Open AccessThermal pretreatment facilitates recovery from prolonged low‐frequency force depression in rat fast‐twitch muscle
Author(s) -
Watanabe Daiki,
Aibara Chihiro,
Okada Naoki,
Wada Masanobu
Publication year - 2018
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.14814/phy2.13853
Subject(s) - myofibril , endoplasmic reticulum , stimulation , contraction (grammar) , chemistry , depolarization , muscle contraction , biophysics , medicine , materials science , endocrinology , biology , biochemistry
The aim of this study was to examine whether thermal pretreatment can accelerate recovery from prolonged low‐frequency force depression. The hindlimbs of thermal treated (T‐treated) rats were immersed in water heated to 42.0°C for 20 min (thermal pretreatment). The thermal pretreatment was performed once a day for 5 days before fatiguing stimulation. Intact gastrocnemius muscles were electrically stimulated via the sciatic nerve until force was reduced to ~50% of the initial and dissected immediately [recovery 0 ( REC 0)] or 60 min [recovery 60 ( REC 60)] following the cessation of stimulation. Using skinned fiber prepared from the superficial region, the ratio of force at 1 Hz to that at 50 Hz (low‐to‐high force ratio), the ratio of depolarization (depol)‐induced force to maximum Ca 2+ ‐activated force (depol/max Ca 2+ force ratio), the steepness of force‐Ca 2+ concentration curves, and myofibrillar Ca 2+ sensitivity were measured. At REC 0, the low‐to‐high force ratio and depol/max Ca 2+ force ratio decreased in stimulated muscles from both non‐ and thermal‐treated rats. At REC 60, these two parameters remained depressed in non‐treated rats, whereas they reverted to resting levels in T‐treated rats. Thermal pretreatment exerted no effect on myofibrillar Ca 2+ sensitivity. The present results reveal that thermal pretreatment can facilitate recovery of submaximum force after vigorous contraction, which is mediated via a quick return of Ca 2+ release from the sarcoplasmic reticulum to resting levels.