title: Predominant cause of prolonged low-frequency force depression changes during recovery after in situ fatiguing stimulation of rat fast-twitch muscle.
abstract: To investigate time-dependent changes in sarcoplasmic reticulum (SR) Ca2+release and myofibrillar (my-) Ca2+sensitivity during recovery from prolonged low-frequency force depression (PLFFD), rat gastrocnemius muscles were electrically stimulated in situ. After 0 h (R0), 0.5 h (R0.5), 2 h (R2), 6 h (R6), or 12 h of recovery, the superficial gastrocnemius muscles were excised and used for biochemical and skinned fiber analyses. At R0, R0.5, R2, and R6, the ratio of force at 1 Hz to that at 50 Hz was decreased in the skinned fibers. The ratio of depolarization-induced force to the maximum Ca2+-activated force (depol/Ca2+force ratio) was utilized as an indicator of SR Ca2+release. At R0, both the depol/Ca2+force ratio and my-Ca2+sensitivity were decreased. At R0.5 and R2, my-Ca2+sensitivity was recovered, while the depol/Ca2+force ratio remained depressed. At R6, my-Ca2+sensitivity was decreased again, whereas the depol/Ca2+force ratio was nearly restored. Western blot analyses demonstrated that decreased my-Ca2+sensitivity at R6 and reduced depol/Ca2+force ratio at R0, R0.5, and R2 were accompanied by depressions in S-glutathionylated troponin I and increases in dephosphorylated ryanodine receptor 1, respectively. These results indicate that, in the early stage of recovery, reduced SR Ca2+release plays a primary role in the etiology of PLFFD, whereas decreased my-Ca2+sensitivity is involved in the late stage, and suggest that S-glutathionylation of troponin I and dephosphorylation of ryanodine receptor 1 contribute, at least partly, to fatiguing contraction-induced alterations in my-Ca2+sensitivity and SR Ca2+release, respectively.
authors.affiliation: Graduate School of Integrated Arts and Sciences, Hiroshima University, Hiroshima, Japan; and.|Research Fellow of Japan Society for the Promotion of Science, Tokyo, Japan.
authors.forename: Daiki
authors.initials: D
authors.lastname: Watanabe
authors.affiliation: Graduate School of Integrated Arts and Sciences, Hiroshima University, Hiroshima, Japan; and wada@hiroshima-u.ac.jp.
authors.forename: Masanobu
authors.initials: M
authors.lastname: Wada
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism; D020013:Calcium Signaling / Q000502:physiology*; D004558:Electric Stimulation / Q000379:methods; D007537:Isometric Contraction / Q000502:physiology*; D036881:Long-Term Synaptic Depression / Q000502:physiology; D008297:Male; D018763:Muscle Fatigue / Q000502:physiology*; D018656:Muscle Fibers, Fast-Twitch / Q000502:physiology*; D053580:Muscle Strength / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D020127:Recovery of Function / Q000502:physiology*; D012519:Sarcoplasmic Reticulum / Q000378:metabolism*; D013314:Stress, Mechanical
chemical_list: D002118:Calcium
keywords: S-glutathionylation; SR Ca2+ release; dephosphorylation; muscle fatigue; myofibrillar Ca2+ sensitivity