Intracellular calcium concentration during low-frequency fatigue in isolated single fibers of mouse skeletal muscle

1993 ◽  
Vol 75 (1) ◽  
pp. 382-388 ◽  
Author(s):  
H. Westerblad ◽  
S. Duty ◽  
D. G. Allen
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Intracellular Calcium ◽  
Calcium Concentration ◽  
Low Frequency ◽  
Intracellular Calcium Concentration ◽  
Low Frequencies ◽  
Single Fibers ◽  
Control Comparison ◽  
Low Frequency Fatigue ◽  
Tetanic Tension

Low-frequency fatigue is a form of muscle fatigue that follows intense muscle activity and is characterized by reduced tetanic tension at low frequencies of stimulation while tetanic tension at high stimulus frequencies is close to normal. The present experiments were performed on isolated single fibers of mouse in which tension and intracellular calcium concentration ([Ca2+]i) were measured. Fatigue was produced by intermittent short tetani continued until tension had declined to 30% of control. Comparison of low- (30- and 50-Hz) and high- (100-Hz) frequency tetani under control conditions and after 30 min of recovery from fatigue showed that low-frequency fatigue was present. During low-frequency fatigue, tetanic [Ca2+]i was substantially reduced at all stimulus frequencies but there was no change in Ca2+ sensitivity or maximum Ca(2+)-activated tension. One possible cause of the reduced tetanic [Ca2+]i is failure of conduction of the action potential in the T tubule, leading to reduced [Ca2+]i in the center of the fiber. However, imaging of [Ca2+]i across the fiber during low-frequency fatigue did not show any such gradient, suggesting that Ca2+ release is uniform across the fiber. Another possible mechanism is that changes in the Ca2+ pumping ability of the sarcoplasmic reticulum might affect tetanic [Ca2+]i. Measurements of the sarcoplasmic reticulum pump function showed a small slowing of Ca2+ uptake rate during low-frequency fatigue, which is unlikely to cause the reduced tetanic [Ca2+]i. In conclusion, the immediate cause of low-frequency fatigue appears to be a reduced tetanic [Ca2+]i, which is probably a consequence of a reduced Ca2+ release from the sarcoplasmic reticulum.

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 Activity-dependent increases in [Ca2+]i contribute to digital-analog plasticity at a molluscan synapse

2017 ◽  
Vol 117 (6) ◽  
pp. 2104-2112 ◽  
Author(s):  
Bjoern Ch. Ludwar ◽  
Colin G. Evans ◽  
Monica Cambi ◽  
Elizabeth C. Cropper
Keyword(s):  
Synaptic Transmission ◽  
Intracellular Calcium ◽  
Time Constant ◽  
Calcium Concentration ◽  
Low Frequency ◽  
Intracellular Calcium Concentration ◽  
Calcium Signal ◽  
Presynaptic Neuron ◽  
Calcium Dependent ◽  
Long Time

In a type of short-term plasticity that is observed in a number of systems, synaptic transmission is potentiated by depolarizing changes in the membrane potential of the presynaptic neuron before spike initiation. This digital-analog form of plasticity is graded. The more depolarized the neuron, the greater the increase in the efficacy of synaptic transmission. In a number of systems, including the system presently under investigation, this type of modulation is calcium dependent, and its graded nature is presumably a consequence of a direct relationship between the intracellular calcium concentration ([Ca2+]i) and the effect on synaptic transmission. It is therefore of interest to identify factors that determine the magnitude of this type of calcium signal. We studied a synapse in Aplysia and demonstrate that there can be a contribution from currents activated during spiking. When neurons spike, there are localized increases in [Ca2+]i that directly trigger neurotransmitter release. Additionally, spiking can lead to global increases in [Ca2+]i that are reminiscent of those induced by subthreshold depolarization. We demonstrate that these spike-induced increases in [Ca2+]i result from the activation of a current not activated by subthreshold depolarization. Importantly, they decay with a relatively slow time constant. Consequently, with repeated spiking, even at a low frequency, they readily summate to become larger than increases in [Ca2+]i induced by subthreshold depolarization alone. When this occurs, global increases in [Ca2+]i induced by spiking play the predominant role in determining the efficacy of synaptic transmission. NEW & NOTEWORTHY We demonstrate that spiking can induce global increases in the intracellular calcium concentration ([Ca2+]i) that decay with a relatively long time constant. Consequently, summation of the calcium signal occurs even at low firing frequencies. As a result there is significant, persistent potentiation of synaptic transmission.

scholarly journals Effects of rapid application of caffeine on intracellular calcium concentration in ferret papillary muscles.

