Length dependence of active force production in skeletal muscle

1999 ◽  
Vol 86 (5) ◽  
pp. 1445-1457 ◽  
Author(s):  
D. E. Rassier ◽  
B. R. MacIntosh ◽  
W. Herzog
Keyword(s):  
Skeletal Muscle ◽  
Muscle Contraction ◽  
Sarcomere Length ◽  
Length Change ◽  
In Vivo Studies ◽  
Active Force ◽  
Moment Arm ◽  
Cross Bridge ◽  
Length Relationship

The sliding filament and cross-bridge theories of muscle contraction provide discrete predictions of the tetanic force-length relationship of skeletal muscle that have been tested experimentally. The active force generated by a maximally activated single fiber (with sarcomere length control) is maximal when the filament overlap is optimized and is proportionally decreased when overlap is diminished. The force-length relationship is a static property of skeletal muscle and, therefore, it does not predict the consequences of dynamic contractions. Changes in sarcomere length during muscle contraction result in modulation of the active force that is not necessarily predicted by the cross-bridge theory. The results of in vivo studies of the force-length relationship suggest that muscles that operate on the ascending limb of the force-length relationship typically function in stretch-shortening cycle contractions, and muscles that operate on the descending limb typically function in shorten-stretch cycle contractions. The joint moments produced by a muscle depend on the moment arm and the sarcomere length of the muscle. Moment arm magnitude also affects the excursion (length change) of a muscle for a given change in joint angle, and the number of sarcomeres arranged in series within a muscle fiber determines the sarcomere length change associated with a given excursion.

HISTORY DEPENDENCE OF SKELETAL MUSCLE FORCE PRODUCTION: A FORGOTTEN PROPERTY

2002 ◽  
Vol 02 (03n04) ◽  
pp. 347-358 ◽  
Author(s):  
W. HERZOG ◽  
D. E. RASSIER
Keyword(s):  
Skeletal Muscle ◽  
Muscle Contraction ◽  
Sarcomere Length ◽  
Force Production ◽  
Passive Component ◽  
Total Force ◽  
Force Enhancement ◽  
Length Relationship ◽  
History Of ◽  
Muscle Force Production

Steady-state force enhancement following active muscle stretching has been observed for well over fifty years, and is a widely accepted property of skeletal muscle contraction. Force enhancement has typically been associated with instability of sarcomere length on the descending limb of the force-length relationship. Here, we demonstrate that the sarcomere length non-uniformity paradigm, based on instability, cannot explain much of the newly discovered results. We provide evidence that force enhancement can occur on the stable ascending limb of the force-length relationship, that force enhancement can exceed the isometric tetanic plateau forces, that it is associated with an increased passive force, and that it occurs for perfectly stable sarcomere lengths on the descending limb of the force-length relationship. Combining all the results, we conclude that force enhancement has at least two components, an active and a passive component, that contribute towards the total force enhancement to varying degrees, depending on the contractile history of muscle contraction.

scholarly journals Autophagy Deficiency by Atg4B Loss Leads to Metabolomic Alterations in Mice

Metabolites ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 481
Author(s):  
Gemma G. Martínez-García ◽  
Raúl F. Pérez ◽  
Álvaro F. Fernández ◽  
Sylvere Durand ◽  
Guido Kroemer ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Amino Acids ◽  
Mammalian Cells ◽  
Tissue Homeostasis ◽  
In Vivo Studies ◽  
Protective Mechanism ◽  
Cardiac Damage ◽  
Wide Range ◽  
First Time

Autophagy is an essential protective mechanism that allows mammalian cells to cope with a variety of stressors and contributes to maintaining cellular and tissue homeostasis. Due to these crucial roles and also to the fact that autophagy malfunction has been described in a wide range of pathologies, an increasing number of in vivo studies involving animal models targeting autophagy genes have been developed. In mammals, total autophagy inactivation is lethal, and constitutive knockout models lacking effectors of this route are not viable, which has hindered so far the analysis of the consequences of a systemic autophagy decline. Here, we take advantage of atg4b−/− mice, an autophagy-deficient model with only partial disruption of the process, to assess the effects of systemic reduction of autophagy on the metabolome. We describe for the first time the metabolic footprint of systemic autophagy decline, showing that impaired autophagy results in highly tissue-dependent alterations that are more accentuated in the skeletal muscle and plasma. These changes, which include changes in the levels of amino-acids, lipids, or nucleosides, sometimes resemble those that are frequently described in conditions like aging, obesity, or cardiac damage. We also discuss different hypotheses on how impaired autophagy may affect the metabolism of several tissues in mammals.

