Changes in contractile properties of skeletal muscle during developmentally programmed atrophy and death

2002 ◽  
Vol 282 (6) ◽  
pp. C1270-C1277 ◽  
Author(s):  
Lawrence M. Schwartz ◽  
Robert L. Ruff
Keyword(s):  
Skeletal Muscle ◽  
Contractile Function ◽  
Adult Emergence ◽  
Calcium Sensitivity ◽  
Resting Potential ◽  
Skeletal Muscle Atrophy ◽  
Tetanic Force ◽  
Death Phase ◽  
Hill Coefficients ◽  
Fiber Organization

Skeletal muscle atrophy and death are protracted processes that accompany aging and pathological insults in mammals. The intersegmental muscles (ISMs) from the tobacco hawkmoth Manduca sexta are composed of giant fibers that undergo distinct hormonally-regulated programs of atrophy and death at the end of metamorphosis. Atrophy occurs during the 3 days preceding adult emergence and results in a 40% reduction of mass, whereas death takes place during the subsequent 30 h and results in the complete loss of the fibers. There are no significant changes in tetanic force or calcium sensitivity in skinned fiber preparations during atrophy. However, the size of caffeine-induced contractions fell by about 50%. With the onset of the death phase, dramatic reductions occur in ISM: tetanic force, twitch amplitude, resting potential, caffeine-induced contractions, calcium sensitivity, and Hill coefficients. Several lines of evidence suggest that ISM atrophy is caused by an increase in protein turnover without significant modification of fiber organization. In contrast, ISM death is accompanied by disorganization of the contractile apparatus and concomitant loss of contractile function.

Estradiol replacement reverses ovariectomy-induced muscle contractile and myosin dysfunction in mature female mice

2007 ◽  
Vol 102 (4) ◽  
pp. 1387-1393 ◽  
Author(s):  
Amy L. Moran ◽  
Steven A. Nelson ◽  
Rachel M. Landisch ◽  
Gordon L. Warren ◽  
Dawn A. Lowe
Keyword(s):  
Skeletal Muscle ◽  
Contractile Function ◽  
Electron Paramagnetic Resonance Spectroscopy ◽  
Eccentric Contraction ◽  
Mature Female ◽  
Resonance Spectroscopy ◽  
Paramagnetic Resonance ◽  
Tetanic Force ◽  
Female Mice

Skeletal muscle contractility and myosin function decline following ovariectomy in mature female mice. In the present study we tested the hypothesis that estradiol replacement can reverse those declines. Four-month-old female C57BL/6 mice ( n = 69) were ovariectomized (OVX) or sham operated. Some mice were treated immediately with placebo or 17β-estradiol (OVX + E2) while other mice were treated 30 days postsurgery. Thirty or sixty days postsurgery, soleus muscles were assessed in vitro for contractile function and susceptibility to eccentric contraction-induced injury. Myosin structural dynamics was analyzed in extensor digitorum longus (EDL) muscles by electron paramagnetic resonance spectroscopy. Maximal isometric tetanic force was affected by estradiol status ( P < 0.001) being ∼10% less in soleus muscles from OVX compared with sham-operated mice [168 mN (SD 16.7) vs. 180 mN (SD 14.4)] and was restored in OVX + E2 mice [187 mN (SD 17.6)]. The fraction of strong-binding myosin during contraction was also affected ( P = 0.045) and was ∼15% lower in EDL muscles from OVX compared with OVX + E2 mice [0.263 (SD 0.034) vs. 0.311 (SD 0.022)]. Plasma estradiol levels were correlated with maximal isometric tetanic force ( r = 0.458; P < 0.001) and active stiffness ( r = 0.329; P = 0.044), indicating that circulating estradiol influenced muscle and myosin function. Estradiol was not effective in protecting muscle against an acute eccentric contraction-induced injury ( P ≥ 0.401) but did restore ovariectomy-induced increases in muscle wet mass caused by fluid accumulation. Collectively, estradiol had a beneficial effect on female mouse skeletal muscle.

Continuous testosterone administration prevents skeletal muscle atrophy and enhances resistance to fatigue in orchidectomized male mice

2006 ◽  
Vol 291 (3) ◽  
pp. E506-E516 ◽  
Author(s):  
Anna-Maree Axell ◽  
Helen E. MacLean ◽  
David R. Plant ◽  
Leah J. Harcourt ◽  
Jennifer A. Davis ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Contractile Function ◽  
Skeletal Muscle Atrophy ◽  
Levator Ani Muscle ◽  
Male Mice ◽  
Testosterone Treatment ◽  
Androgen Withdrawal ◽  
Rigorous Model ◽  
Fast Twitch

