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18/06/2013 | Etudes Compléments alimentaires



L. VELLA       Journal of Strength and Conditioning Research VOLUME 27 | SUPPLEMENT 4 | APRIL 2013 | S107

Purpose: Current approaches in the treatment of exerciseinduced
muscle injury rely of the inhibition of pro-inflammatory
mediators and alleviating the cardinal signs of inflammation:
redness, swelling, heat and pain. However, recent research
suggests that the molecular events occurring early in acute
inflammation engage an active and coordinated inflammatory
resolution program characterized by a switch to production of
pro-resolution factors that govern the withdrawal of proinflammatory
signals and the restoration of tissue homeostasis
and function. This line of research has lead to the identification
of novel classes of lipid derived eicosanoid species
which may provide new targets in the successful resolution of

Methods: Sixteen untrained male subjects
(age 23 6 0.7 yr, mass 88 6 3.1 kg) were assigned to a placebo
(PLA) (n = 8) or ibuprofen (IBU) (n = 8) group. Subjects
completed a single bout of resistance exercise consisting of 3
sets of 8–12 repetitions of a squat, leg press and leg extension
at 80% 1RM. Muscle biopsies were obtained at rest and
at 0, 3 and 24 h post exercise. Intravenous blood samples
were obtained at rest, at 30 min intervals between 0 and 3 h
and again at 24 h post exercise. The IBU group orally consumed
400 mg of ibuprofen immediately prior to the first
muscle biopsy and at 5 and 10 h post exercise. Serum concentrations
of eicosanoid species were analyzed by liquid
chromatography mass spectrometry. The mRNA expression
of white blood cell surface markers, inflammatory cytokines
and indirect markers of inflammatory resolution was analyzed
in muscle tissue by RT-PCR. Results: Acute exercise
increased the serum expression of traditional pro-inflammatory
eicosanoid species derived from both the COX (PGF2a,
PGE2, PGD2, TXB2) and LOX (LTB4, LTB5) pathways.
Additionally, heightened circulating levels of novel pro-resolution
bioactive lipid mediators derived from EPA (RvE1 isoforms),
DHA (RvD1) and arachidonic acid (LXA4 and LXA5)
were detected post exercise.
These responses were blunted
by the administration of the COX inhibiting non-steroidal antiinflammatory
drug ibuprofen. Contrastingly, IBU elicited
a trend for an increased exercise induced expression of the
pro-inflammatory cytokines IL-8 and IL-6, with a significant
interaction achieved for MCP-1. The mRNA expression of
alternative macrophage cell surface marker CD163 and
TGF-b increased at 24 h in the placebo group.

Novel classes of bioactive lipid mediators are up regulated
following resistance exercise that may play a crucial role in
the resolution of exercise induced inflammation. An increase
in inflammatory cytokines within the IBU group suggests the
post exercise inflammation program may be impaired while
no change in CD163 expression may provide preliminary
evidence that an inflammatory resolution program involving
the phagocytosis of apoptotic neutrophils may also be
inhibited. In alternative models of acute inflammation, these
pathways appear necessary for the successful resolution of
acute inflammation and the restoration of homeostatic tissue

Practical Application: The active resolution of
exercise induced inflammation may be a key process in
post-exercise recovery. A shift from traditional anti-inflammatory
treatments towards those which promote active resolution
may enhance the efficiency with which inflammation
naturally subsides in the body whilst governing the successful
repair and regeneration of damaged muscle tissue.

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