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- Turmeric (Curcuma longa)
- Curcumin
- Muscle Soreness
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Date:
09-15-2014 | HC# 081461-504
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Re: Curcumin Formulation Reduces Delayed Muscle Soreness after Eccentric Exercise
Drobnic
F, Riera J, Appendino G, et al. Reduction of delayed onset muscle soreness by a
novel curcumin delivery system (Meriva®): a randomised,
placebo-controlled trial. J Int Soc
Sports Nutr. June 18, 2014;11:31. doi: 10.1186/1550-2783-11-31.
Eccentric exercise refers to forced muscle elongation
during muscle contraction. This form of exercise may lead to mild muscle damage
and delayed onset muscle soreness (DOMS), the generation of reactive oxygen
species (ROS), and subsequent inflammation. Curcumin, a compound isolated from
turmeric (Curcuma longa) root, has
been shown to have anti-inflammatory activity1 by attenuating the
modulators of inflammation, including nuclear factor kappa B (NF-ĸB) and
cyclooxygenase-2 (COX-2)2,3; curcumin has also been reported to
activate endogenous antioxidant response modulator nuclear factor erythroid 2-related
factor 2 (Nrf2).4 This randomized,
placebo-controlled, single-blind trial investigated the potential of curcumin
product Meriva®
(Indena S.p.A.; Milan, Italy), formulated with soy (Glycine max) lecithin to enhance bioavailability, to alleviate muscle injury, ROS damage, and
inflammation due to eccentric exercise.
This study enrolled 20 healthy men that engaged
in aerobic exercise for 4 hours per week or more. Included subjects did not
smoke, had no diseases of the musculoskeletal system, and had a maximal oxygen
consumption (VO2max) of 35 ml/kg or greater during a treadmill
exercise test. Those taking anti-inflammatory, analgesic, or antioxidant medications
in the past month; with liver or kidney problems; or with current inflammation
or disease were excluded. Subjects were randomly assigned to either 1 g of
Meriva 2 times per day at breakfast and dinner, for a total curcumin dosage of
400 mg daily, or placebo. Meriva contains curcumin (20%), soy lecithin in a 1:2
weight ratio, and 2 parts of microcrystalline cellulose. Contents of the placebo were not described. Treatments
were given 48 hours before downhill-run testing and continued for 24 hours
following the testing for a total of 4 days.
Subjects underwent a baseline treadmill exercise
test at a 3% grade starting at 6 km/h, raised by 1 km/h per minute until either
VO2max was steady or began to decrease, or muscle fatigue occurred.
VO2max, maximum speed (Spdmax), and speed at anaerobic
threshold (Spdat) was determined. After 2 days of curcumin, to
induce eccentric muscle injury, a downhill running test was conducted, consisting
of a 10-minute warm-up and a downhill run at constant speed on a treadmill at
-10% for 45 minutes. At 7 and 5 days before the curcumin intake began, subjects
had conducted 10-minute exercise regimes to practice the study protocol and
ensure a consistent baseline of muscle tone. Additionally, subjects were given
a "nutritional supplement" of 25-30 g of carbohydrates and 2-4 g of
protein 1 hour before the downhill running test. Subjects were given access to
water ad lib during the downhill running test after consuming 500 ml of mineral
water 30 minutes before the test began.
Magnetic resonance imaging (MRI) was used to
gauge thigh muscle damage, and muscle biopsies were taken 48 hours after the
downhill running test to assess for muscle myeloperoxidase (MPO) activity,
albumin, and cluster of differentiation 3 (CD3) positive cells using
immunohistochemistry (all markers of muscle injury or inflammation). A week
before the test, blood cell and blood chemistry parameters had been assessed. Blood
was also taken right before the downhill running test, and 2 and 24 hours after
the test, to measure markers of both oxidative stress and inflammation. Pain
was also measured 48 hours after the test by a scale ranging from 0 (no pain)
to 4 (disabling pain) while climbing up or down stairs.
Of the 20 subjects enrolled, 1 subject randomly
assigned to the Meriva group dropped out for personal reasons prior to the
test, leaving 9 subjects in the Meriva group. Between the placebo and Meriva
groups, no significant differences were noted in Spdmax (13.7 ± 1.8
km/h vs. 14.8 ± 1.1 km/h) or downhill running speed (10.9 ± 1.2 km/h vs. 11.4 ±
0.9 km/h). According to the MRI measurements, a significantly less percentage
of subjects had muscle damage in the Meriva group as compared to the placebo
group in the posterior (44.4% vs. 90%, P=0.0329) or medial (33.3% vs. 80%,
P=0.0397) areas of the right thigh. Results were similar in the left thigh
(33.3% vs. 80%, P=0.0397, and 33.3% vs. 90%, P=0.0106, respectively).
Overall, the difference in pain experienced by
the Meriva group as compared to the placebo group approached significance (23.3
± 7.9 vs. 30.6 ± 7.9, P=0.06). When analyzing the anterior thigh area, both
right and left comparisons showed significantly less pain in the Meriva group
(right=4.4 ± 2.5 vs. 7.8 ± 3.9, left=4.4 ± 2.4 vs. 8.2 ± 4.6, P<0.05 for
both). Also, at the 2-hour post-exercise test, interleukin-8 (IL-8, a marker of
inflammation) was significantly lower in the Meriva group as compared to the
control (196.8 ± 66.1 pg/ml vs. 274.7 ± 70.7 pg/ml, P<0.05). Markers of
oxidant stress were not significantly different between groups at any time.
Muscle biopsy endpoints (n=4 from the Meriva group, and n=5 from the placebo
group) were not significantly different between groups.
This study showed a significant reduction in
muscle damage, pain in certain areas, and IL-8 concentrations associated with
Meriva consumption during eccentric exercise, pointing to its potential use in preventing
DOMS. No effect was noted on markers of oxidative stress; this suggests that
curcumin likely attenuates inflammation as opposed to oxidant damage. The
authors mention that curcumin may activate endogenous antioxidant regulatory
cellular mechanisms and may also act as an analgesic. Limitations of this study
include the short duration, single type of aerobic exercise employed, the
overall small amount of oxidative damage, and the limited amount of biopsy
samples. Ideally, future studies will focus on specific mechanism of action
during use with exercise.
—Amy C.
Keller, PhD
References
1Blumenthal M, Goldberg
A, Brinckmann J, eds. Herbal Medicine:
Expanded Commission E Monographs. Austin,
TX: American Botanical Council; Newton, MA: Integrative Medicine
Communications; 2000.
2Singh S, Aggarwal BB.
Activation of transcription factor NF-kappa B is suppressed by curcumin
(diferuloylmethane) [corrected]. J Biol
Chem. October 1995;270(42):24995-25000.
3Chun K-S, Keum Y-S,
Han SS, Song Y-S, Kim S-H, Surh Y-J. Curcumin inhibits phorbol ester-induced
expression of cyclooxygenase-2 in mouse skin through suppression of
extracellular signal-regulated kinase activity and NF-kappaB activation. Carcinogenesis. September
2003;24(9):1515-1524.
4Shehzad A, Lee YS.
Molecular mechanisms of curcumin action: signal transduction. Biofactors. January-February
2013;39(1):27-36.
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