The importance of limitations in aerobic metabolism, glycolysis, and membrane excitability for the development of high-frequency fatigue in isolated rat soleus muscle

2007 ◽  
Vol 292 (5) ◽  
pp. R2001-R2011 ◽  
Author(s):  
K. T. Murphy ◽  
T. Clausen
Keyword(s):  
Soleus Muscle ◽  
High Frequency ◽  
Receptor Agonist ◽  
Aerobic Metabolism ◽  
Membrane Excitability ◽  
M Wave ◽  
Force Transducers ◽  
Rat Soleus Muscle ◽  
Isolated Rat

We investigated the role of limitations in aerobic metabolism, glycolysis, and membrane excitability for development of high-frequency fatigue in isolated rat soleus muscle. Muscles mounted on force transducers were incubated in buffer bubbled with 5% CO2 and either 95% O2 (oxygenated) or 95% N2 (anoxic) and stimulated at 60 Hz continuously for 30–120 s or intermittently for 120 s. Cyanide (2 mM) and 2-deoxyglucose (10 mM) were used to inhibit aerobic metabolism and both glycolysis and aerobic metabolism, respectively. Excitability was reduced by carbacholine (10 μM), a nicotinic ACh receptor agonist, or ouabain (10 μM), an Na+-K+ pump inhibitor. Membrane excitability was measured by recording M waves. Intracellular Na+ and K+ contents and membrane potentials were measured by flame photometry and microelectrodes, respectively. During 120 s of continuous stimulation, oxygenated and anoxic muscles showed the same force loss. In oxygenated muscles, cyanide did not alter force loss for up to 90 s, whereas 2-deoxyglucose increased force loss (by 19–69%; P < 0.01) from 14 s of stimulation. In oxygenated muscles, 60 s of stimulation reduced force, M wave area, and amplitude by 70–90% ( P < 0.001). Carbacholine or ouabain increased intracellular Na+ content ( P < 0.001), induced a 7- to 8-mV membrane depolarization ( P < 0.001), and accelerated the rate of force loss (by 250–414%) during 30 s of stimulation ( P < 0.001). Similar effects were seen with intermittent stimulation. In conclusion, limitations in glycolysis and subsequently also in aerobic metabolism, as well as membrane excitability but not aerobic metabolism alone, appear to play an important role in the development of high-frequency fatigue in isolated rat soleus muscle.

On the role of 5-hydroxytryptamine in the peripheral action of fenfluramine: studies with the isolated rat soleus muscle

1990 ◽  
Vol 39 (5) ◽  
pp. 965-968 ◽  
Author(s):  
Shlomo Sasson ◽  
Baruch Kunievsky ◽  
Christine Nathan ◽  
Erol Ceras
Keyword(s):  
Soleus Muscle ◽  
Rat Soleus Muscle ◽  
Peripheral Action ◽  
Isolated Rat

scholarly journals PO-064 A potential role of stretch-activated channels in anabolic mechanotransduction in the atrophied rat soleus muscle

2018 ◽  
Vol 1 (3) ◽  
Author(s):  
Timur Mirzoev ◽  
Sergey Tyganov ◽  
Boris Shenkman
Keyword(s):  
Skeletal Muscle ◽  
Soleus Muscle ◽  
Contractile Function ◽  
Mammalian Skeletal Muscle ◽  
Mechanical Unloading ◽  
Mtorc1 Signaling ◽  
Significant Difference ◽  
Rat Soleus Muscle ◽  
Isolated Rat

Objective Prolonged immobilization or unloading of skeletal muscle causes muscle disuse atrophy, which is characterized by a reduction in muscle cross-sectional area and compromised contractile function. To date, the mechanisms of anabolic mechanotransduction in the atrophied mammalian skeletal muscle remain poorly understood. The aim of the present study was to assess a possible role of stretch-activated ion channels (SAC) in the propagation of a mechanical signal to anabolic signaling and protein synthesis (PS) in an isolated rat soleus muscle following mechanical unloading. Methods The mechanical unloading was performed via hindlimb suspension (HS). Twenty-eight male Wistar rats weighing were randomly assigned to the following 4 groups (n=7/group): 1) vivarium control (C), 2) control + SAC inhibitor (gadolinium) (C+Gd3+), 3) 7-day HS (HS), 4) 7-day HS + SAC inhibitor (HS+Gd3+). Following unloading, an isolated rat soleus was placed in an organ culture medium and subjected to a bout of eccentric contractions (EC). Upon completion of the EC, muscles were collected for Western blot analyses to determine the content of the key anabolic markers. The rate of PS was measured by SUnSET technique. Results EC-induced increase in PS was significantly less in the HS and HS+ Gd3+ groups vs. the C group. There was no statistically significant difference between the HS and HS+ Gd3+ groups in terms of EC-induced increase in muscle PS. A decrease in EC-induced phosphorylation of p70S6K, 4E-BP1, RPS6 and GSK-3beta in the 7-day unloaded soleus treated with SAC inhibitor did not differ from that of the 7-day unloaded soleus without SAC blockade. Thus, the inhibition of SAC with gadolinium did not lead to further decline in EC-induced phosphorylation of the key anabolic markers and muscle PS. Conclusions The results of the study suggest that attenuation of mTORC1-signaling and PS in response to EC in unloaded soleus muscle may be associated with inactivation of SAC. The study was supported by the RFBR grant # 16-34-60055.

Mechanism of insulin-induced activation of Na(+)-K(+)-ATPase in isolated rat soleus muscle

1991 ◽  
Vol 261 (2) ◽  
pp. C224-C230 ◽  
Author(s):  
E. Weil ◽  
S. Sasson ◽  
Y. Gutman
Keyword(s):  
Soleus Muscle ◽  
Time Course ◽  
Maximal Effect ◽  
Dependent Manner ◽  
Insulin Stimulation ◽  
K Uptake ◽  
Sequence Of Events ◽  
Rat Soleus Muscle ◽  
Isolated Rat ◽  
Stimulation Of

Insulin augments Na(+)-K(+)-ATPase activity in skeletal muscles. It has been proposed that the sequence of events is activation of Na(+)-H+ antiporter, increased intracellular Na+ concentration ( [Na+]i), and stimulation of Na(+)-K+ pump. We have used isolated rat soleus muscles to test this hypothesis. Insulin increased the ouabain-suppressible K+ uptake in a dose- and time-dependent manner. The maximal effect was observed at 50-100 mU/ml insulin. Stimulation of K+ uptake was accompanied by increased specific [3H]ouabain binding and lowered [Na+]i. The ionophore monensin, which promotes Na(+)-H+ exchange, also increased the rate of ouabain-suppressible K+ uptake in soleus muscle, with a maximal effect obtained at 10-100 microM ionophore. However, this increase was accompanied by an elevation of [Na+]i. In the presence of 10-100 microM monensin, addition of 100 mU/ml insulin further increased K+ uptake but reduced [Na+]i. The effect on K+ uptake was additive. Ouabain (10(-3) M) completely suppressed the effect of insulin on [Na+]i. Insulin had no effect on the magnitude or the time course of insulin stimulation of K+ uptake. Thus equal stimulation of Na(+)-K(+)-ATPase by insulin was observed when [Na+]i was elevated (under monensin) or lowered (under amiloride). These data suggest that activation of Na(+)-K(+)-ATPase in soleus muscle by insulin is not secondary to stimulation of Na(+)-H+ antiporter.

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