scholarly journals Effects of Muscle Length and Physiological Cross Sectional Area on Muscle Force Production: a Comparative Study

2018 ◽  
Vol 1048 ◽  
pp. 012008
Author(s):  
F Romero-Sánchez ◽  
F J Alonso ◽  
J Barrios-Muriel ◽  
G Rodríguez-Jiménez
2000 ◽  
Vol 88 (3) ◽  
pp. 1127-1132 ◽  
Author(s):  
Brenda Russell ◽  
Delara Motlagh ◽  
William W. Ashley

What determines the shape, size, and force output of cardiac and skeletal muscle? Chicago architect Louis Sullivan (1856–1924), father of the skyscraper, observed that “form follows function.” This is as true for the structural elements of a striated muscle cell as it is for the architectural features of a building. Function is a critical evolutionary determinant, not form. To survive, the animal has evolved muscles with the capacity for dynamic responses to altered functional demand. For example, work against an increased load leads to increased mass and cross-sectional area (hypertrophy), which is directly proportional to an increased potential for force production. Thus a cell has the capacity to alter its shape as well as its volume in response to a need for altered force production. Muscle function relies primarily on an organized assembly of contractile and other sarcomeric proteins. From analysis of homogenized cells and molecular and biochemical assays, we have learned about transcription, translation, and posttranslational processes that underlie protein synthesis but still have done little in addressing the important questions of shape or regional cell growth. Skeletal muscles only grow in length as the bones grow; therefore, most studies of adult hypertrophy really only involve increased cross-sectional area. The heart chamber, however, can extend in both longitudinal and transverse directions, and cardiac cells can grow in length and width. We know little about the regulation of these directional processes that appear as a cell gets larger with hypertrophy or smaller with atrophy. This review gives a brief overview of the regulation of cell shape and the composition and aggregation of contractile proteins into filaments, the sarcomere, and myofibrils. We examine how mechanical activity regulates the turnover and exchange of contraction proteins. Finally, we suggest what kinds of experiments are needed to answer these fundamental questions about the regulation of muscle cell shape.


2008 ◽  
Vol 22 (1) ◽  
pp. 128-131 ◽  
Author(s):  
Shigeki Ikegawa ◽  
Kazuo Funato ◽  
Naoya Tsunoda ◽  
Hiroaki Kanehisa ◽  
Tetsuo Fukunaga ◽  
...  

2012 ◽  
Vol 28 (6) ◽  
pp. 701-707 ◽  
Author(s):  
Marcelo Peduzzi de Castro ◽  
Daniel Cury Ribeiro ◽  
Felipe de Camargo Forte ◽  
Joelly Mahnic de Toledo ◽  
Roberto Costa Krug ◽  
...  

The aim of this study was to compare shoulder muscle force and moment production during external rotation performed in the transverse and sagittal planes. An optimization model was used for estimating shoulder muscle force production of infraspinatus, teres minor, supraspinatus, anterior deltoid, middle deltoid and posterior deltoid muscles. The model uses as input data the external rotation moment, muscle moment arm magnitude, muscle physiologic cross-sectional area and muscle specific tension. The external rotation moment data were gathered from eight subjects in transverse and six subjects in sagittal plane using an isokinetic dynamometer. In the sagittal plane, all studied muscles presented larger estimated force in comparison with the transverse plane. The infraspinatus, teres minor, supraspinatus and posterior deltoid muscles presented larger moment in sagittal when compared with transverse plane. When prescribing shoulder rehabilitation exercises, therapists should bear in mind the described changes in muscle force production.


2010 ◽  
Vol 298 (1) ◽  
pp. C149-C162 ◽  
Author(s):  
Nadège Zanou ◽  
Georges Shapovalov ◽  
Magali Louis ◽  
Nicolas Tajeddine ◽  
Chiara Gallo ◽  
...  

Skeletal muscle contraction is reputed not to depend on extracellular Ca2+. Indeed, stricto sensu , excitation-contraction coupling does not necessitate entry of Ca2+. However, we previously observed that, during sustained activity (repeated contractions), entry of Ca2+is needed to maintain force production. In the present study, we evaluated the possible involvement of the canonical transient receptor potential (TRPC)1 ion channel in this entry of Ca2+and investigated its possible role in muscle function. Patch-clamp experiments reveal the presence of a small-conductance channel (13 pS) that is completely lost in adult fibers from TRPC1−/−mice. The influx of Ca2+through TRPC1 channels represents a minor part of the entry of Ca2+into muscle fibers at rest, and the activity of the channel is not store dependent. The lack of TRPC1 does not affect intracellular Ca2+concentration ([Ca2+]i) transients reached during a single isometric contraction. However, the involvement of TRPC1-related Ca2+entry is clearly emphasized in muscle fatigue. Indeed, muscles from TRPC1−/−mice stimulated repeatedly progressively display lower [Ca2+]itransients than those observed in TRPC1+/+fibers, and they also present an accentuated progressive loss of force. Interestingly, muscles from TRPC1−/−mice display a smaller fiber cross-sectional area, generate less force per cross-sectional area, and contain less myofibrillar proteins than their controls. They do not present other signs of myopathy. In agreement with in vitro experiments, TRPC1−/−mice present an important decrease of endurance of physical activity. We conclude that TRPC1 ion channels modulate the entry of Ca2+during repeated contractions and help muscles to maintain their force during sustained repeated contractions.


1982 ◽  
Vol 97 (1) ◽  
pp. 411-420
Author(s):  
R. B. Armstrong ◽  
C. R. Taylor

This experiment was designed to study the relationship between the cross-sectional area of rat skeletal muscle showing glycogen loss and the muscle forces exerted during exercise. Muscular force exerted by the extensors of the elbows and ankle was increased by 24% by loading rats with 24% of their body mass while running them on a treadmill at 30 m.min-1. VO2 increased by 24% and stride frequency was unchanged when the rats ran with loads. Cross-sectional areas of the elbow and ankle extensor muscles showing glycogen loss were compared from rats running with and without the load. We found a nearly direct proportionality between the changes in force and the changes in muscle area showing glycogen loss, i.e. when the force of the extensors was increased by 24%, the cross-sectional area of the elbow extensors showing glycogen loss increased by 28%, and that of the ankle extensor group increased by 24%. The more peripheral muscles in each group accounted for a greater proportion of the increase in cross-sectional area of the group showing glycogen loss (i.e. lateral and long heads of triceps brachii muscle accounted for 91% of the increase in the elbow extensor group, and gastrocnemius muscle accounted for 84% of the increase in the ankle extensor group). Most of the increases in muscle area showing glycogen loss occurred in fast-twitch-glycolytic fibres (84% in the elbow and 88% in the ankle). The data suggest that increasing muscle force requirements by 24% by loading resulted in proportional increases in cross-sectional area of muscles recruited to produce the force, i.e. that spatial recruitment primarily accounted for the elevation in force. The relatively greater increases in cross-sectional area showing glycogen loss of peripheral muscles within a group indicate the importance of studying whole groups of muscles when considering muscular recruitment patterns during exercise.


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