scholarly journals Reversible inhibition of sarcoplasmic reticulum Ca-ATPase by altered neuromuscular activity in rabbit fast-twitch muscle

1987 ◽  
Vol 162 (3) ◽  
pp. 555-561 ◽  
Author(s):  
Ekkehard LEBERER ◽  
Karl-Thomas HARTNER ◽  
Dirk PETTE
1993 ◽  
Vol 264 (4) ◽  
pp. R816-R819 ◽  
Author(s):  
G. J. Etgen ◽  
R. P. Farrar ◽  
J. L. Ivy

Insulin- and contraction-stimulated skeletal muscle glucose transport is governed largely by the GLUT-4 isoform of the glucose transporter. Recently, it has been demonstrated that denervated muscle has decreased GLUT-4 protein content, suggesting that regulation of GLUT-4 protein is related to neuromuscular activity. However, until now the effects of the opposite situation, enhanced neuromuscular activity, could only be speculated on from exercise training studies. In the present investigation the effect of chronic low-frequency electrical stimulation (10 Hz, 8 h/day) on GLUT-4 protein content and citrate synthase activity was determined in the predominantly fast-twitch plantaris. Chronic electrical stimulation enhanced GLUT-4 protein content and citrate synthase activity in the muscles stimulated for 10-20 days. Electrical stimulation lasting 30-40 days resulted in no further enhancement of GLUT-4 protein content while citrate synthase activity continued to increase. Further prolongation of electrical stimulation (60-90 days) resulted in a plateauing of citrate synthase activity. The results suggest that increased neuromuscular activity can act independently of systemic changes to increase total GLUT-4 protein content. They also suggest that both GLUT-4 protein content and citrate synthase activity are positively related to increased neuromuscular activity but that their rates of increase differ substantially.


2019 ◽  
Vol 316 (5) ◽  
pp. R543-R551 ◽  
Author(s):  
Daiki Watanabe ◽  
Chihiro Aibara ◽  
Masanobu Wada

Skeletal muscles undergoing vigorous activity can enter a state of prolonged low-frequency force depression (PLFFD). This study was conducted to examine whether antioxidant treatment is capable of accelerating the recovery from PLFFD, with a focus on the function of the sarcoplasmic reticulum (SR) and myofibril. One hour before fatiguing stimulation (FS) was administered, rats received an intraperitoneal injection of Eukarion (EUK-134), which mimics the activities of superoxide dismutase and catalase. Intact muscles of the hindlimbs were electrically stimulated via the sciatic nerve until the force was reduced to ~50% of the initial force (FS). Thirty minutes after cessation of FS, the superficial regions of gastrocnemius muscles were dissected and used for biochemical and skinned-fiber analyses. Whole muscle analyses revealed that antioxidant alleviated the FS-induced decrease in the reduced glutathione content. Skinned-fiber analyses showed that the antioxidant did not affect the FS-induced decrease in the ratio of force at 1 Hz to that at 50 Hz. However, the antioxidant partially inhibited the FS-mediated decrease in the ratio of depolarization-induced force to the maximum Ca2+-activated force. Furthermore, the antioxidant completely suppressed the FS-induced increase in myofibrillar Ca2+ sensitivity. These results suggest that antioxidant treatment is ineffective in facilitating the restoration of PLFFD, probably due to its negative effect on myofibrillar Ca2+ sensitivity, which supersedes its positive effect on SR Ca2+ release.


1989 ◽  
Vol 185 (1) ◽  
pp. 51-54 ◽  
Author(s):  
Ekkehard LEBERER ◽  
Karl-Thomas HARTNER ◽  
Christopher J. BRANDL ◽  
Junichi FUJII ◽  
Michihiko TADA ◽  
...  

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