Ischemia/reperfusion-induced changes in intracellular free Ca2+ levels in rat skeletal muscle fibers – an in vivo study

2000 ◽  
Vol 440 (2) ◽  
pp. 302-308 ◽  
Author(s):  
Tamás Ivanics ◽  
Zsuzsa Miklós ◽  
Zoltán Ruttner ◽  
Sándor Bátkai ◽  
Dick W. Slaaf ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Ischemia Reperfusion ◽  
Muscle Fibers ◽  
In Vivo Study ◽  
Rat Skeletal Muscle ◽  
Skeletal Muscle Fibers ◽  
Induced Changes

scholarly journals ROS-Mediated Decline in Maximum Ca2+-Activated Force in Rat Skeletal Muscle Fibers following In Vitro and In Vivo Stimulation

PLoS ONE ◽  
2012 ◽  
Vol 7 (5) ◽  
pp. e35226 ◽  
Author(s):  
Travis L. Dutka ◽  
Esther Verburg ◽  
Noni Larkins ◽  
Kristin H. Hortemo ◽  
Per K. Lunde ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Fibers ◽  
Rat Skeletal Muscle ◽  
Skeletal Muscle Fibers

scholarly journals In vivo Ca2+ dynamics induced by Ca2+ injection in individual rat skeletal muscle fibers

2017 ◽  
Vol 5 (5) ◽  
pp. e13180 ◽  
Author(s):  
Mario Wakizaka ◽  
Hiroaki Eshima ◽  
Yoshinori Tanaka ◽  
Hideki Shirakawa ◽  
David C. Poole ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Fibers ◽  
Rat Skeletal Muscle ◽  
Skeletal Muscle Fibers

Effects of Creatine Supplementation During Resistance Training on Myosin Heavy Chain (MHC) Expression in Rat Skeletal Muscle Fibers

2010 ◽  
Vol 24 (1) ◽  
pp. 88-96 ◽  
Author(s):  
Andreo F Aguiar ◽  
Danilo H Aguiar ◽  
Alan DS Felisberto ◽  
Fernanda R Carani ◽  
Rachel C Milanezi ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Resistance Training ◽  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
Muscle Fibers ◽  
Creatine Supplementation ◽  
Rat Skeletal Muscle ◽  
Skeletal Muscle Fibers

Glycogen Depletion in Rat Skeletal Muscle Fibers During Exercise

1975 ◽  
pp. 397-401 ◽  
Author(s):  
R. B. Armstrong ◽  
C. W. Saubert ◽  
W. L. Sembrowich ◽  
R. E. Shepherd ◽  
P. D. Gollnick
Keyword(s):  
Skeletal Muscle ◽  
Muscle Fibers ◽  
Glycogen Depletion ◽  
Rat Skeletal Muscle ◽  
Skeletal Muscle Fibers

scholarly journals Exercise: Teaching myocytes new tricks

2017 ◽  
Vol 123 (2) ◽  
pp. 460-472 ◽  
Author(s):  
Scott K. Powers
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Cardiac Myocytes ◽  
Endurance Exercise ◽  
Ischemia Reperfusion ◽  
Muscle Fibers ◽  
Cardiac Phenotype ◽  
Endurance Exercise Training ◽  
Skeletal Muscle Fibers ◽  
Exercise Induced

Endurance exercise training promotes numerous cellular adaptations in both cardiac myocytes and skeletal muscle fibers. For example, exercise training fosters changes in mitochondrial function due to increased mitochondrial protein expression and accelerated mitochondrial turnover. Additionally, endurance exercise training alters the abundance of numerous cytosolic and mitochondrial proteins in both cardiac and skeletal muscle myocytes, resulting in a protective phenotype in the active fibers; this exercise-induced protection of cardiac and skeletal muscle fibers is often referred to as “exercise preconditioning.” As few as 3–5 consecutive days of endurance exercise training result in a preconditioned cardiac phenotype that is sheltered against ischemia-reperfusion-induced injury. Similarly, endurance exercise training results in preconditioned skeletal muscle fibers that are resistant to a variety of stresses (e.g., heat stress, exercise-induced oxidative stress, and inactivity-induced atrophy). Many studies have probed the mechanisms responsible for exercise-induced preconditioning of cardiac and skeletal muscle fibers; these studies are important, because they provide an improved understanding of the biochemical mechanisms responsible for exercise-induced preconditioning, which has the potential to lead to innovative pharmacological therapies aimed at minimizing stress-induced injury to cardiac and skeletal muscle. This review summarizes the development of exercise-induced protection of cardiac myocytes and skeletal muscle fibers and highlights the putative mechanisms responsible for exercise-induced protection in the heart and skeletal muscles.

scholarly journals Defective Acetylcholine Receptor Subunit Switch Precedes Atrophy of Slow-Twitch Skeletal Muscle Fibers Lacking ERK1/2 Kinases in Soleus Muscle

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Shuo Wang ◽  
Bonnie Seaberg ◽  
Ximena Paez-Colasante ◽  
Mendell Rimer
Keyword(s):  
Skeletal Muscle ◽  
Acetylcholine Receptor ◽  
Soleus Muscle ◽  
Muscle Fibers ◽  
Neuromuscular Synapse ◽  
Fiber Morphology ◽  
Skeletal Muscle Fibers ◽  
Slow Twitch

Abstract To test the role of extracellular-signal regulated kinases 1 and 2 (ERK1/2) in slow-twitch, type 1 skeletal muscle fibers, we studied the soleus muscle in mice genetically deficient for myofiber ERK1/2. Young adult mutant soleus was drastically wasted, with highly atrophied type 1 fibers, denervation at most synaptic sites, induction of “fetal” acetylcholine receptor gamma subunit (AChRγ), reduction of “adult” AChRε, and impaired mitochondrial biogenesis and function. In weanlings, fiber morphology and mitochondrial markers were mostly normal, yet AChRγ upregulation and AChRε downregulation were observed. Synaptic sites with fetal AChRs in weanling muscle were ~3% in control and ~40% in mutants, with most of the latter on type 1 fibers. These results suggest that: (1) ERK1/2 are critical for slow-twitch fiber growth; (2) a defective γ/ε-AChR subunit switch, preferentially at synapses on slow fibers, precedes wasting of mutant soleus; (3) denervation is likely to drive this wasting, and (4) the neuromuscular synapse is a primary subcellular target for muscle ERK1/2 function in vivo.

Excitation-contraction latencies in postnatal rat skeletal muscle fibers

1970 ◽  
Vol 29 (1) ◽  
pp. 142-151 ◽  
Author(s):  
Edward R. Chaplin ◽  
George W. Nell ◽  
Sheppard M. Walker
Keyword(s):  
Skeletal Muscle ◽  
Muscle Fibers ◽  
Rat Skeletal Muscle ◽  
Skeletal Muscle Fibers
Sign in / Sign up

Export Citation Format

Share Document