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Specific Force (specific + force)

Distribution by Scientific Domains

Life Sciences	50%
Medical Sciences	33%

Selected Abstracts

Increased CaV,1a expression with aging contributes to skeletal muscle weakness

AGING CELL, Issue 5 2009
Jackson R. Taylor
Summary Ca2+ release from the sarcoplasmic reticulum (SR) into the cytosol is a crucial part of excitation,contraction (E-C) coupling. Excitation,contraction uncoupling, a deficit in Ca2+ release from the SR, is thought to be responsible for at least some of the loss in specific force observed in aging skeletal muscle. Excitation,contraction uncoupling may be caused by alterations in expression of the voltage-dependent calcium channel ,1s (CaV1.1) and ,1a (CaV,1a) subunits, both of which are necessary for E-C coupling to occur. While previous studies have found CaV1.1 expression declines in old rodents, CaV,1a expression has not been previously examined in aging models. Western blot analysis shows a substantial increase of CaV,1a expression over the full lifespan of Friend Virus B (FVB) mice. To examine the specific effects of CaV,1a overexpression, a CaV,1a -YFP plasmid was electroporated in vivo into young animals. The resulting increase in expression of CaV,1a corresponded to decline of CaV1.1 over the same time period. YFP fluorescence, used as a measure of CaV,1a -YFP expression in individual fibers, also showed an inverse relationship with charge movement, measured using the whole-cell patch-clamp technique. Specific force was significantly reduced in young CaV,1a -YFP electroporated muscle fibers compared with sham-electroporated, age-matched controls. siRNA interference of CaV,1a in young muscles reduced charge movement, while charge movement in old was restored to young control levels. These studies imply CaV,1a serves as both a positive and negative regulator CaV1.1 expression, and that endogenous overexpression of CaV,1a during old age may play a role in the loss of specific force. [source]

Single muscle fiber size and contractility after spinal cord injury in rats

MUSCLE AND NERVE, Issue 1 2006
Walter R. Frontera MD
Abstract Spinal cord injury (SCI) results in muscle weakness but the degree of impairment at the level of single fibers is not known. The purpose of this study was to examine the effects of T9,level SCI on single muscle fibers from the tibialis anterior of rats. Significant decreases in cross-sectional area (CSA), maximal force (Po), and specific force (SF = Po/CSA) were noted at 2 weeks. Atrophy and force-generating capacity were reversed at 4 weeks, but SF remained impaired. Maximum shortening velocity (Vo) did not change after injury. SCI thus appears to affect various contractile properties of single muscle fibers differently. Normal cage activity may partially restore function but new interventions are needed to restore muscle fiber quality. Muscle Nerve, 2006 [source]

Alterations in inorganic phosphate in mouse hindlimb muscles during limb disuse,

NMR IN BIOMEDICINE, Issue 2 2008
Neeti Pathare
Abstract Muscle disuse induces a wide array of structural, biochemical, and neural adaptations in skeletal muscle, which can affect its function. We recently demonstrated in patients with an orthopedic injury that cast immobilization alters the resting Pi content of skeletal muscle, which may contribute to loss of specific force. The goal of this study was to determine the direct effect of disuse on the basal phosphate content in skeletal muscle in an animal model, avoiding the confounding effects of injury/surgery. 31P and 1H MRS data were acquired from the gastrocnemius muscle of young adult mice (C57BL6 female, n,=,8), at rest and during a reversible ischemia experiment, before and after 2 weeks of cast immobilization. Cast immobilization resulted in an increase in resting Pi content (75%; p,<,0.001) and the Pi to phosphocreatine (PCr) ratio (Pi/PCr; 80%, p,<,0.001). The resting concentrations of ATP, PCr and total creatine (PCr,+,creatine) and the intracellular pH were not significantly different after immobilization. During ischemia (30,min), PCr concentrations decreased to 54,±,2% and 52,±,6% of the resting values in pre-immobilized and immobilized muscles, respectively, but there were no detectable differences in the rates of Pi increase or PCr depletion (0.55,±,0.01,mM min,1 and 0.52,±,0.03,mM min,1 before and after immobilization, respectively; p,=,0.78). At the end of ischemia, immobilized muscles had a twofold higher phosphorylation potential ([ADP][Pi]/[ATP]) and intracellular buffering capacity (3.38,±,0.54 slykes vs 6.18,±,0.57 slykes). However, the rate of PCr resynthesis (kPCr) after ischemia, a measure of in vivo mitochondrial function, was significantly lower in the immobilized muscles (0.31,±,0.04,min,1) than in pre-immobilized muscles (0.43,±,0.04,min,1). In conclusion, our findings indicate that 2 weeks of cast immobilization, independent of injury-related alterations, leads to a significant increase in the resting Pi content of mouse skeletal muscle. The increase in Pi with muscle disuse has a significant effect on the cytosolic phosphorylation potential during transient ischemia and increases the intracellular buffering capacity of skeletal muscle. Copyright © 2007 John Wiley & Sons, Ltd. [source]

