The Sarcoplasmic Reticulum in Muscle Fatigue and Disease: Role of the Sarco(endo)plasmic Reticulum Ca2+-ATPase

2004 ◽  
Vol 29 (3) ◽  
pp. 308-329 ◽  
Author(s):  
A. Russell Tupling
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Calcium Release ◽  
Contractile Activity ◽  
Muscle Relaxation ◽  
Low Frequency ◽  
Free Calcium ◽  
Cellular Mechanisms ◽  
Plasmic Reticulum ◽  
Low Frequency Fatigue

Skeletal muscles induced to contract repeatedly respond with a progressive loss in their ability to generate a target force or power. This condition is known simply as fatigue. Commonly, fatigue may persist for prolonged periods of time, particularly at low activation frequencies, which is called low-frequency fatigue. Failure to activate the contractile apparatus with the appropriate intracellular free calcium ([Ca2+]f) signal contributes to fatigue but the precise mechanisms involved are unknown. The sarcoplasmic reticulum (SR) is the major organelle in muscle that is responsible for the regulation of [Ca2+]f, and numerous studies have shown that SR function, both Ca2+ release and Ca2+ uptake, is impaired following fatiguing contractile activity. The major aim of this review is to provide insight into the various cellular mechanisms underlying the alterations in SR Ca2+ cycling and cytosolic [Ca2+]f that are associated both with the development of fatigue during repeated muscle contraction and with low-frequency or long-lasting fatigue. The primary focus will be on the role of the sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) in normal muscle function, fatigue, and disease. Key words: calcium release, calcium uptake, muscle relaxation, low-frequency fatigue, Brody disease

Role of intracellular calcium and metabolites in low-frequency fatigue of mouse skeletal muscle

1997 ◽  
Vol 272 (2) ◽  
pp. C550-C559 ◽  
Author(s):  
E. R. Chin ◽  
C. D. Balnave ◽  
D. G. Allen
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Low Frequency ◽  
Single Muscle ◽  
Low Frequencies ◽  
Time Integral ◽  
Metabolic Component ◽  
Dependent Component ◽  
Low Frequency Fatigue

We have examined the extent to which prolonged reductions in low-frequency force (i.e., low-frequency fatigue) result from increases in intracellular free Ca2+ concentration ([Ca2+]i) and alterations in muscle metabolites. Force and [Ca2+]i were measured in mammalian single muscle fibers in response to short, intermediate, and long series of tetani that elevated the [Ca2+]i-time integral to 5, 17, and 29 microM x s, respectively. Only the intermediate and long series resulted in prolonged (>60 x min) reductions in Ca2+ release and low-frequency fatigue. When fibers recovered from the long series of tetani without glucose, Ca2+ release was reduced to a greater extent and force was reduced at high and low frequencies. These findings indicate that the decrease in sarcoplasmic reticulum Ca2+ release associated with fatigue has at least two components: 1) a metabolic component, which, in the presence of glucose, recovers within 1 h, and 2) a component dependent on the elevation of the [Ca2+]i-time integral, which recovers more slowly. It is this Ca2+-dependent component that is primarily responsible for low-frequency fatigue.

scholarly journals Patterns of sarcomere activation, temperature dependence, and effect of ryanodine in chemically skinned cardiac fibers.

1986 ◽  
Vol 87 (6) ◽  
pp. 885-905 ◽  
Author(s):  
A Lundblad ◽  
H Gonzalez-Serratos ◽  
G Inesi ◽  
J Swanson ◽  
P Paolini
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Temperature Dependence ◽  
Calcium Release ◽  
Contractile Activity ◽  
The Other ◽  
Calcium Blockers ◽  
Calcium Accumulation ◽  
Contractile Activation

Functionally skinned and electrochemically shunted myocytes were prepared by perfusing rat hearts with collagenase in order to obtain a technically improved measurement of sarcomere dynamics and to evaluate the role of sarcoplasmic reticulum in situ with respect to contractile activation. In the presence of micromolar calcium, the myocytes exhibited phasic and propagated contraction waves beginning at one end and proceeding along the myocyte. Beating rates, the propagation velocity of the activation wave, and single sarcomere shortening and relaxation velocities were obtained by manual or automated analysis of 16-mm film recorded at 170 frames/s from a camera attached to a microscope that was equipped with a temperature-controlled stage. In parallel experiments, calcium accumulation by the sarcoplasmic reticulum of the myocytes in situ was measured by direct isotopic tracer methods. The frequency (10-38 min-1) of spontaneous contractions, the velocity (1.9-7.4 microns . s-1) of sarcomere shortening, and the velocity (1.7-6.8 microns . s-1) of sarcomere relaxation displayed identical temperature dependences (Q10 = 2.2), which are similar to that of the calcium pump of sarcoplasmic reticulum and are consistent with a rate limit imposed by enzyme-catalyzed mechanisms on all these parameters. On the other hand, the velocity (77-159 microns . s-1) of sequential sarcomere activation displayed a lower temperature dependence (Q10 = 1.5), which is consistent with a diffusion-limited and self-propagating release of calcium from one sarcomere to the other. The phasic contractile activity of the dissociated myocytes was inhibited by 10(-8)-10(6) M ryanodine (and not by myolemmal calcium blockers) under conditions in which calcium accumulation by sarcoplasmic reticulum in situ was demonstrated to proceed optimally. The effect of ryanodine is attributed to an interaction of this drug with sarcotubular structures, producing inhibition of calcium release from the sarcoplasmic reticulum. The consequent lack of sarcomere activation underlines the role of sarcoplasmic reticulum uptake and release in the phasic contractile activation of the electrochemically shunted myocytes.

