Contractile and Electrical Characteristics of Extensor Muscle from Alloxan-Diabetic Rats: An In Vitro Study

Grossie, J.

doi:10.2337/diab.31.3.194

Cited by 25 publications

(18 citation statements)

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“…Thus, although these results show interesting changes with diabetes, they do not reflect true tension-generating capability, which is best revealed by conventional tetanic measurements. Other in vitro experiments with 0.1-ms pulse width did not demonstrate hypercontractility but support our conclusion that fast muscles exhibit hypocontractility (11).…”

Section: Discussionsupporting

confidence: 76%

“…In slow soleus, time to peak twitch tension (TTP) and half-relaxation time (HRT) are prolonged in alloxan-induced (10) and streptozocin-induced (STZ-D; 9) diabetes. However, contraction times of fast-twitch extensor digitorum longus (EDL) were unaffected (9)(10)(11), but there was a decline in tension evoked by tetanic stimulation that could be prevented by insulin treatment (11).…”

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confidence: 99%

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Changes in Skeletal Muscle Contractile Properties in Streptozocin-Induced Diabetic Rats and Role of Polyol Pathway and Hypoinsulinemia

1990

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Functional changes in slow-twitch soleus and fast-twitch extensor digitorum longus muscles were assessed after 2 mo of streptozocin-induced diabetes in rats. For soleus, there was a slowing of twitch times both for contraction and relaxation and a reduction of maximum tetanic relaxation rate. There was little effect on strength performance assessed by maximal tetanic tension production. Treatment with the aldose reductase inhibitor ponalrestat largely prevented relaxation defects but had little effect on contraction. For the fast muscle, twitch times were relatively unaffected, but maximum tetanic relaxation rate was reduced. In addition, tetanic tension output decreased. These changes were largely prevented by ponalrestat treatment. The effects of partial insulin therapy were also investigated. This regimen reduced hypoinsulinemia, but sufficient hyperglycemia remained to stimulate the polyol pathway. It prevented the slowing of soleus twitch contraction but had no effect on relaxation. For extensor digitorum longus, insulin produced further deleterious effects on tetanic tension and maximum relaxation rate, which were antagonized by ponalrestat. A 1% dietary myo-inositol supplement had little effect on contractile function in slow or fast muscles. It was concluded that polyol-pathway activity is an important factor underlying skeletal muscle functional changes in diabetes, probably acting through disruption of Ca2+ handling. Hypoinsulinemia was considered a secondary factor causing atrophy, particularly of fast muscles. There was no evidence of effects dependent on neuropathy.

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Section: Discussionsupporting

confidence: 76%

mentioning

confidence: 99%

Changes in Skeletal Muscle Contractile Properties in Streptozocin-Induced Diabetic Rats and Role of Polyol Pathway and Hypoinsulinemia

1990

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“…[From Nielsen and Clausen (313).] (91,177). More recent studies showed that the endurance of diaphragm, soleus, and EDL prepared from streptozotocin diabetic rats was reduced (293,294).…”

Section: Effects Of Na ؉ -K ؉ Pump Inhibition or Downregulationmentioning

confidence: 96%

Na⁺-K⁺Pump Regulation and Skeletal Muscle Contractility

Clausen

2003

Physiological Reviews

514

673

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In skeletal muscle, excitation may cause loss of K+, increased extracellular K+ ([K+]o), intracellular Na+ ([Na+]i), and depolarization. Since these events interfere with excitability, the processes of excitation can be self-limiting. During work, therefore, the impending loss of excitability has to be counterbalanced by prompt restoration of Na+-K+ gradients. Since this is the major function of the Na+-K+ pumps, it is crucial that their activity and capacity are adequate. This is achieved in two ways: 1) by acute activation of the Na+-K+ pumps and 2) by long-term regulation of Na+-K+ pump content or capacity. 1) Depending on frequency of stimulation, excitation may activate up to all of the Na+-K+ pumps available within 10 s, causing up to 22-fold increase in Na+ efflux. Activation of the Na+-K+ pumps by hormones is slower and less pronounced. When muscles are inhibited by high [K+]o or low [Na+]o, acute hormone- or excitation-induced activation of the Na+-K+ pumps can restore excitability and contractile force in 10-20 min. Conversely, inhibition of the Na+-K+ pumps by ouabain leads to progressive loss of contractility and endurance. 2) Na+-K+ pump content is upregulated by training, thyroid hormones, insulin, glucocorticoids, and K+ overload. Downregulation is seen during immobilization, K+ deficiency, hypoxia, heart failure, hypothyroidism, starvation, diabetes, alcoholism, myotonic dystrophy, and McArdle disease. Reduced Na+-K+ pump content leads to loss of contractility and endurance, possibly contributing to the fatigue associated with several of these conditions. Increasing excitation-induced Na+ influx by augmenting the open-time or the content of Na+ channels reduces contractile endurance. Excitability and contractility depend on the ratio between passive Na+-K+ leaks and Na+-K+ pump activity, the passive leaks often playing a dominant role. The Na+-K+ pump is a central target for regulation of Na+-K+ distribution and excitability, essential for second-to-second ongoing maintenance of excitability during work.