Androgens promote anabolism in skeletal muscle; however, effects on subsequent muscle function are less well defined because of a lack of reliable experimental models. We established a rigorous model of androgen withdrawal and administration in male mice and assessed androgen regulation of muscle mass, structure, and function. Adult C57Bl/6J male mice were orchidectomized (Orx) or sham-operated (Sham) and received 10 wk of continuous testosterone (T) or control treatment (C) via intraperitoneal implants. Mass, fiber cross-sectional area (CSA), and in vitro contractile function were assessed for fast-twitch extensor digitorum longus (EDL) and slow-twitch soleus (SOL) muscles. After 10 wk, Orx+C mice had reduced body weight gain ( P < 0.05), seminal vesicle mass ( P < 0.01), and levator ani muscle mass ( P < 0.001) compared with Sham+C mice, and these effects were prevented with testosterone treatment. Orx+T mice had greater EDL ( P < 0.01) and SOL ( P < 0.01) muscle mass compared with Orx+C mice; however, median fiber CSA was not significantly altered in these muscles. EDL and SOL muscle force was greater in Sham+T compared with Orx+C mice ( P < 0.05) in proportion to muscle mass. Unexpectedly, Orx+T mice had increased fatigue resistance of SOL muscle compared with Orx+C mice ( P < 0.001). We used a rigorous model of androgen withdrawal and administration in male mice to demonstrate an essential role of androgens in the maintenance of muscle mass and force. In addition, we showed that testosterone treatment increases resistance to fatigue of slow- but not fast-twitch muscle.

Hyperbaric oxygen improves contractile function of regenerating rat skeletal muscle after myotoxic injury

2000 ◽  
Vol 89 (4) ◽  
pp. 1477-1482 ◽  
Author(s):  
Paul Gregorevic ◽  
Gordon S. Lynch ◽  
David A. Williams
Keyword(s):  
Skeletal Muscle ◽  
Hyperbaric Oxygen ◽  
Contractile Function ◽  
Adjunctive Treatment ◽  
Muscle Degeneration ◽  
Muscle Injuries ◽  
Rat Skeletal Muscle ◽  
Tetanic Force ◽  
Edl Muscle

There is growing interest in hyperbaric oxygen (HBO) as an adjunctive treatment for muscle injuries. This experiment tested the hypothesis that periodic inhalation of HBO hastens the functional recovery and myofiber regeneration of skeletal muscle after myotoxic injury. Injection of the rat extensor digitorum longus (EDL) muscle with bupivacaine hydrochloride causes muscle degeneration. After injection, rats breathed air with or without periodic HBO [100% O2 at either 2 or 3 atmospheres absolute (ATA)]. In vitro maximum isometric tetanic force of injured EDL muscles and regenerating myofiber size were unchanged between 2 ATA HBO-treated and untreated rats at 14 days postinjury but were ∼11 and ∼19% greater, respectively, in HBO-treated rats at 25 days postinjury. Maximum isometric tetanic force of injured muscles was ∼27% greater, and regenerating myofibers were ∼41% larger, in 3 ATA HBO-treated rats compared with untreated rats at 14 days postinjury. These findings demonstrate that periodic HBO inhalation increases maximum force-producing capacity and enhances myofiber growth in regenerating skeletal muscle after myotoxic injury with greater effect at 3 than at 2 ATA.

scholarly journals Temporal Adaptive Changes in Contractility and Fatigability of Diaphragm Muscles from Streptozotocin-Diabetic Rats

2010 ◽  
Vol 2010 ◽  
pp. 1-8 ◽  
Author(s):  
Marco Brotto ◽  
Leticia Brotto ◽  
J.-P. Jin ◽  
Thomas M. Nosek ◽  
Andrea Romani
Keyword(s):  
Insulin Treatment ◽  
Contractile Function ◽  
Fiber Type ◽  
Calcium Sensitivity ◽  
Diabetic Rats ◽  
Time Interval ◽  
Gradual Improvement ◽  
Tetanic Force ◽  
Streptozotocin Induced Diabetes ◽  
Streptozotocin Diabetic Rats

Diabetes is characterized by ventilatory depression due to decreased diaphragm (DPH) function. This study investigated the changes in contractile properties of rat DPH muscles over a time interval encompassing from 4 days to 14 weeks after the onset of streptozotocin-induced diabetes, with and without insulin treatment for 2 weeks. Maximum tetanic force in intact DPH muscle strips and recovery from fatiguing stimulation were measured. An early (4-day) depression in contractile function in diabetic DPH was followed by gradual improvement in muscle function and fatigue recovery (8 weeks). DPH contractile function deteriorated again at 14 weeks, a process that was completely reversed by insulin treatment. Maximal contractile force and calcium sensitivity assessed in Triton-skinned DPH fibers showed a similar bimodal pattern and the same beneficial effect of insulin treatment. While an extensive analysis of the isoforms of the contractile and regulatory proteins was not conducted, Western blot analysis of tropomyosin suggests that the changes in diabetic DPH response depended, at least in part, on a switch in fiber type.

