Temperature-dependent skeletal muscle dysfunction in rats with congestive heart failure

Abnormalities in the excitation-contraction coupling of slow-twitch muscle seem to explain the slowing and increased fatigue observed in congestive heart failure (CHF). However, it is not known which elements of the excitation-contraction coupling might be affected. We hypothesize that the temperature sensitivity of contractile properties of the soleus muscle might be altered in CHF possibly because of alterations of the temperature sensitivity of intracellular Ca2+ handling. We electrically stimulated the in situ soleus muscle of anesthetised rats that had 6-wk postinfarction CHF using 1 and 50 Hz and using a fatigue protocol (5-Hz stimulation for 30 min) at 35, 37, and 40°C. Ca2+ uptake and release were measured in sarcoplasmic reticulum vesicles at various temperatures. Contraction and relaxation rates of the soleus muscle were slower in CHF than in sham at 35°C, but the difference was almost absent at 40°C. The fatigue protocol revealed that force development was more temperature sensitive in CHF, whereas contraction and relaxation rates were less temperature sensitive in CHF than in sham. The Ca2+ uptake and release rates did not correlate to the difference between CHF and sham regarding contractile properties or temperature sensitivity. In conclusion, the discrepant results regarding altered temperature sensitivity of contraction and relaxation rates in the soleus muscle of CHF rats compared with Ca2+ release and uptake rates in vesicles indicate that the molecular cause of slow-twitch muscle dysfunction in CHF is not linked to the intracellular Ca2+ cycling.

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The stiffness of slow-twitch muscle lags behind twitch tension: Implications for contractile mechanisms and behavior

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y79-178 ◽

1979 ◽

Vol 57 (10) ◽

pp. 1189-1192 ◽

Cited By ~ 8

Author(s):

R. B. Stein ◽

F. Parmiggiani

Keyword(s):

Soleus Muscle ◽

Muscle Stiffness ◽

Plantaris Muscle ◽

Rigor State ◽

Slow Twitch Muscle ◽

Slow Twitch ◽

And Behavior

Small, square stretches were applied during contractions of soleus and plantaris muscles in the cat to measure muscle stiffness. The stiffness of the slow-twitch soleus muscle (but not of the fast plantaris muscle) reaches a maximum after the peak in twitch tension. Since the number of active bonds should be maximum before the peak in tension, we suggest that many bonds are in the rigor state during the falling phase of the twitch. The stiffness of the bonds in this state may be useful for prolonging the twitch in slow-twitch muscles and for maintaining a posture.

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THE TIMING OF TEMPERATURE SENSITIVITY OF LEAKY FERTILITY FACTOR MUTATIONS IN MALE DROSOPHILA MELANOGASTER

Genetics ◽

10.1093/genetics/74.1.115 ◽

1973 ◽

Vol 74 (1) ◽

pp. 115-132

Author(s):

Anne W Koopmans Frankel

Keyword(s):

Temperature Sensitivity ◽

Cytological Study ◽

Adult Life ◽

Pupal Stage ◽

Sensitive Period ◽

Temperature Sensitive ◽

Fertility Factor ◽

Temperature Regimen ◽

Two Temperatures ◽

The Difference

ABSTRACT Some of the mutations of the male fertility factors on the Y chromosome give rise to a small proportion of fertile males, each of which produces only a small number of progeny. Many of these mutations are temperature-sensitive, producing a larger proportion of fertile males at 25°C than at 19°C. One of these mutants was carefully analyzed and it was found that only sperm which mature in the first five days of adult life can effect fertilization, regardless of the temperature regimen. A unique temperature-sensitive period was localized to the mid-pupal stage by single twenty-four-hour 25°C treatments applied at various times in the life cycle to flies otherwise grown at 19°C. The temperature sensitivity associated with this pupal sensitive period is adequate to account for all of the difference in fertility between flies. grown continuously at the two temperatures. The timing of the temperature-sensitive process in combination with a cytological study of spermiogenesis indicates that temperature sensitivity occurs after the first meiotic metaphase during a spermatid stage. Thus it affects some post-transcriptional event in the expression of the phenotype of the fertility factor.

