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Spinal μ‐opioid receptor sensitive locomotor muscle afferents decrease responsiveness of motor cortical cells and diminish cortical voluntary activation (705.1)
Author(s) -
Sidhu Simranjit,
Weavil Joshua,
Mangum Tyler,
Morgan David,
Jessop Jacob,
Richardson Russell,
Amann Markus
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.705.1
Subject(s) - transcranial magnetic stimulation , stimulation , silent period , medicine , opioid , neuroscience , endocrinology , chemistry , receptor , psychology
We investigated the influence of group III/IV locomotor muscle afferents on the development of supraspinal fatigue and changes in motor cortical cell responsiveness by comparison of cortical versus spinal excitability during sustained cycling exercise. Six males performed constant‐load cycling exercise (80% peak power‐output) to exhaustion under control conditions (CTRL) and with lumbar intrathecal fentanyl (FENT) impairing feedback from µ‐opioid receptor‐sensitive lower limb muscle afferents. Pre‐to‐post exercise changes in voluntary activation (VA) and potentiated quadriceps twitch force (∆Qtw) were assessed via transcranial magnetic (TMS) and electrical femoral nerve stimulation (FNS). During cycling, vastus lateralis responses evoked by TMS (MEP) and electrical cervicomedullary stimulation (CMEP) were normalized to FNS‐evoked M‐waves. Although maximum voluntary quadriceps torque was similarly reduced following both trials (~14%; P<0.05), ∆Qtw was greater in FENT vs. CTRL (51 ± 5% vs. 62 ± 7%; P<0.05). Furthermore, VA was reduced by 6% in CTRL (P<0.05) but remained unchanged in FENT. MEP increased throughout the exercise in FENT (14 ± 5%; P<0.05) but remained unchanged in CTRL. CMEP did not change in either session. Our findings suggest that group III/IV muscle afferents compromise motor cortical cell responsiveness during locomotor exercise and facilitate supraspinal fatigue. Grant Funding Source : HL_103786; HL‐116579