LEU versus CON (60%, ±20%) but was unaffected relative to 5LEU. Regression analysis revealed p70S6K-rpS6 phosphorylation moderately predicted FSR, but the associations with plasma leucine and essential amino acids were small. Conclusions: Ingesting 23 g of protein with 5 g of added leucine achieved near-maximal FSR after endurance exercise, an effect unlikely attributable to mTORC1-S6K-rpS6 signaling, insulin, or amino acids. Translating the effects of protein-leucine quantity on protein synthesis to optimizing adaptation and performance requires further research.