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Decreased nerve growth factor upregulation is a mechanism for reduced mechanical hyperalgesia after the second bout of exercise in rats
Author(s) -
Urai H.,
Murase S.,
Mizumura K.
Publication year - 2013
Publication title -
scandinavian journal of medicine and science in sports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.575
H-Index - 115
eISSN - 1600-0838
pISSN - 0905-7188
DOI - 10.1111/sms.12013
Subject(s) - downregulation and upregulation , hyperalgesia , nerve growth factor , bradykinin , endocrinology , delayed onset muscle soreness , antagonist , medicine , chemistry , anesthesia , receptor , nociception , muscle damage , biochemistry , gene
Delayed onset muscle soreness ( DOMS ) is reduced when the same exercise is repeated after a certain interval. However, the mechanism for this adaptation, called a repeated bout effect, is still not well understood. Recently, we showed that upregulated nerve growth factor ( NGF ) triggered by B 2 bradykinin receptor ( B2R ) activation in exercised muscle was responsible for DOMS . In this study, we investigated whether NGF upregulation was reduced after repeated bouts of exercise in rats, and if so, whether this change occurred upstream of B2R . A bout of 500 lengthening contractions ( LC ) was applied on day 0 and again 5 days later. DOMS was evaluated by the mechanical withdrawal threshold of the exercised extensor digitorum longus ( EDL ) muscle. Mechanical hyperalgesia and NGF m RNA upregulation in EDL were observed after the first LC , but not after the second LC . We then injected HOE 140, a B2R antagonist with effects lasting only several hours, once before the first LC . This blocked the development of mechanical hyperalgesia and NGF m RNA upregulation not only after the first LC but also after the second LC . This suggests that adaptation occurred upstream of B2R , as the influence of the first LC was limited to that area by HOE 140.