scholarly journals Low-Frequency Fatigue as an Indicator of Eccentric Exercise-Induced Muscle Injury: The Role of Vitamin E

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Antonios Kyparos ◽  
Michalis G. Nikolaidis ◽  
Konstantina Dipla ◽  
Andreas Zafeiridis ◽  
Vassilis Paschalis ◽  
...  
Keyword(s):  
Vitamin E ◽  
Eccentric Exercise ◽  
Muscle Injury ◽  
Low Frequency ◽  
Low Frequency Fatigue ◽  
Exercise Induced

Cholinergic effects on intracellular free calcium concentration in renal corpuscle: role of parietal sheet

1992 ◽  
Vol 262 (2) ◽  
pp. F248-F255
Author(s):  
F. Lebrun ◽  
F. Morel ◽  
G. Vassent ◽  
J. Marchetti
Keyword(s):  
Calcium Release ◽  
Intracellular Free Calcium ◽  
Free Calcium ◽  
Response Curves ◽  
Glomerular Function ◽  
Intracellular Free Calcium Concentration ◽  
Free Calcium Concentration ◽  
External Calcium ◽  
Cholinergic Effects

To investigate a possible effect of cholinergic agonists on the renal glomerular function, fura-2 microfluorometric measurements of intracellular free calcium [( Ca2+]i) were performed on single intact glomeruli, single isolated parietal sheets of the Bowman's capsule and single parietal sheet-deprived glomeruli (PS-D glomerulus). Carbachol (10(-4) M), in the presence of 2 mM external calcium, induced a biphasic increase in [Ca2+]i characterized by a sharp initial peak followed by a sustained plateau in the whole glomerulus (delta [Ca2+]i = 177 +/- 13 and 70 +/- 7 nM, respectively; n = 21) and in the parietal sheet (418 +/- 30 and 111 +/- 13 nM, respectively; n = 21). In the PS-D glomerulus (n = 9), the response was less marked and included a barely visible peak (77 +/- 13 nM) and a relatively low plateau (49 +/- 11 nM). In the absence of external calcium, the peak phase was preserved in the three structures, indicating a calcium release from intracellular pools, whereas the plateau, due to the entry of external calcium, was suppressed. These effects were fully inhibited by 10(-4) M of either atropine or pirenzepine, demonstrating the muscarinic nature of the receptors. Dose-response curves showed that the parietal sheet was more sensitive to the physiological agonist (acetylcholine) than to carbachol. A still unexplained difference in sensitivity was noted between peak and plateau, respectively (half-maximal responses were 5 x 10(-6) vs. 5 x 10(-7) M for carbachol and 2 x 10(-7) vs. 3 x 10(-8) M for acetylcholine).(ABSTRACT TRUNCATED AT 250 WORDS)

Postulated role of calsequestrin in the regulation of calcium release from sarcoplasmic reticulum

Biochemistry ◽  
1989 ◽  
Vol 28 (16) ◽  
pp. 6764-6771 ◽  
Author(s):  
Noriaki Ikemoto ◽  
Michel Ronjat ◽  
Laszlo G. Meszaros ◽  
Makoto Koshita
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Calcium Release

scholarly journals The role of cytoskeleton in the regulation of contractile activity in smooth muscle cells from aorta of rats

2007 ◽  
Vol 6 (1) ◽  
pp. 78-82
Author(s):  
S. V. Gousakova
Keyword(s):  
Smooth Muscle ◽  
Contractile Activity ◽  
Muscle Relaxation ◽  
Smooth Muscle Relaxation ◽  
Aortic Smooth Muscle ◽  
Physiologically Active Substances ◽  
Cytochalasine B ◽  
Smooth Muscle Contractions ◽  
System Operating

Influence of cytoskeleton modulation by Colchicine and Cytochalasine B on contractile reactions of smooth muscle segments of rat's aorta caused by physiologically active substances, the membrane's depolarization and cells' striction was investigated by mechanographical method. Microtubules and actinic elements of the cytoskeleton were established to participate in the development of hyper-potassic and phenylephrine -induced contractions as well as in the smooth muscle relaxation induced by cAMP. Cytochalasine B suppresses both kinds of aortic smooth muscle contractions more effectively than Colchicine. Contractile reactions at isoosmotic striction are suppressed only by Cytochalasine. Efficacy of cAMP signal system operating depends on actinic cyto-skeleton integrity.

