Effects of distribution of muscle fiber length on active length-force characteristics of rat gastrocnemius medialis

1994 ◽  
Vol 239 (4) ◽  
pp. 414-420 ◽  
Author(s):  
Gertjan J. C. Ettema ◽  
Peter A. Huijing
Keyword(s):  
Muscle Fiber ◽  
Fiber Length ◽  
Gastrocnemius Medialis ◽  
Active Length ◽  
Force Characteristics

501 Changes of muscle fiber length in vivo during walking as revealed by ultrasound images

2008 ◽  
Vol 2007.20 (0) ◽  
pp. 165-166
Author(s):  
Naoto SASAGAWA ◽  
Tasuku MIYOSHI ◽  
Hiroyuki KOYAMA ◽  
Takashi KOMEDA ◽  
Shin-Ichiro YAMAMOTO
Keyword(s):  
Muscle Fiber ◽  
Fiber Length ◽  
Ultrasound Images

scholarly journals Dynamic left ventricular elastance: a model for integrating cardiac muscle contraction into ventricular pressure-volume relationships

2008 ◽  
Vol 104 (4) ◽  
pp. 958-975 ◽  
Author(s):  
Kenneth B. Campbell ◽  
Amy M. Simpson ◽  
Stuart G. Campbell ◽  
Henk L. Granzier ◽  
Bryan K. Slinker
Keyword(s):  
Muscle Fiber ◽  
Fiber Length ◽  
Phase 1 ◽  
Left Ventricular ◽  
Isolated Rat Heart ◽  
Rate Of Change ◽  
Lv Function ◽  
Elastic Distortion ◽  
Length Changes ◽  
Incremental Step

To integrate myocardial contractile processes into left ventricular (LV) function, a mathematical model was built. Muscle fiber force was set equal to the product of stiffness and elastic distortion of stiffness elements, i.e., force-bearing cross bridges (XB). Stiffness dynamics arose from recruitment of XB according to the kinetics of myofilament activation and fiber-length changes. Elastic distortion dynamics arose from XB cycling and the rate-of-change of fiber length. Muscle fiber stiffness and distortion dynamics were transformed into LV chamber elastance and volumetric distortion dynamics. LV pressure equaled the product of chamber elastance and volumetric distortion, just as muscle-fiber force equaled the product of muscle-fiber stiffness and lineal elastic distortion. Model validation was in terms of its ability to reproduce cycle-time-dependent LV pressure response, ΔP( t), to incremental step-like volume changes, ΔV, in the isolated rat heart. All ΔP( t), regardless of the time in the cycle at which ΔP( t) was elicited, consisted of three phases: phase 1, concurrent with the leading edge of ΔV; phase 2, a brief transient recovery from phase 1; and phase 3, sustained for the duration of systole. Each phase varied with the time in the cycle at which ΔP( t) was elicited. When the model was fit to the data, cooperative activation was required to sustain systole for longer periods than was possible with Ca2+ activation alone. The model successfully reproduced all major features of the measured ΔP( t) responses, and thus serves as a credible indicator of the role of underlying contractile processes in LV function.

8J-20 Measurement of Gastrocnemius muscle fiber length during passive postural modulation

2011 ◽  
Vol 2010.23 (0) ◽  
pp. 311-312
Author(s):  
Hideaki TABEI ◽  
Hiroki OBATA ◽  
Tasuku MIYOSHI ◽  
Shin-ichiroh YAMAMOTO
Keyword(s):  
Muscle Fiber ◽  
Fiber Length ◽  
Gastrocnemius Muscle

Muscle fiber length: a determinant of left ventricular contraction pattern

1966 ◽  
Vol 211 (2) ◽  
pp. 301-306 ◽  
Author(s):  
VJ Fisher ◽  
RJ Lee ◽  
A Gourin ◽  
H Bolooki ◽  
JH Stuckey ◽  
...  
Keyword(s):  
Muscle Fiber ◽  
Fiber Length ◽  
Left Ventricular ◽  
Ventricular Contraction ◽  
Contraction Pattern

scholarly journals Abelson tyrosine-protein kinase 2 regulates myoblast proliferation and controls muscle fiber length

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Jennifer K Lee ◽  
Peter T Hallock ◽  
Steven J Burden
Keyword(s):  
Protein Kinase ◽  
Muscle Fiber ◽  
Fiber Length ◽  
Myoblast Fusion ◽  
Mutant Mice ◽  
Diaphragm Muscle ◽  
Tendon Cells ◽  
Limb Muscles ◽  
Myoblast Proliferation ◽  
Tyrosine Protein Kinase

Muscle fiber length is nearly uniform within a muscle but widely different among different muscles. We show that Abelson tyrosine-protein kinase 2 (Abl2) has a key role in regulating myofiber length, as a loss of Abl2 leads to excessively long myofibers in the diaphragm, intercostal and levator auris muscles but not limb muscles. Increased myofiber length is caused by enhanced myoblast proliferation, expanding the pool of myoblasts and leading to increased myoblast fusion. Abl2 acts in myoblasts, but as a consequence of expansion of the diaphragm muscle, the diaphragm central tendon is reduced in size, likely contributing to reduced stamina of Abl2 mutant mice. Ectopic muscle islands, each composed of myofibers of uniform length and orientation, form within the central tendon of Abl2+/− mice. Specialized tendon cells, resembling tendon cells at myotendinous junctions, form at the ends of these muscle islands, suggesting that myofibers induce differentiation of tendon cells, which reciprocally regulate myofiber length and orientation.

scholarly journals Errors in Predicting Muscle Fiber Lengths from Joint Kinematics Point to the Need to Include Tendon Tension in Computational Neuromuscular Models

2020 ◽  
Author(s):  
Daniel A Hagen ◽  
Francisco J Valero-Cuevas
Keyword(s):  
Muscle Fiber ◽  
Fiber Length ◽  
Functional Relationship ◽  
Parametric Uncertainty ◽  
Muscle Spindles ◽  
Joint Kinematics ◽  
Effective Control ◽  
Golgi Tendon Organs ◽  
Limb Kinematics ◽  
Tendon Tension

Accurate predictions of tendon forces must consider musculotendon mechanics; specifically muscle fiber lengths and velocities. These are either predicted explicitly by simulating musculoskeletal dynamics or approximated from measured limb kinematics. The latter is complicated by the fact that tendon lengths and pennation angles vary with both limb kinematics and tendon tension. We now derive the error in kinematically-approximated muscle fiber lengths as a general equation of muscle geometry and tendon tension. This enables researchers to objectively evaluate this error’s significance—which can reach ~ 80% of the optimal muscle fiber length—with respect to the scientific or clinical question being asked. Although this equation provides a detailed functional relationship between muscle fiber lengths, joint kinematics and tendon tension, the parameters used to characterize musculotendon architecture are subject- and muscle-specific. This parametric uncertainty limits the accuracy of any generic musculoskeletal model that hopes to explain subject-specific phenomena. Nevertheless, the existence of such a functional relationship has profound implications to biological proprioception. These results strongly suggest that tendon tension information (from Golgi tendon organs) is likely integrated with muscle fiber length information (from muscle spindles) at the spinal cord to produce useful estimates of limb configuration to enable effective control of movement.

POTENTIAL MECHANISMS MODULATING MUSCLE FIBER LENGTH DURING LIMB LENGTHENING

1999 ◽  
Vol 31 (Supplement) ◽  
pp. S172
Author(s):  
V. J. Caiozzo ◽  
M. J. Baker ◽  
F. Haddad ◽  
A. Qin
Keyword(s):  
Muscle Fiber ◽  
Fiber Length ◽  
Limb Lengthening
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