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Calcium binding protein changes of sarcoplasmic reticulum from rat denervated skeletal muscle

Bioscience Reports ◽

10.1007/bf01115228 ◽

1988 ◽

Vol 8 (4) ◽

pp. 369-378 ◽

Cited By ~ 9

Author(s):

Marie-Jeanne Loirat ◽

Brigitte Lucas-Heron ◽

Béatrice Ollivier ◽

Claude Leoty

Keyword(s):

Skeletal Muscle ◽

Sarcoplasmic Reticulum ◽

Atpase Activity ◽

Soleus Muscle ◽

Calcium Binding ◽

Neural Control ◽

Calcium Binding Protein ◽

Slow Twitch Muscle ◽

Slow Twitch ◽

Fast Twitch

Two Ca2+ sequestering proteins were studied in fast-twitch (EDL) and slow-twitch (soleus) muscle sarcoplasmic reticulum (SR) as a function of denervation time. Ca2+-ATPase activity measured in SR fractions of normal soleus represented 5% of that measure in SR fractions of normal EDL. Denervation caused a severe decrease in activity only in fast-twich muscle. Ca2+-ATPase and calsequestrin contents were affected differently by denervation. In EDL SR, Ca2+-ATPase content decreased progressively, whereas in soleus SR, no variation was observed. Calsequestrin showed a slight increase in both muscles as a function of denervation time correlated with increased45Ca-binding. These results indicate first that Ca2+-ATPase activity in EDL was under neural control, and that because of low Ca2+-ATPase activity and content in slow-twitch muscle no variation could be detected, and secondly that greater calsequestrin content might represent a relative increasing of heavy vesicles or decreasing of light vesicles as a function of denervation time in the whole SR fraction isolated in both types of muscles.

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Centrifugal intensity and duration as countermeasures to soleus muscle atrophy

Journal of Applied Physiology ◽

10.1152/jappl.1990.69.4.1387 ◽

1990 ◽

Vol 69 (4) ◽

pp. 1387-1389 ◽

Cited By ~ 14

Author(s):

D. S. D'Aunno ◽

D. B. Thomason ◽

F. W. Booth

Keyword(s):

Muscle Atrophy ◽

Soleus Muscle ◽

Weight Bearing ◽

Slow Twitch Muscle ◽

Wet Weight ◽

Slow Twitch

Mechanical acceleration is a countermeasure that may be employed to prevent atrophy of slow-twitch muscle during non-weight bearing. In the present study, daily centrifugation of rats for different durations (1 or 2 h) and at different gravitational intensities (1.5 or 2.6 G) was used to test whether mechanical acceleration could ameliorate the atrophy of the soleus muscle induced by non-weight bearing (tail-traction model). The soleus muscle atrophied 32% during 7 days of non-weight bearing without countermeasures. Centrifugation treatment did not completely prevent atrophy relative to precontrol wet weight of the soleus muscle. Non-weight-bearing groups receiving 2-h daily treatments of 1, 1.5, or 2.6 G had 48, 56, and 65%, respectively, of the atrophy observed in the non-weight-bearing-only group compared with the precontrol group. No evidence was obtained that centrifugation at 2.6 G was more effective than exposure to 1 or 1.5 G as a countermeasure to non-weight-bearing-induced atrophy of the soleus muscle.

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Atrophy of the soleus muscle by hindlimb unweighting

Journal of Applied Physiology ◽

10.1152/jappl.1990.68.1.1 ◽

1990 ◽

Vol 68 (1) ◽

pp. 1-12 ◽

Cited By ~ 354

Author(s):

D. B. Thomason ◽

F. W. Booth

Keyword(s):

Soleus Muscle ◽

Oxidative Capacity ◽

Glycolytic Enzyme ◽

Hindlimb Unweighting ◽

Degradation Rates ◽

Applied Physiology ◽

Slow Twitch Muscle ◽

Specific Mrnas ◽

Slow Twitch ◽

Fast Twitch

The unweighting model is a unique whole animal model that will permit the future delineation of the mechanism(s) by which gravity maintains contractile mass in postural (slow-twitch) skeletal muscle. Since the origination of the model of rodent hindlimb unweighting almost one decade ago, about half of the 59 refereed articles in which this model was utilized have been published in the Journal of Applied Physiology. Thus the purpose of this review is to provide, for those researchers with an interest in the hindlimb unweighting model, a summation of the data derived from this model to data and hopefully to stimulate research interest in aspects of the model for which data are lacking. The stress response of the animal to hindlimb unweighting is transient, minimal in magnitude, and somewhat variable. After 1 wk of unweighting, the animal exhibits no chronic signs of stress. The atrophy of the soleus muscle, a predominantly slow-twitch muscle, is emphasized because unweighting preferentially affects it compared with other calf muscles, which are mainly fast-twitch muscles. The review considers the following information about the unweighted soleus muscle: electromyogram activity, amount and type of protein lost, capillarization, oxidative capacity, glycolytic enzyme activities, fiber cross section, contractile properties, glucose uptake, sensitivity to insulin, protein synthesis and degradation rates, glucocorticoid receptor numbers, responses of specific mRNAs, and changes in metabolite concentrations.