The Modulation of the Calcium Transport by Skeletal Muscle Sarcoplasmic Reticulum in the Hibernating European Hamster

1991 ◽  
Vol 46 (11-12) ◽  
pp. 1109-1126 ◽  
Author(s):  
◽  
Luisa De Martino ◽  
Barbara Soltau ◽  
Wilhelm Hasselbach
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Calcium Transport ◽  
Calcium Uptake ◽  
Calcium Release ◽  
Ion Homeostasis ◽  
Free Calcium ◽  
Type I ◽  
Calcium Dependent ◽  
Calcium Affinity

Calcium transport of skeletal muscle sarcoplasmic reticulum was comparatively studied in hibernating and summer active European hamsters (Cricetus cricetus L.). Crude homogenates from psoas, soleus and mixed skeletal muscles were used. Protein yield was strongly reduced in the muscle homogenates of hibernating hamsters. The calcium concentration in the muscle of hibernating hamsters was increased to a much higher content than in the serum. In the same animals the maximal rate of calcium uptake and the calcium storing capacity of sarcoplasmic reticulum were augmented by 43% and respectively 17%. Kinetic experiments with various concentrations of free calcium revealed in the hibernating animals higher uptake rates and a lower apparent calcium affinity than in the summer active hamsters. Some shift of calcium uptake rate and calcium affinity similar to that of a fast-twitch muscle was also observed in winter active animals kept at 22 C under natural photoperiod. By contrast, the activity of the calcium dependent ATPase was not increased, suggesting a tighter coupling during hibernation between calcium dependent ATP-hydrolysis and calcium transport. No seasonal difference was observed in the calcium release by KCl-caffeine from calcium loaded vesicles of sarcoplasmic reticulum.Proportion and size of fibre types were studied with cold cross sections from psoas and soleus muscles. An average atrophy of about 25% was found during hibernation in both muscles. Cytochemistry revealed, however, a different reduction of cross area between type-I- and type-11-fibres, which reaches values up to 46% in the type-I I-fast-fibres of the slow soleus muscle. Electron microscopy did not show any definite change in the distribution and amount of sarcoplasmic reticulum.The results suggest that during hibernation a modulation in the properties of calcium transport ATPase of sarcoplasmic reticulum occurs to better support the calcium transport function at low temperatures, which in turn warrants the restoration of ion homeostasis in the course of the arousal.

Erg K+ channels modulate contractile activity in the bovine epididymal duct

2008 ◽  
Vol 294 (3) ◽  
pp. R895-R904 ◽  
Author(s):  
Marco Mewe ◽  
Iris Wulfsen ◽  
Anna M. E. Schuster ◽  
Ralf Middendorff ◽  
Günter Glassmeier ◽  
...  
Keyword(s):  
Calcium Release ◽  
Calcium Influx ◽  
Contractile Activity ◽  
Physiological Role ◽  
Inhibitory Effect ◽  
Isometric Tension ◽  
Channel Blockers ◽  
Current Increase ◽  
Epididymal Duct

The expression and functional role of ether-à-go-go-related gene (erg) K+ channels were examined in the bovine epididymal duct. Sperm transit through the epididymal duct relies on spontaneous phasic contractions (SC) of the peritubular smooth muscle wall. Isometric tension studies revealed SC-enhancing effects of the erg channel blockers E-4031, dofetilide, cisapride, and haloperidol and SC-suppressing effects of the activator NS-1643. In the corpus epididymidis, EC50 values of 32 nM and 8.3 μM were determined for E-4031 and NS-1643, respectively. E-4031 was also able to elicit contraction in epithelium-denuded corpus segments, which lacked SC. In the cauda region, E-4031 and NS-1643 exerted effects on agonist-induced contraction similar to those observed in the proximal duct. Experiments with nifedipine and thapsigargin suggested that the excitatory effects of E-4031 depended mainly on external calcium influx and not on intracellular calcium release. Western blot and RT-PCR assays revealed the expression of both, erg1a and erg1b, in all duct regions. Because erg1b appears to predominate in the epididymal duct, patch-clamp experiments were performed on heterologously expressed erg1b channels to investigate the sensitivity of this splice variant to NS-1643. In contrast to its effects on erg1a, NS-1643 induced a concentration-dependent current increase mainly due to a marked leftward shift in erg1b channel activation by ∼30 mV at 10 μM, explaining the inhibitory effect of the drug on epididymal SC. In summary, these data provide strong evidence for a physiological role of erg1 channels in regulating epididymal motility patterns.

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