Effect of sarcomere length on total capillary length in skeletal muscle: In vivo evidence for longitudinal stretching of capillaries

1990 ◽  
Vol 40 (1) ◽  
pp. 63-72 ◽  
Author(s):  
C.G. Ellis ◽  
O. Mathieu-Costello ◽  
R.F. Potter ◽  
I.C. MacDonald ◽  
A.C. Groom
Keyword(s):  
Skeletal Muscle ◽  
Sarcomere Length ◽  
Capillary Length

scholarly journals Effects of myofiber isolation technique on sarcolemma biomechanics

BioTechniques ◽  
2020 ◽  
Vol 69 (5) ◽  
pp. 388-391
Author(s):  
Karla P Garcia-Pelagio ◽  
Stephen JP Pratt ◽  
Richard M Lovering
Keyword(s):  
Skeletal Muscle ◽  
Extensor Digitorum Longus ◽  
Sarcomere Length ◽  
Biomechanical Properties ◽  
Isolation Technique ◽  
Enzymatic Dissociation ◽  
Flexor Digitorum Brevis ◽  
Flexor Digitorum ◽  
Biomechanical Measurements

Isolated myofibers are commonly used to understand the function of skeletal muscle in vivo. This can involve single isolated myofibers obtained from dissection or from enzymatic dissociation. Isolation via dissection allows control of sarcomere length and preserves tendon attachment but is labor-intensive, time-consuming and yields few viable myofibers. In contrast, enzymatic dissociation is fast and facile, produces hundreds of myofibers, and more importantly reduces the number of muscles/animals needed for studies. Biomechanical properties of the sarcolemma have been studied using myofibers from the extensor digitorum longus, but this has been limited to dissected myofibers, making data collection slow and difficult. We have modified this tool to perform biomechanical measurements of the sarcolemma in dissociated myofibers from the flexor digitorum brevis.

scholarly journals Stretch of active muscle during the declining phase of the calcium transient produces biphasic changes in calcium binding to the activating sites.

1990 ◽  
Vol 96 (5) ◽  
pp. 1013-1035 ◽  
Author(s):  
A M Gordon ◽  
E B Ridgway
Keyword(s):  
Calcium Binding ◽  
Time Course ◽  
Control Level ◽  
Calcium Transient ◽  
Length Change ◽  
Positive Phase ◽  
Active Force ◽  
Cross Bridge ◽  
Calcium Affinity ◽  
Cross Bridges

In voltage-clamped barnacle single muscle fibers, muscle shortening during the declining phase of the calcium transient increases myoplasmic calcium. This extra calcium is probably released from the activating sites by a change in affinity when cross-bridges break (Gordon, A. M., and E. B. Ridgway, 1987. J. Gen. Physiol. 90:321-340). Stretching the muscle at similar times causes a more complex response, a rapid increase in intracellular calcium followed by a transient decrease. The amplitudes of both phases increase with the rate and amplitude of stretch. The rapid increase, however, appears only when the muscle is stretched more than approximately 0.4%. This is above the length change that produces the breakpoint in the force record during a ramp stretch. This positive phase in response to large stretches is similar to that seen on equivalent shortening at the same point in the contraction. For stretches at different times during the calcium transient, the peak amplitude of the positive phase has a time course that is delayed relative to the calcium transient, while the peak decrease during the negative phase has an earlier time course that is more similar to the calcium transient. The amplitudes of both phases increase with increasing strength of stimulation and consequent force. When the initial muscle the active force. A large decrease in length (which drops the active force to zero) decreases the extra calcium seen on a subsequent restretch. After such a shortening step, the extra calcium on stretch recovers (50 ms half time) toward the control level with the same time course as the redeveloped force. Conversely, stretching an active fiber decreases the extra calcium on a subsequent shortening step that is imposed shortly afterward. Enhanced calcium binding due to increased length alone cannot explain our data. We hypothesize that the calcium affinity of the activating sites increases with cross-bridge attachment and further with cross-bridge strain. This accounts for the biphasic response to stretch as follows: cross-bridges detached by stretch first decrease calcium affinity, then upon reattachment increase calcium affinity due to the strained configuration brought on by the stretch. The experiments suggest that cross-bridge attachment and strain can modify calcium binding to the activating sites in intact muscle.