1988 ◽  
Vol 92 (3) ◽  
pp. 351-368 ◽  
Author(s):  
G L Smith ◽  
M Valdeolmillos ◽  
D A Eisner ◽  
D G Allen
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Intracellular Calcium ◽  
Papillary Muscle ◽  
Calcium Concentration ◽  
Isometric Tension ◽  
Transient Increase ◽  
Intracellular Calcium Concentration ◽  
Papillary Muscles ◽  
Releasable Pool ◽  
Rapid Removal

In this paper we investigate the effects of caffeine (5-20 mM) on ferret papillary muscle. The intracellular Ca2+ concentration ( [Ca2+]i) was measured from the light emitted by the photoprotein aequorin, which had previously been microinjected into superficial cells. Isometric tension was measured simultaneously. The rapid application of caffeine produced a transient increase of [Ca2+]i, which decayed spontaneously within 2-3 s and was accompanied by a transient contracture. The removal of extracellular Na+ or an increase in the concentration of intracellular Na+ (produced by strophanthidin) increased the magnitude of the caffeine response. Cessation of stimulation for several minutes or stimulation at low rates decreased the magnitude of the stimulated twitch and Ca2+ transient. These maneuvers also decreased the size of the caffeine response. These results are consistent with the hypothesis that the caffeine-releasable pool of Ca2+ (sarcoplasmic reticulum) is modulated by maneuvers that affect contraction. Ryanodine (10 microM) decreased the magnitude of the caffeine response as well as that of the stimulated twitch. In contrast, the rapid removal of external Ca2+ abolished the systolic Ca2+ transient within 5 s, but had no effect on the caffeine response. From this we conclude that the abolition of twitch by Ca2+-free solutions is not due to depletion of the sarcoplasmic reticulum of Ca2+, but may be due to a requirement of Ca2+ entry into the cell to trigger Ca2+ release from the sarcoplasmic reticulum.

β-Amyloid-induced increase in the resting intracellular calcium concentration gives support to tell Alzheimer lymphocytes from control ones

2002 ◽  
Vol 58 (2) ◽  
pp. 203-205 ◽  
Author(s):  
András Palotás ◽  
János Kálmán ◽  
Miklós Palotás ◽  
Anna Juhász ◽  
Zoltán Janka ◽  
...  
Keyword(s):  
Intracellular Calcium ◽  
Calcium Concentration ◽  
Intracellular Calcium Concentration ◽  
Β Amyloid

scholarly journals Low-Frequency Fatigue at Different Muscle Length Following Intermittent Eccentric Drop Jumps in 12—14 Year-Old Boys

2018 ◽  
Vol 3 (57) ◽  
Author(s):  
Vytautas Streckis ◽  
Giedrius Gorianovas ◽  
Birutė Miseckaitė ◽  
Valerija Streckienė ◽  
Ronaldas Endrijaitis ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Eccentric Exercise ◽  
Mechanical Damage ◽  
Low Frequency ◽  
Muscle Length ◽  
Contraction Force ◽  
Low Frequencies ◽  
Drop Jumps ◽  
Low Frequency Fatigue ◽  
Initial Force

Low frequency fatigue (LFF) in 12—14 year-old adolescent boys (n = 10) doing 75 eccentric jumps performed every20 s from a platform 80 cm high was investigated.Thus the aim of this study was to find out if LFF manifests itself in the muscles of boys aged 12—14 years doing 75 dropjumps performed every 20 s at angles of 90˚ and 135˚ from a platform 80 cm high. The results of the research have shownthat doing 75 eccentric jumps performed every 20 s calls forth LFF in the muscles of boys that is particularly strong anddisappears more slowly at a shorter length of the muscle exercised. Thus, the hypothesis as to the sarcomeric origin ofLFF in the muscles of boys and men has been confirmed. Besides, the muscles of men of mature age are more resistantto LFF than those of boys. This fact, as well as a more acute pain brought about in the muscles of boys, indicates thatthe muscles of boys are less resistant to mechanical damage than those of men of mature age.It is maintained that as a result of the eccentric exercise performed, some portion of the weak sarcomeres gets tornand then the strong sarcomeres, i.e. the ones that develop contraction force have to work at a shorter muscle length.When muscle contraction length is short the sensitiveness of miofibrillas to Ca 2+  decreases. It is rather unexpectedthough that 24 h after the end of the exercise the force developed by electrostimulation at low frequencies (20 Hz) issmaller (p < 0.05), as compared to the initial force registered at a shorter muscle length. Since after the exercise therewas also a decrease in the force developed at a shorter muscle length in particular, the sarcomeres are believed tohave been damaged during eccentric exercise.Keywords: electrical stimulation, force, age, muscle damage, stretch-shortening exercise.

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