Low-frequency stimulation of rat fast-twitch muscle enhances the expression of hexokinase II and both the translocation and expression of glucose transporter 4 (GLUT-4)

1994 ◽  
Vol 219 (1-2) ◽  
pp. 307-315 ◽  
Author(s):  
Sabine HOFMANN ◽  
Dirk PETTE
Keyword(s):  
Glucose Transporter ◽  
Low Frequency ◽  
Glucose Transporter 4 ◽  
Hexokinase Ii ◽  
Glut 4 ◽  
Low Frequency Stimulation ◽  
Fast Twitch Muscle ◽  
Frequency Stimulation ◽  
Fast Twitch ◽  
Stimulation Of

Effect of chronic electrical stimulation on GLUT-4 protein content in fast-twitch muscle

1993 ◽  
Vol 264 (4) ◽  
pp. R816-R819 ◽  
Author(s):  
G. J. Etgen ◽  
R. P. Farrar ◽  
J. L. Ivy
Keyword(s):  
Electrical Stimulation ◽  
Protein Content ◽  
Glucose Transporter ◽  
Citrate Synthase ◽  
Low Frequency ◽  
Neuromuscular Activity ◽  
Glut 4 ◽  
Fast Twitch Muscle ◽  
Chronic Electrical Stimulation ◽  
Fast Twitch

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.

scholarly journals Neural control of gene expression in skeletal muscle. Calcium-sequestering proteins in developing and chronically stimulated rabbit skeletal muscles

1986 ◽  
Vol 239 (2) ◽  
pp. 295-300 ◽  
Author(s):  
E Leberer ◽  
U Seedorf ◽  
D Pette
Keyword(s):  
Neural Control ◽  
Low Frequency ◽  
Neuron Activity ◽  
Control Of Gene Expression ◽  
Low Frequency Stimulation ◽  
Fast Twitch Muscle ◽  
Frequency Stimulation ◽  
Slow Twitch ◽  
Fast Twitch

Tissue contents of the sarcoplasmic-reticulum Ca2+-ATPase (Ca2+ +Mg2+-dependent ATPase), of calsequestrin and of parvalbumin were immunochemically quantified in homogenates of fast- and slow-twitch muscles of embryonic, maturing and adult rabbits. Unlike parvalbumin, Ca2+-ATPase and calsequestrin were expressed in embryonic muscles. Presumptive fast-twitch muscles displayed higher contents of these two proteins than did presumptive slow-twitch muscles. Calsequestrin steeply increased before birth and reached adult values in the two muscle types 4 days after birth. The main increase in Ca2+-ATPase occurred during the first 2 weeks after birth. Denervation of postnatal fast- and slow-twitch muscles decreased calsequestrin to amounts typical of embryonic muscle and suppressed further increases of Ca2+-ATPase. Denervation caused slight decreases in Ca2+-ATPase in adult fast-twitch, but not in slow-twitch, muscles, whereas calsequestrin was greatly decreased in both. Chronic low-frequency stimulation induced a rapid decrease in parvalbumin in fast-twitch muscle, which was preceded by a drastic decrease in the amount of its polyadenylated RNA translatable in vitro. Tissue amounts of Ca2+-ATPase and calsequestrin were essentially unaltered up to periods of 52 days stimulation. These results indicate that in fast- and slow-twitch muscles different basal amounts of Ca2+-ATPase and calsequestrin are expressed independent of innervation, but that neuromuscular activity has a modulatory effect. Conversely, the expression of parvalbumin is greatly enhanced by phasic, and drastically decreased by tonic, motor-neuron activity.

scholarly journals Cachectic skeletal muscle response to a novel bout of low-frequency stimulation

2014 ◽  
Vol 116 (8) ◽  
pp. 1078-1087 ◽  
Author(s):  
Melissa J. Puppa ◽  
E. Angela Murphy ◽  
Raja Fayad ◽  
Gregory A. Hand ◽  
James A. Carson
Keyword(s):  
Muscle Contraction ◽  
Cancer Cachexia ◽  
Glucose Transporter ◽  
Low Frequency ◽  
Pyrrolidine Dithiocarbamate ◽  
Peroxisome Proliferator ◽  
Glucose Transporter 4 ◽  
Peroxisome Proliferator Activated Receptor ◽  
Low Frequency Stimulation ◽  
Frequency Stimulation

