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.

Changes in EMG power spectrum (high-to-low ratio) with force fatigue in humans

1982 ◽  
Vol 53 (5) ◽  
pp. 1094-1099 ◽  
Author(s):  
J. Moxham ◽  
R. H. Edwards ◽  
M. Aubier ◽  
A. De Troyer ◽  
G. Farkas ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Electrical Stimulation ◽  
Power Spectrum ◽  
Low Frequency ◽  
Normal Subjects ◽  
Quadriceps Muscle ◽  
Force Response ◽  
Low Frequencies ◽  
Emg Power Spectrum ◽  
Low Frequency Fatigue

During and following high-load fatiguing voluntary contractions, the force response of skeletal muscle to electrical stimulation is altered so that the frequency-force curve is moved to the right. Fatiguing contractions also result in a shift to the left of the electromyographic (EMG) power spectrum. In the quadriceps muscle and the diaphragm of normal subjects the change in the force response to electrical stimulation has been correlated with the EMG changes. After repeated submaximal contractions in the quadriceps and diaphragm, the forces produced by electrical stimulation at low frequencies were reduced, indicating low-frequency fatigue. This type of fatigue persisted for several hours but did not result in any change in the EMG high-to-low ratio. Low-frequency fatigue is probably an important aspect of the failure of skeletal muscle to generate adequate force, and the EMG high-to-low ratio may not recognize this type of fatigue.

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.

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

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.

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

Hg2+-induced contracture in mechanically skinned fibers of frog skeletal muscle

1985 ◽  
Vol 63 (9) ◽  
pp. 1070-1074 ◽  
Author(s):  
Takako Aoki ◽  
Toshiharu Oba ◽  
Ken Hotta
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Sulfhydryl Groups ◽  
Skinned Fibers ◽  
Frog Skeletal Muscle ◽  
Semitendinosus Muscle ◽  
Skinned Fiber ◽  
Brij 58 ◽  
Develop Tension

In mechanically skinned fibers of the semitendinosus muscle of bullfrogs, we examined the role of membrane sulfhydryl groups on Ca2+ release from the sarcoplasmic reticulum (SR). Hg2+, a sulfhydryl reagent (20–100 μM), induced a repetitive contracture of skinned fibers, and this contracture did not occur in skinned fibers in which the SR had been disrupted by treatment with a detergent (Brij 58). Procaine (10 mM), Mg2+ (5 mM), or dithiothreitol (1 mM) blocked the Hg2+-induced contracture. Ag+ or p-chloromercuribenzenesulfonic acid produced similar contractures to that induced by Hg2+. We conclude that Hg2+ releases Ca2+ from SR of a skinned fiber by modifying sulfhydryl groups on the SR membrane, and suggest that the Ca2+ released by Hg2+ may trigger a greater release of Ca2+ from SR to develop tension.

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