Cross-sectional area and force production of the quadriceps muscle in elderly osteoarthritic subjects

1998 ◽  
Vol 2 (1) ◽  
pp. 37-38
Author(s):  
J.A. Oldham ◽  
T.E. Howe
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.


1999 ◽  
Vol 276 (2) ◽  
pp. R591-R596 ◽  
Author(s):  
H. Green ◽  
C. Goreham ◽  
J. Ouyang ◽  
M. Ball-Burnett ◽  
D. Ranney

To examine the hypothesis that increases in fiber cross-sectional area mediated by high-resistance training (HRT) would result in a decrease in fiber capillarization and oxidative potential, regardless of fiber type, we studied six untrained males (maximum oxygen consumption, 45.6 ± 2.3 ml ⋅ kg−1 ⋅ min−1; mean ± SE) participating in a 12-wk program designed to produce a progressive hypertrophy of the quadriceps muscle. The training sessions, which were conducted 3 times/wk, consisted of three sets of three exercises, each performed for 6–8 repetitions maximum (RM). Measurements of fiber-type distribution obtained from tissue extracted from the vastus lateralis at 0, 4, 7, and 12 wk indicated reductions ( P < 0.05) in type IIB fibers (15.1 ± 2.1% vs. 7.2 ± 1.3%) by 4 wk in the absence of changes in the other fiber types (types I, IIA, and IIAB). Training culminated in a 17% increase ( P < 0.05) in cross-sectional area by 12 wk with initial increases observed at 4 wk. The increase was independent of fiber type-specific changes. The number of capillaries in contact with each fiber type increased by 12 wk, whereas capillary contacts-to-fiber area ratios remained unchanged. In a defined cross-sectional field, HRT also increased the capillaries per fiber at 12 wk. Training failed to alter cellular oxidative potential, as measured by succinic dehydrogenase (SDH) activity, regardless of fiber type and training duration. It is concluded that modest hypertrophy induced by HRT does not compromise cellular tissue capillarization and oxidative potential regardless of fiber type.


2019 ◽  
Vol 47 (5) ◽  
pp. 423-434 ◽  
Author(s):  
Luke M Weinel ◽  
Matthew J Summers ◽  
Lee-Anne Chapple

Muscle wasting in the intensive care unit (ICU) is common and may impair functional recovery. Ultrasonography (US) presents a modern solution to quantify skeletal muscle size and monitor muscle wasting. However, no standardised methodology for the conduct of ultrasound-derived quadriceps muscle layer thickness or cross-sectional area in this population exists. The aim of this study was to compare methodologies reported for the measurement of quadriceps muscle layer thickness (MLT) and cross-sectional area (CSA) using US in critically ill patients. Databases PubMed, Ovid, Embase, and CINAHL were searched for original research publications that reported US-derived quadriceps MLT and/or CSA conducted in critically ill adult patients. Data were extracted from eligible studies on parameters relating to US measurement including anatomical location, patient positioning, operator technique and image analysis. It was identified that there was a clear lack of reported detail and substantial differences in the reported methodology used for all parameters. A standardised protocol and minimum reporting standards for US-derived measurement of quadriceps muscle size in ICU is required to allow for consistent measurement techniques and hence interpretation of results.


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.


1990 ◽  
Vol 69 (3) ◽  
pp. 861-867 ◽  
Author(s):  
S. C. Kandarian ◽  
T. P. White

Hypotheses were tested that the deficit in maximum isometric force normalized to muscle cross-sectional area (i.e., specific Po, N/cm2) of hypertrophied muscle would return to control value with time and that the rate and magnitude of adaptation of specific force would not differ between soleus and plantaris muscles. Ablation operations of the gastrocnemius and plantaris muscles or the gastrocnemius and soleus muscles were done to induce hypertrophy of synergistic muscle left intact in female Wistar rats (n = 47) at 5 wk of age. The hypertrophied soleus and plantaris muscles and control muscles from other age-matched rats (n = 22) were studied from days 30 to 240 thereafter. Po was measured in vitro at 25 degrees C in oxygenated Krebs-Ringer bicarbonate. Compared with control values, soleus muscle cross-sectional area increased 41-15% from days 30 to 240 after ablation, whereas Po increased 11 and 15% only at days 60 and 90. Compared with control values, plantaris muscle cross-sectional area increased 52% at day 30, 40% from days 60 through 120, and 15% at day 240. Plantaris muscle Po increased 25% from days 30 to 120 but at day 240 was not different from control value. Changes in muscle architecture were negligible after ablation in both muscles. Specific Po was depressed from 11 to 28% for both muscles at all times. At no time after the ablation of synergistic muscle did the increased muscle cross-sectional area contribute fully to isometric force production.


1982 ◽  
Vol 62 (2) ◽  
pp. 227-234 ◽  
Author(s):  
A. Young ◽  
I. Hughes ◽  
J. M. Round ◽  
R. H. T. Edwards

1. By means of ultrasound scanning, bilateral measurements of the cross-sectional area of the quadriceps muscle group were made in 14 young adults with unilateral thigh muscle wasting after knee injury. Needle biopsy specimens from the lateral mass of the muscle were used to estimate the myofibre cross-sectional area for both quadriceps of each subject. 2. The cross-sectional area of the quadriceps of each patient's injured limb was always smaller than that of the contralateral muscle. The wasting was largely localized to the quadriceps, with relative sparing of the other thigh muscles. 3. None of the biopsies showed any abnormality apart from a reduction in fibre size. In each case, the injured limb's reduced quadriceps cross-sectional area was associated with a reduced mean fibre area. 4. The ratio of the cross-sectional area of a muscle to its mean fibre area is a function of the number of fibres it contains. The ratio varied considerably from patient to patient but there was close agreement between the values obtained for the two limbs of each patient. 5. The quadriceps wasting produced by knee injury was due to muscle fibre atrophy. There was no evidence for a change in the number of fibres in the muscle.


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