While exercise benefits have been well documented in patients with chronic diseases, the mechanistic understanding of cachectic muscle's response to contraction is essentially unknown. We previously demonstrated that treadmill exercise training attenuates the initiation of cancer cachexia and the development of metabolic syndrome symptoms (Puppa MJ, White JP, Velazquez KT, Baltgalvis KA, Sato S, Baynes JW, Carson JA. J Cachexia Sarcopenia Muscle 3: 117–137, 2012). However, cachectic muscle's metabolic signaling response to a novel, acute bout of low-frequency contraction has not been determined. The purpose of this study was to determine whether severe cancer cachexia disrupts the acute contraction-induced response to low-frequency muscle contraction [low-frequency stimulation (LoFS)]. Metabolic gene expression and signaling was examined 3 h after a novel 30-min bout of contraction (10 Hz) in cachectic ApcMin/+(Min) and C57BL/6 (BL-6) mice. Pyrrolidine dithiocarbamate, a STAT/NF-κB inhibitor and free radical scavenger, was administered systemically to a subset of mice to determine whether this altered the muscle contraction response. Although glucose transporter-4 mRNA was decreased by cachexia, LoFS increased muscle glucose transporter-4 mRNA in both BL-6 and Min mice. LoFS also induced muscle peroxisome proliferator-activated receptor-γ and peroxisome proliferator-activated receptor-α coactivator-1 mRNA. However, in Min mice, LoFS was not able to induce muscle proliferator-activated receptor-α coactivator-1 targets nuclear respiratory factor-1 and mitochondrial transcription factor A mRNA. LoFS induced phosphorylated-S6 in BL-6 mice, but this induction was blocked by cachexia. Administration of pyrrolidine dithiocarbamate for 24 h rescued LoFS-induced phosphorylated-S6 in cachectic muscle. LoFS increased muscle phosphorylated-AMP-activated protein kinase and p38 in BL-6 and Min mice. These data demonstrate that cachexia alters the muscle metabolic response to acute LoFS, and combination therapies in concert with muscle contraction may be beneficial for improving muscle mass and function during cachexia.

Calcium transients in single fibers of low-frequency stimulated fast-twitch muscle of rat

1999 ◽  
Vol 277 (6) ◽  
pp. C1122-C1129 ◽  
Author(s):  
Stefanie Carroll ◽  
Pierluigi Nicotera ◽  
Dirk Pette
Keyword(s):  
Rate Constant ◽  
Binding Capacity ◽  
Low Frequency ◽  
Partial Recovery ◽  
Single Fibers ◽  
Low Frequency Stimulation ◽  
Fast Twitch Muscle ◽  
Frequency Stimulation ◽  
Slow Twitch Fibers ◽  
Fast Twitch

Ca2+transients were investigated in single fibers isolated from rat extensor digitorum longus muscles exposed to chronic low-frequency stimulation for different time periods up to 10 days. Approximately 2.5-fold increases in resting Ca2+ concentration ([Ca2+]) were observed 2 h after stimulation onset and persisted throughout the stimulation period. The elevated [Ca2+] levels were in the range characteristic of slow-twitch fibers from soleus muscle. In addition, we noticed a transitory elevation of the integral [Ca2+] per pulse with a maximum (∼5-fold) after 1 day. Steep decreases in rate constant of [Ca2+] decay could be explained by an immediate impairment of Ca2+ uptake and, with longer stimulation periods, by an additional loss of cytosolic Ca2+ binding capacity resulting from a decay in parvalbumin content. A partial recovery of the rate constant of [Ca2+] decay in 10-day stimulated muscle could be explained by an increasing mitochondrial contribution to Ca2+ sequestration.

