Physiological measurement of functional muscle length and its relationship to muscle and muscle fiber length

1988 ◽  
Vol 21 (10) ◽  
pp. 860
Author(s):  
Peter V. Loubert
2001 ◽  
Vol 91 (6) ◽  
pp. 2466-2470 ◽  
Author(s):  
Thomas J. Burkholder

Muscle fiber length adaptation to static stretch or shortening depends on age, with sarcomere addition in young muscle being dependent on mobility. Series sarcomere number can also increase in young animals in response to increased muscle excursion, but it is not clear whether adult muscles respond similarly. The ankle flexor retinaculum was transected in neonatal and adult rats to increase tibialis anterior muscle excursion. Sarcomere number in tibialis anterior was determined after 8 wk of adaptation. Muscle moment arm and excursion were increased 30% ( P < 0.01) in both age groups. Muscle cross-sectional area was reduced by 12% ( P < 0.01) in response to the increased mechanical advantage, and this reduction was unaffected by age. Fiber length change was also unaffected by age, with both groups showing a trend ( P < 0.10) for slightly (6%) increased fiber length. Retinaculum transection results in shorter muscle length in all joint configurations, so this trend opposes the fiber length decrease predicted by an adaptation to muscle length and indicates that fiber length is influenced by dynamic mechanical signals in addition to static length.


2001 ◽  
Vol 280 (1) ◽  
pp. R156-R165 ◽  
Author(s):  
Aladin M. Boriek ◽  
Deshen Zhu ◽  
Mark Zeller ◽  
Joseph R. Rodarte

Functional properties of the diaphragm are mediated by muscle structure. Modeling of force transmission necessitates a precise knowledge of muscle fiber architecture. Because the diaphragm experiences loads both along and transverse to the long axes of its muscle fibers in vivo, the mechanism of force transmission may be more complex than in other skeletal muscles that are loaded uniaxially along the muscle fibers. Using a combination of fiber microdissections and histological and morphological methods, we determined regional muscle fiber architecture and measured the shape of the cell membrane of single fibers isolated from diaphragm muscles from 11 mongrel dogs. We found that muscle fibers were either spanning fibers (SPF), running uninterrupted between central tendon (CT) and chest wall (CW), or were non-spanning fibers (NSF) that ended within the muscle fascicle. NSF accounted for the majority of fibers in the midcostal, dorsal costal, and lateral crural regions but were only 25–41% of fibers in the sternal region. In the midcostal and dorsal costal regions, only ∼1% of the NSF terminated within the fascicle at both ends; the lateral crural region contained no such fibers. We measured fiber length, tapered length, fiber diameters along fiber length, and the taper angle for 271 fibers. The lateral crural region had the longest mean length of SPF, which is equivalent to the mean muscle length, followed by the costal and sternal regions. For the midcostal and crural regions, the percentage of tapered length of NSF was 45.9 ± 5.3 and 40.6 ± 7.5, respectively. The taper angle was ∼0.15° for both, and, therefore, the shear component of force was ∼380 times greater than the tensile component. When the diaphragm is submaximally activated, as during normal breathing and maximal inspiratory efforts, muscle forces could be transmitted to the cell membrane and to the extracellular intramuscular connective tissue by shear linkage, presumably via structural transmembrane proteins.


Author(s):  
Naoto SASAGAWA ◽  
Tasuku MIYOSHI ◽  
Hiroyuki KOYAMA ◽  
Takashi KOMEDA ◽  
Shin-Ichiro YAMAMOTO

2008 ◽  
Vol 104 (4) ◽  
pp. 958-975 ◽  
Author(s):  
Kenneth B. Campbell ◽  
Amy M. Simpson ◽  
Stuart G. Campbell ◽  
Henk L. Granzier ◽  
Bryan K. Slinker

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.


Author(s):  
Hideaki TABEI ◽  
Hiroki OBATA ◽  
Tasuku MIYOSHI ◽  
Shin-ichiroh YAMAMOTO

1966 ◽  
Vol 211 (2) ◽  
pp. 301-306 ◽  
Author(s):  
VJ Fisher ◽  
RJ Lee ◽  
A Gourin ◽  
H Bolooki ◽  
JH Stuckey ◽  
...  

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Jennifer K Lee ◽  
Peter T Hallock ◽  
Steven J Burden

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.


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