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“…The increase in membrane input resistance reflects a reduced Cl --conductance, congruent with the elevated tetanus/twitch ratio observed in diaphragm form LPS-treated mice. Some agents, and the diabetic state, that interfere with Cl --conductance also increase twitch force (Hodgkin and Horowicz 1960;Taylor et al 1969, Grossie 1982. Therefore, these findings imply that the sarcolemmal Cl --channel is markedly affected in endotoxemia and that this may account for, at least in part, the altered contractile responses of the mouse diaphragm.…”

Section: Discussionmentioning

confidence: 83%

“…A reduction in membrane Cl --conductance is associated with myotonia in skeletal muscle (Barchi 1975;Palade and Barchi 1977 a, b;LinShiau et al 1991). An alteration of membrane conductance is intimately related to some pathological conditions, for example, the skeletal muscle of diabetic rats or mice has a lower membrane potential and a higher membrane resistance (Grossie 1982;Kimura et al 1988;LinShiau et al 1993). Thus, the possibility of changes in the contractile and electrical properties of skeletal muscle during endotoxemia was tested in this study.…”

Section: Introductionmentioning

confidence: 99%

Involvement of nitric oxide in the in vivo effects of lipopolysaccharide on the contractile and electrical properties of mouse diaphragm

Liu

Lai

Lin

et al. 1997

Naunyn-Schmiedeberg's Arch Pharmacol

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The contractile and electrical properties of the mouse diaphragm during endotoxemia were studied, and the possible role of nitric oxide (NO) on these changes was investigated. The mice were injected intraperitoneally with E. coli. lipopolysaccharide (endotoxin, LPS) at various times before isolation of the diaphragm to induce endotoxemia. It was observed that direct twitch tension was slightly increased, and that there was a significant increase in tetanic tension when compared with controls. The potentiation of direct twitch tension induced by a Cl--channel blocker (9-anthracene carboxylic acid), but not the potentiation by a Na+-channel activator (veratridine) or by K+-channel blockers (uranyl ion, 4-aminopyridine and tetraethylammonium ion), was attenuated in the diaphragm of LPS-treated mice. Moreover, the resting membrane potential was significantly reduced and the membrane input resistance was significantly increased, largely due to a decrease in Cl--conductance. However, the membrane K+-conductance remained unaltered. These results imply that the sarcolemmal Cl--channel is markedly affected in the mouse diaphragm during endotoxemia. These changes of contractile and electrical characteristics of the mouse diaphragm during endotoxemia could be reversed by treatment with dexamethasone and N(G)-nitro-L-arginine (NO synthase inhibitors). On the other hand, in in vitro studies, LPS (20 microg/ml), by itself, applied directly to the diaphragm, did not alter the muscle contractions or the membrane potentials. A NO donor, added to the diaphragm bath, increased the tetanus/twitch ratio and induced a transient depolarization. All of these findings suggest that LPS may, at least in part, affect the sarcolemmal electrical properties and muscle contractions during endotoxemia through the L-arginine:NO pathway.

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Contractile and Electrical Characteristics of Extensor Muscle from Alloxan-Diabetic Rats: An In Vitro Study

Cited by 25 publications

References 0 publications

Changes in Skeletal Muscle Contractile Properties in Streptozocin-Induced Diabetic Rats and Role of Polyol Pathway and Hypoinsulinemia

Changes in Skeletal Muscle Contractile Properties in Streptozocin-Induced Diabetic Rats and Role of Polyol Pathway and Hypoinsulinemia

Na⁺-K⁺Pump Regulation and Skeletal Muscle Contractility

Involvement of nitric oxide in the in vivo effects of lipopolysaccharide on the contractile and electrical properties of mouse diaphragm

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Contractile and Electrical Characteristics of Extensor Muscle from Alloxan-Diabetic Rats: An In Vitro Study

Cited by 25 publications

References 0 publications

Changes in Skeletal Muscle Contractile Properties in Streptozocin-Induced Diabetic Rats and Role of Polyol Pathway and Hypoinsulinemia

Changes in Skeletal Muscle Contractile Properties in Streptozocin-Induced Diabetic Rats and Role of Polyol Pathway and Hypoinsulinemia

Na+-K+Pump Regulation and Skeletal Muscle Contractility

Involvement of nitric oxide in the in vivo effects of lipopolysaccharide on the contractile and electrical properties of mouse diaphragm

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Na⁺-K⁺Pump Regulation and Skeletal Muscle Contractility