Abstract
Sports-related pain and injury is directly linked to tissue inflammation, thus involving the autonomic nervous system (ANS). In the present experimental study, we disable the sympathetic part of the ANS by applying a stellate ganglion block (SGB) in an experimental model of delayed onset muscle soreness (DOMS) of the biceps muscle. We included 45 healthy participants (female 11, male 34, age 24.16 ± 6.67 years [range 18–53], BMI 23.22 ± 2.09 kg/m2) who were equally randomized to receive either (i) an SGB prior to exercise-induced DOMS (preventive), (ii) sham intervention in addition to DOMS (control/sham), or (iii) SGB after the induction of DOMS (rehabilitative). The aim of the study was to determine whether and to what extent sympathetically maintained pain (SMP) is involved in DOMS processing. Focusing on the muscular area with the greatest eccentric load (biceps distal fifth), a significant time × group interaction on the pressure pain threshold was observed between preventive SGB and sham (p = 0.034). There was a significant effect on pain at motion (p = 0.048), with post hoc statistical difference at 48 h (preventive SGB Δ1.09 ± 0.82 cm VAS vs. sham Δ2.05 ± 1.51 cm VAS; p = 0.04). DOMS mediated an increase in venous cfDNA -as a potential molecular/inflammatory marker of DOMS- within the first 24 h after eccentric exercise (time effect p = 0.018), with a peak at 20 and 60 min. After 60 min, cfDNA levels were significantly decreased comparing preventive SGB to sham (unpaired t-test p = 0.008). At both times, 20 and 60 min, cfDNA significantly correlated with observed changes in PPT. The 20-min increase was more sensitive, as it tended toward significance at 48 h (r = 0.44; p = 0.1) and predicted the early decrease of PPT following preventive stellate blocks at 24 h (r = 0.53; p = 0.04). Our study reveals the broad impact of the ANS on DOMS and exercise-induced pain. For the first time, we have obtained insights into the sympathetic regulation of pain and inflammation following exercise overload. As this study is of a translational pilot character, further research is encouraged to confirm and specify our observations.
Highlights
Acute pain is generally accompanied by acute inflammation, a protective response involving immune cells, blood vessels, and molecular mediators, which is physiologically thought to eliminate the initial cause of cell injury and initiate tissue repair
Since microtraumas and inflammation seem to play a role in athletic overload (Seidel et al, 2012; Wilke et al, 2017), we investigated the association of alterations in cell-free DNA (cfDNA) as a secondary outcome upon studying the association of the SNS with delayed onset muscle soreness (DOMS)
We evaluated the role of cfDNA as a potential molecular marker of DOMS in preventive stellate ganglion block (SGB) and sham control
Summary
Acute pain is generally accompanied by acute inflammation, a protective response involving immune cells, blood vessels, and molecular mediators, which is physiologically thought to eliminate the initial cause of cell injury and initiate tissue repair. Inflammatory mediators are able to bind to nociceptors in the peripheral nervous system innervating areas such as fascia and muscle (Ji et al, 2016) They induce vasodilation, extravasation of plasma proteins, and the release of further chemical mediators (Rittner and Stein, 2005). Being an information and control system, the ANS balances all organ systems against each other, maintaining homeostasis For this reason, it is logical that the ANS is involved in pain, inflammation, and immune processes in a “coordinating” way and plays an important role in microcirculation (Elenkov et al, 2000; Tracey, 2002, 2009; Jänig, 2006; Schaible et al, 2011; Janig, 2014)
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