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Effects of Temperature on Calcium Transients and Ca2+-Dependent Afterhyperpolarizations in Neocortical Pyramidal Neurons

Journal of Neurophysiology ◽

10.1152/jn.01017.2004 ◽

2005 ◽

Vol 93 (4) ◽

pp. 2012-2020 ◽

Cited By ~ 30

Author(s):

J. C. F. Lee ◽

J. C. Callaway ◽

R. C. Foehring

Keyword(s):

Action Potential ◽

Temperature Sensitivity ◽

Pyramidal Neurons ◽

Membrane Properties ◽

Temperature Sensitive ◽

Voltage Dependent ◽

Intracellular Ca ◽

Slow Rise ◽

Kinetics Of ◽

Neocortical Pyramidal Neurons

In neocortical pyramidal neurons, the medium (mAHP) and slow AHP (sAHP) have different relationships with intracellular [Ca2+]. To further explore these differences, we varied bath temperature and compared passive and active membrane properties and Ca2+ transients in response to a single action potential (AP) or trains of APs. We tested whether Ca2+-dependent events are more temperature sensitive than voltage-dependent ones, the slow rise time of the sAHP is limited by diffusion, and temperature sensitivity differs between the mAHP and sAHP. The onset and decay kinetics of the sAHP were very temperature sensitive (more so than diffusion). We found that the decay time course of Ca2+ transients was also very temperature sensitive. In contrast, the mAHP (amplitude, time to peak, and exponential decay) and sAHP peak amplitude were moderately sensitive to temperature. The amplitudes of intracellular Ca2+ transients evoked either by a single spike or a train of spikes showed modest temperature sensitivities. Pyramidal neuron input resistance was increased by cooling. With the exception of threshold, which remained unchanged between 22 and 35°C, action potential parameters (amplitude, half-width, maximum rates of rise and fall) were modestly affected by temperature. Collectively, these data suggest that temperature sensitivity was higher for the Ca2+-dependent sAHP than for voltage-dependent AP parameters or for the mAHP, diffusion of Ca2+ over distance cannot explain the slow rise of the sAHP in these cells, and the kinetics of the sAHP and mAHP are affected differently by temperature.

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ATP-sensitive potassium channels mediate hyperosmotic stimulation of NKCC in slow-twitch muscle

AJP Cell Physiology ◽

10.1152/ajpcell.00247.2003 ◽

2004 ◽

Vol 286 (3) ◽

pp. C586-C595 ◽

Cited By ~ 4

Author(s):

Aidar R. Gosmanov ◽

Zheng Fan ◽

Xianqiang Mi ◽

Edward G. Schneider ◽

Donald B. Thomason

Keyword(s):

Skeletal Muscle ◽

Soleus Muscle ◽

Potassium Current ◽

Plantaris Muscle ◽

Channel Inhibition ◽

Slow Twitch Muscle ◽

Inhibition Of Glycolysis ◽

Slow Twitch ◽

Mapk Inhibitors ◽

Fast Twitch

In mildly hyperosmotic medium, activation of the Na+-K+-2Cl- cotransporter (NKCC) counteracts skeletal muscle cell water loss, and compounds that stimulate protein kinase A (PKA) activity inhibit the activation of the NKCC. The aim of this study was to determine the mechanism for PKA inhibition of NKCC activity in resting skeletal muscle. Incubation of rat slow-twitch soleus and fast-twitch plantaris muscles in isosmotic medium with the PKA inhibitors H-89 and KT-5720 caused activation of the NKCC only in the soleus muscle. NKCC activation caused by PKA inhibition was insensitive to MEK MAPK inhibitors and to insulin but was abolished by the PKA stimulators isoproterenol and forskolin. Furthermore, pinacidil [an ATP-sensitive potassium (KATP) channel opener] or inhibition of glycolysis increased NKCC activity in the soleus muscle but not in the plantaris muscle. Preincubation of the soleus muscle with glibenclamide (a KATP channel inhibitor) prevented the NKCC activation by hyperosmolarity, PKA inhibition, pinacidil, and glycolysis inhibitors. In contrast, glibenclamide stimulated NKCC activity in the plantaris muscle. In cells stably transfected with the Kir6.2 subunit of the of KATP channel, inhibition of glycolysis activated potassium current and NKCC activity. We conclude that activation of KATP channels in slow-twitch muscle is necessary for activation of the NKCC and cell volume restoration in hyperosmotic conditions.

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