Document Detail


Bradykinin and nerve growth factor play pivotal roles in muscular mechanical hyperalgesia after exercise (delayed-onset muscle soreness).
MedLine Citation:
PMID:  20220009     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Unaccustomed strenuous exercise that includes lengthening contraction (LC) often causes delayed-onset muscle soreness (DOMS), a kind of muscular mechanical hyperalgesia. The substances that induce this phenomenon are largely unknown. Peculiarly, DOMS is not perceived during and shortly after exercise, but rather is first perceived after approximately 1 d. Using B(2) bradykinin receptor antagonist HOE 140, we show here that bradykinin released during exercise plays a pivotal role in triggering the process that leads to muscular mechanical hyperalgesia. HOE 140 completely suppressed the development of muscular mechanical hyperalgesia when injected before LC, but when injected 2 d after LC failed to reverse mechanical hyperalgesia that had already developed. B(1) antagonist was ineffective, regardless of the timing of its injection. Upregulation of nerve growth factor (NGF) mRNA and protein occurred in exercised muscle over a comparable time course (12 h to 2 d after LC) for muscle mechanical hyperalgesia. Antibodies to NGF injected intramuscularly 2 d after exercise reversed muscle mechanical hyperalgesia. HOE 140 inhibited the upregulation of NGF. In contrast, shortening contraction or stretching induced neither mechanical hyperalgesia nor NGF upregulation. Bradykinin together with shortening contraction, but not bradykinin alone, reproduced lasting mechanical hyperalgesia. We also showed that rat NGF sensitized thin-fiber afferents to mechanical stimulation in the periphery after 10-20 min. Thus, NGF upregulation through activation of B(2) bradykinin receptors is essential (though not satisfactory) to mechanical hyperalgesia after exercise. The present observations explain why DOMS occurs with a delay, and why lengthening contraction but not shortening contraction induces DOMS.
Authors:
Shiori Murase; Etsuji Terazawa; Fernando Queme; Hiroki Ota; Teru Matsuda; Kenji Hirate; Yasuko Kozaki; Kimiaki Katanosaka; Toru Taguchi; Hisako Urai; Kazue Mizumura
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of neuroscience : the official journal of the Society for Neuroscience     Volume:  30     ISSN:  1529-2401     ISO Abbreviation:  J. Neurosci.     Publication Date:  2010 Mar 
Date Detail:
Created Date:  2010-03-11     Completed Date:  2010-04-09     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8102140     Medline TA:  J Neurosci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  3752-61     Citation Subset:  IM    
Affiliation:
Department of Neuroscience II, Research Institute of Environmental Medicine, Nagoya University, Nagoya 464-8601, Japan.
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MeSH Terms
Descriptor/Qualifier:
Animals
Bradykinin / physiology*,  secretion
Electric Stimulation / methods
Hyperalgesia / physiopathology*
Male
Mechanoreceptors / physiology
Muscle Contraction / physiology
Muscle, Skeletal / physiology*
Nerve Fibers, Unmyelinated / physiology
Pain Measurement* / methods
Physical Conditioning, Animal* / methods
Rats
Rats, Sprague-Dawley
Time Factors
Chemical
Reg. No./Substance:
58-82-2/Bradykinin

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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