Effects of cocaine on leakage of creatine kinase from skeletal muscle: In vitro and in vivo studies in mice

Life Sciences ◽  
1995 ◽  
Vol 57 (17) ◽  
pp. 1569-1578 ◽  
Author(s):  
Gayle A. Brazeau ◽  
Anne McArdle ◽  
Malcolm J. Jackson
Keyword(s):  
Skeletal Muscle ◽  
Creatine Kinase ◽  
In Vivo Studies

scholarly journals Optogenetic activation of muscle contraction in vivo

2020 ◽  
Author(s):  
Elahe Ganji ◽  
C. Savio Chan ◽  
Christopher W. Ward ◽  
Megan L. Killian
Keyword(s):  
Skeletal Muscle ◽  
Electrical Stimulation ◽  
Muscle Contraction ◽  
Fluorescent Imaging ◽  
Triceps Surae ◽  
Light Activation ◽  
Non Invasive ◽  
Optogenetic Stimulation ◽  
Stimulation Of

AbstractOptogenetics is an emerging alternative to traditional electrical stimulation to initiate action potentials in activatable cells both ex vivo and in vivo. Optogenetics has been commonly used in mammalian neurons and more recently, it has been adapted for activation of cardiomyocytes and skeletal muscle. Therefore, the aim of this study was to evaluate the stimulation feasibility and sustain isometric muscle contraction and limit decay for an extended period of time (1s), using non-invasive transdermal light activation of skeletal muscle (triceps surae) in vivo. We used inducible Cre recombination to target expression of Channelrhodopsin-2 (ChR2(H134R)-EYFP) in skeletal muscle (Acta1-Cre) in mice. Fluorescent imaging confirmed that ChR2 expression is localized in skeletal muscle and does not have specific expression in sciatic nerve branch, therefore, allowing for non-nerve mediated optical stimulation of skeletal muscle. We induced muscle contraction using transdermal exposure to blue light and selected 10Hz stimulation after controlled optimization experiments to sustain prolonged muscle contraction. Increasing the stimulation frequency from 10Hz to 40Hz increased the muscle contraction decay during prolonged 1s stimulation, highlighting frequency dependency and importance of membrane repolarization for effective light activation. Finally, we showed that optimized pulsed optogenetic stimulation of 10 Hz resulted in comparable ankle torque and contractile functionality to that of electrical stimulation. Our results demonstrate the feasibility and repeatability of non-invasive optogenetic stimulation of muscle in vivo and highlight optogenetic stimulation as a powerful tool for non-invasive in vivo direct activation of skeletal muscle.

Steroid effects on permeability of rat thymic lymphocytes to α-aminoisobutyrate

1963 ◽  
Vol 205 (3) ◽  
pp. 446-452 ◽  
Author(s):  
Melvin Blecher
Keyword(s):  
Skeletal Muscle ◽  
Extracellular Fluid ◽  
In Vivo Studies ◽  
Metabolic Inhibitors ◽  
Active Process ◽  
Low Concentrations ◽  
Significant Difference ◽  
Adrenalectomized Rats

In vitro studies of the flux of α-aminoisobutyrate-1-C14 (AIB) between rat thymic lymphocytes and extracellular fluid have revealed that: a) the amino acid enters cells but is not further metabolized; b) at low concentrations, similar to those of amino acids in plasma, the net influx and efflux of AIB exhibit properties of an active process; and c) influx of AIB is inhibited, and efflux stimulated, by deoxycorticosterone (DOC), by metabolic inhibitors, and by other specific steroids. In vivo studies of the distribution of AIB between serum and tissue demonstrated that administration of DOC to adrenalectomized rats inhibited concentration of AIB by thymus, diaphragm, and skeletal muscle, augmented uptake by liver, and increased the serum level of AIB. Prior adrenalectomy of donor rats resulted in no change from normal in the in vitro capacity of thymic lymphocytes to take up AIB. There was no significant difference from normal in the in vivo concentration of AIB by thymus, liver, and skeletal muscle of adrenalectomized rats, although uptake by diaphragm was decreased compared to normal control animals.

scholarly journals A proposed role for non-junctional transverse tubules in skeletal muscle as flexible segments allowing expansion of the transverse network

2019 ◽  
Vol 29 (2) ◽  
Author(s):  
Manuela Lavorato ◽  
Ramesh Iyer ◽  
Clara Franzini-Armstrong
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Skeletal Muscles ◽  
Sarcomere Length ◽  
Muscle Fibers ◽  
Entire Length ◽  
Small Fish ◽  
Transverse Tubules ◽  
T Tubules

Using a variety of technical approaches, we have detected the presence of continuous triads that cover the entire length of T tubules in the main white body muscles of several small fish. This is in contrast to the discontinuous association of sarcoplasmic reticulum with T tubules in the red muscles from the same fish as well as in all other previously described muscles in a large variety of skeletal muscles. We suggest that continuous triads are permissible only in muscle fibers that are not normally subject to significant changes in sarcomere length during normal in vivo activity, as is the case for white muscles in the trunk of fish.

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