Preconditioning contractions prevent prolonged force depression and Ca2+-dependent proteolysis of STAC3 after damaging eccentric contractions

Preconditioning contractions (PCs) have been shown to markedly improve recovery from eccentric contractions (ECCs)-induced force depression. We here examined the mechanism behind the effects of PCs with focusing on the SH3 and cysteine-rich domain 3 (STAC3) that is essential for coupling membrane de...

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Bibliographic Details
Published inJournal of applied physiology (1985) Vol. 131; no. 5; pp. 1399 - 1407
Main Authors Ashida, Yuki, Himori, Koichi, Tamai, Katsuyuki, Kimura, Iori, Yamada, Takashi
Format Journal Article
LanguageEnglish
Published Bethesda American Physiological Society 01.11.2021
Subjects
Calcium (reticular)
Calcium ions
Calpain
Cell activation
Cell membranes
Depolarization
Membrane permeability
Membrane potential
Muscle contraction
Muscles
Preconditioning
Proteolysis
Recovery
Sarcoplasmic reticulum
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Summary:Preconditioning contractions (PCs) have been shown to markedly improve recovery from eccentric contractions (ECCs)-induced force depression. We here examined the mechanism behind the effects of PCs with focusing on the SH3 and cysteine-rich domain 3 (STAC3) that is essential for coupling membrane depolarization to Ca2+ release from the sarcoplasmic reticulum. Rat medial gastrocnemius (MG) muscles were excised immediately (REC0), 1 day (REC1), and 4 days (REC4) after exposure to 100 repeated damaging ECCs in vivo. PCs with 10 repeated nondamaging ECCs were applied 2 days before the damaging ECCs. Damaging ECCs induced in vivo isometric torque depression at 50 and 100 Hz stimulation frequencies, which was accompanied by a significant decrease in the amount of full-length STAC3, an activation of calpain 1, and an increased number of Evans Blue dye-positive fibers in MG muscles at REC1 and REC4. Interestingly, PCs attenuated all these deleterious alterations induced by damaging ECCs. Moreover, mechanistic experiments performed on normal muscle samples exposed to various concentration of Ca2+ showed a Ca2+-dependent proteolysis of STAC3, which was prevented by calpain inhibitor MDL-28170. In conclusion, PCs may improve recovery from force depression after damaging ECCs, in part by inhibiting the loss of STAC3 due to the increased permeability of cell membrane and subsequent activation of calpain 1.
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ISSN:8750-7587
1522-1601
DOI:10.1152/japplphysiol.00463.2021