Reversible changes in Ca2+ -activation properties of rat skeletal muscle exposed to elevated physiological temperatures

THE JOURNAL OF PHYSIOLOGY, Issue 3 2002
Chris van der Poel
Exposure of relaxed rat extensor digitorum longus (EDL; predominantly fast-twitch) muscle to temperatures in the upper physiological range for mammalian skeletal muscle (43-46 °C) led to reversible alterations of the contractile activation properties. These properties were studied using the mechanically skinned fibre preparation activated in Ca2+ -buffered solutions. The maximum Ca2+ -activated force (maximum force per cross-sectional area) and the steepness of force-pCa (-log10[Ca2+]) curves as measured by the Hill coefficient (nH) reversibly decreased by factors of 8 and 2.5, respectively, when the EDL muscle was treated at 43 °C for 30 min and 5 and 2.8, respectively, with treatment at 46 °C for 5 min. Treatment at 47 °C for 5 min produced an even more marked depression in maximum specific force, which fully recovered after treatment, and in the Hill coefficient, which did not recover after treatment. After all temperature treatments there was no change in the level of [Ca2+] at which 50 % maximum force was generated. The temperature-induced depression in force production and steepness of the force-pCa curves were shown to be associated with superoxide (O2,) production in muscle (apparent rate of O2, production at room temperature, 0.055 ± 0.008 nmol min,1 (g wet weight),1; and following treatment to 46 °C for 5 min, 1.8 ± 0.2 nmol min,1 (g wet weight),1) because 20 mm Tiron, a membrane-permeant O2, scavenger, was able to markedly suppress the net rate of O2, production and prevent any temperature-induced depression of contractile parameters. The temperature-induced depression in force production of the contractile apparatus could be reversed either by allowing the intact muscle to recover for 3-4 h at room temperature or by treatment of the skinned fibre preparation with dithiothreitol (a potent reducing agent) in the relaxing solution. These results demonstrate that mammalian skeletal muscle has the ability to uncouple force production reversibly from the activator Ca2+ as the temperature increases in the upper physiological range through an increase in O2, production. [source]

Antisocial Security: The Puzzle of Beggar-Thy-Children Policies

AMERICAN JOURNAL OF POLITICAL SCIENCE, Issue 3 2009
Robert Grafstein
The U.S. Social Security program has irrevocably transferred substantial wealth from workers to their ostensibly altruistic parents. After some alternative explanations for this paradox are addressed, a formal model is developed to show that a majority of rational voters who care about their descendants can support the preservation of current benefits for themselves but accept the prospect of Social Security's future retrenchment. Incorporating elements of Tabellini's (2000) positive theory of Social Security and Bénabou and Ok's (2001) analysis of income mobility, the model identifies specific forces affecting this time-varying individual support for Social Security. These forces are embodied in three hypotheses related to income mobility, relative income level, and age. An ordered logit analysis of cumulative ANES data supports these hypotheses. [source]