Altered gene expression in fast-twitch muscle induced by chronic low-frequency stimulation

1992 ◽  
Vol 262 (3) ◽  
pp. R333-R338 ◽  
Author(s):  
D. Pette ◽  
S. Dusterhoft
Keyword(s):  
Fiber Type ◽  
Low Frequency ◽  
Protein Isoforms ◽  
Control Factor ◽  
Phenotypic Properties ◽  
Altered Expression ◽  
Low Frequency Stimulation ◽  
Fast Twitch Muscle ◽  
Frequency Stimulation ◽  
Fast Twitch

Increased neuromuscular activity via chronic low-frequency stimulation induces multiple fast-to-slow transitions in phenotypic properties that ultimately lead to fiber type conversions in the fast-twitch muscle of small mammals. Most of these alterations occur in an ordered sequence and result from the sequentially altered expression of myofibrillar and other protein isoforms. These changes relate to altered levels of specific mRNAs, followed by alterations in protein synthesis. As shown by the exchange of myosin heavy chain isoforms, protein degradation may be an additional control factor involved in the rearrangement of the myofibrillar apparatus. The degree of the various fast-to-slow transitions is species dependent and may be related to differences in thyroid hormone levels. It is suggested that the drastically and persistently depressed phosphorylation potential of the ATP system possibly serves to trigger the transformation process.

Creatine loading elevates the intracellular phosphorylation potential and alters adaptive responses of rat fast-twitch muscle to chronic low-frequency stimulation

2015 ◽  
Vol 40 (7) ◽  
pp. 671-682 ◽  
Author(s):  
Charles T. Putman ◽  
Maria Gallo ◽  
Karen J.B. Martins ◽  
Ian M. MacLean ◽  
Michelle J. Jendral ◽  
...  
Keyword(s):  
Low Frequency ◽  
Adaptive Responses ◽  
Slow Fibre ◽  
Phosphorylation Potential ◽  
Time To Peak ◽  
Low Frequency Stimulation ◽  
Fast Twitch Muscle ◽  
Frequency Stimulation ◽  
Induced Changes ◽  
Fast Twitch

This study tested the hypothesis that elevating the intracellular phosphorylation potential (IPP = [ATP]/[ADP]free) within rat fast-twitch tibialis anterior muscles by creatine (Cr) loading would prevent fast-to-slow fibre transitions induced by chronic low-frequency electrical stimulation (CLFS, 10 Hz, 12 h/day). Creatine-control and creatine-CLFS groups drank a solution of 1% Cr + 5% dextrose, ad libitum, for 10 days before and during 10 days of CLFS; dextrose-control and dextrose-CLFS groups drank 5% dextrose. Cr loading increased total Cr (P < 0.025), phosphocreatine (PCr) (P < 0.003), and the IPP (P < 0.0008) by 34%, 45%, and 64%, respectively. PCr and IPP were 46% (P < 0.002) and 76% (P < 0.02) greater in creatine-CLFS than in dextrose-CLFS. Higher IPP was confirmed by a 58% reduction in phospho-AMP-activated protein kinase α (Thr172) (P < 0.006). In dextrose-CLFS, myosin heavy chain (MyHC) I and IIa transcripts increased 32- and 38-fold (P < 0.006), respectively, whereas MyHC-IIb mRNA decreased by 75% (P < 0.03); the corresponding MyHC-I and MyHC-IIa protein contents increased by 2.0- (P < 0.03) and 2.7-fold (P < 0.05), respectively, and MyHC-IIb decreased by 30% (P < 0.03). In contrast, within creatine-CLFS, MyHC-I and MyHC-IIa mRNA were unchanged and MyHC-IIb mRNA decreased by 75% (P < 0.003); the corresponding MyHC isoform contents were not altered. Oxidative reference enzymes were similarly elevated (P < 0.01) in dextrose-CLFS and creatine-CLFS, but reciprocal reductions in glycolytic reference enzymes occurred only in dextrose-CLFS (P < 0.02). Preservation of the glycolytic potential and greater SERCA2 and parvalbumin contents in creatine-CLFS coincided with prolonged time to peak tension and half-rise time (P < 0.01). These results highlight the IPP as an important physiological regulator of muscle fibre plasticity and demonstrate that training-induced changes typically associated with improvements in muscular endurance or increased power output are not mutually exclusive in Cr-loaded muscles.

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