scholarly journals Effects of glucose on contractile function, [Ca2+]i, and glycogen in isolated mouse skeletal muscle

2002 ◽  
Vol 282 (6) ◽  
pp. C1306-C1312 ◽  
Author(s):  
Ingrid Helander ◽  
Håkan Westerblad ◽  
Abram Katz
Keyword(s):  
Skeletal Muscle ◽  
Extensor Digitorum Longus ◽  
Contractile Function ◽  
Extensor Digitorum ◽  
Fluorescence Ratio ◽  
Tetanic Force ◽  
Mouse Skeletal Muscle ◽  
Control Value ◽  
Extracellular Glucose ◽  
Initial Force

Extensor digitorum longus muscles were stimulated to contract to fatigue and allowed to recover for 2 h in the absence or presence of 5.5 or 11 mM extracellular glucose. This was followed by a second fatigue run, which ended when the absolute force was the same as at the end of the first run. During the first fatigue run, the fluorescence ratio for indo 1 increased [reflecting an increase in myoplasmic free Ca2+ concentration ([Ca2+]i)] during the initial tetani, peaking at ∼115% of the first tetanic value, followed by a continuous decrease to ∼90% at fatigue. During the first fatigue run, myofibrillar Ca2+ sensitivity was significantly decreased. During the second run, the number of tetani was 57 ± 6% of initial force in muscles that recovered in the absence of glucose and 110 ± 6 and 119 ± 2% of initial force in muscles that recovered in 5.5 and 11 mM glucose, respectively. Fluorescence ratios during the first, peak, and last tetani did not differ significantly between the first and second fatigue runs during any of the three conditions. Glycogen decreased by almost 50% during the first fatigue run and did not change further after recovery in the absence of glucose. After recovery in the presence of 5.5 and 11 mM glucose, glycogen increased 32 and 42% above the nonstimulated control value ( P < 0.01). These data demonstrate that extracellular glucose delays the decrease of tetanic force and [Ca2+]i during fatiguing stimulation and that glycogen supercompensation following contraction can occur in the absence of insulin.

scholarly journals Functional and biochemical responses of skeletal muscle following a moderate degree of systemic iron loading in mice

2019 ◽  
Vol 126 (4) ◽  
pp. 799-809
Author(s):  
Chen Liang ◽  
Marisa C. Mickey ◽  
Candace N. Receno ◽  
Mustafa Atalay ◽  
Keith C. DeRuisseau
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Ryanodine Receptor ◽  
Contractile Function ◽  
Iron Concentration ◽  
Skeletal Muscle Atrophy ◽  
Protein Carbonyls ◽  
Moderate Degree ◽  
Iron Loading ◽  
Biochemical Responses

Excessive iron loading may cause skeletal muscle atrophy and weakness because of its free radical generating properties. To determine whether a clinically relevant degree of iron loading impairs skeletal muscle function, young male mice received injections of iron dextran (4 mg iron/200 µl) or 2 mM d-glucose (control) 5 days/week for 2 weeks ( n = 10/group). Systemic iron loading induced an approximate fourfold increase in the skeletal muscle nonheme iron concentration. Soleus specific tension (1, 30–250 Hz) was lower among iron-loaded animals compared with controls despite similar body mass and muscle mass. Soleus lipid peroxidation (4-hydroxynonenal adducts) and protein oxidation (protein carbonyls) levels were similar between groups. In gastrocnemius muscle, reduced glutathione (GSH) and glutathione peroxidase activity were similar but glutathione disulfide (GSSG) and the GSSG/GSH ratio were greater in iron-loaded muscle. A greater protein expression level of endogenous thiol antioxidant thioredoxin (TRX) was observed among iron-loaded muscle whereas its endogenous inhibitor thioredoxin-interacting protein (TXNip) and the TRX/TXNip ratio were similar. Glutaredoxin2, a thiol-disulfide oxidoreductase activated by GSSG-induced destabilization of its iron-sulfur [2Fe-2S] cluster, was lower following iron loading. Additionally, protein levels of α-actinin and αII-spectrin at 240 kDa were lower in the iron-loaded group. Ryanodine receptor stabilizing subunit calstabin1 was also lower following iron loading. In summary, the contractile dysfunction that resulted from moderate iron loading may be mediated by a disturbance in the muscle redox balance and from changes arising from an increased proteolytic response and aberrant sarcoplasmic reticulum Ca2+ release. NEW & NOTEWORTHY Although severe iron loading is known to cause muscle oxidative stress and dysfunction, the effects of a moderate degree of systemic iron loading on muscle contractile function and biochemical responses remain unclear. This study demonstrates that a pathophysiological elevation in the skeletal muscle iron load leads to force deficits that coincide with impaired redox status, structural integrity, and lower ryanodine receptor-associated calstabin1 in the absence of muscle mass changes or oxidative damage.

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