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Low back pain in athletes can be controlled with acupuncture by a catecholaminergic pathway: clinical trial
Arriaga-Pizano L, Gomez-Jimenez DC, Flores-Mejia LA, Perez-Cervera Y, Solorzano-Mata CJ, Lopez-Macias C, Isibasi A, Torres-Rosas R
Acupuncture in Medicine 2020 May 20:Epub ahead of print
clinical trial
5/10 [Eligibility criteria: No; Random allocation: Yes; Concealed allocation: Yes; Baseline comparability: No; Blind subjects: Yes; Blind therapists: No; Blind assessors: Yes; Adequate follow-up: No; Intention-to-treat analysis: No; Between-group comparisons: Yes; Point estimates and variability: No. Note: Eligibility criteria item does not contribute to total score] *This score has been confirmed*

BACKGROUND: Activation of the sympathetic nervous system attenuates inflammation via catecholamines. Recent evidence has shown that electroacupuncture (EA) activates neuronal networks involved in the release of dopamine and norepinephrine that control systemic inflammation. In muscle, catecholamines are related to cyclic adenosine monophosphate (cAMP). This signaling molecule has been implicated in recovery from sustained contractile activity, which may induce muscular pain, such as that which occurs during low back pain (LBP). OBJECTIVE: Our aim was to evaluate the effects of EA used for the control of LBP on the activation of the sympathetic nervous system in a randomized controlled clinical trial in athletes. METHODS: Two groups of athletes with acute or chronic low back pain were studied. EA, sham EA and pharmacological treatment (diclofenac sodium) were evaluated. The outcome measures included a pain score represented by a visual analogue scale (VAS) and serum levels of catecholamines quantified by enzyme-linked immunosorbent assay. In addition, blood was collected into chilled heparin tubes, placed in 96-well cell culture plates and incubated with an equal volume of Roswell Park Memorial Institute (RPMI) medium, with lipopolysaccharide (LPS) alone or with catecholamines. Tumor necrosis factor (TNF)-alpha levels in the supernatants were analyzed. RESULTS: The results indicated that the initial pain ratings did not differ between the groups analyzed. EA induced epinephrine secretion but not norepinephrine or dopamine secretion. Although EA and pharmacological treatment did not differ in terms of pain relief, in vitro epinephrine and norepinephrine reduced TNF-alpha production in response to LPS stimuli. CONCLUSION: EA activates the sympathetic nervous system and induces the release of epinephrine, which could ameliorate inflammation and protect muscular tissue in addition to relieving pain.

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