Influence of fiber-type composition on recovery from tourniquet-induced skeletal muscle ischemia–reperfusion injury

2008 ◽  
Vol 33 (2) ◽  
pp. 272-281 ◽  
Author(s):  
Thomas J. Walters ◽  
John F. Kragh ◽  
David G. Baer
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Contractile Function ◽  
Fiber Type ◽  
Ischemia Reperfusion ◽  
Fiber Types ◽  
Fiber Type Composition ◽  
Type Composition ◽  
Slow Twitch ◽  
Fast Twitch

This study was designed to determine if previously reported differences in the functional impairment of muscles composed of predominantly different fiber types occurs following extended periods of ischemia. We hypothesized that the soleus (Sol) muscle, a predominantly slow-twitch muscle, would be less vulnerable to tourniquet-induced ischemia–reperfusion than the plantaris (Plant), a predominantly fast-twitch muscle, as determined by the assessment of isometric contractile function. Male Sprague–Dawley rats were assigned to one of the following groups to undergo tourniquet application (TKA) (n = 6/group): 2 h TKA, 2 d recovery; 4 h TKA, 2 d recovery; 2 h TKA, 14 d recovery; or 4 h TKA, 14 d recovery. In situ isometric contractile properties were assessed in the predominantly slow-twitch Sol and the predominantly fast-twitch Plant; the contralateral muscle served as the internal control. At 2 d, muscle contraction could not be elicited via neural stimulation, but muscles did contract with direct stimulation, which indicates neural injury. This condition was resolved by day 14. At this time point, tetanic tension (Po) in the Plant was reduced by 45% and 69% in the 2 and 4 h groups, respectively. Po for the Sol was unaffected in the 2 h group, but was reduced by 30% in the 4 h group. The fatigue resistance of the Plant was increased 2 fold in the 4 h group and was unchanged in all other groups. These results demonstrate that vulnerability to tourniquet-induced ischemia–reperfusion injury is dramatically different with respect to muscle fiber-type composition.

Slow to fast alterations in skeletal muscle fibers caused by clenbuterol, a beta 2-receptor agonist

1988 ◽  
Vol 254 (6) ◽  
pp. E726-E732 ◽  
Author(s):  
R. J. Zeman ◽  
R. Ludemann ◽  
T. G. Easton ◽  
J. D. Etlinger
Keyword(s):  
Muscle Fiber ◽  
Receptor Agonist ◽  
Fiber Type ◽  
Fiber Types ◽  
Cross Sectional ◽  
Type Composition ◽  
Slow Twitch ◽  
Beta 2 ◽  
Slow Twitch Fibers ◽  
Fast Twitch

Chronic treatment of rats with clenbuterol, a beta 2-receptor agonist (8–12 wk), caused hypertrophy of histochemically identified fast- but not slow-twitch fibers within the soleus, while the mean areas of both fiber types were increased in the extensor digitorum longus (EDL). In contrast, treatment with the beta 2-receptor antagonist, butoxamine, reduced fast-twitch fiber size in both muscles. In the solei and to a lesser extent in the EDLs, the ratio of the number of fast- to slow-twitch fibers was increased by clenbuterol, while the opposite was observed with butoxamine. The muscle fiber hypertrophy observed in the EDL was accompanied by parallel increases in maximal tetanic tension and muscle cross-sectional area, while in the solei, progressive increases in rates of force development and relaxation toward values typical of fast-twitch muscles were also observed. Our results suggest a role of beta 2-receptors in regulating muscle fiber type composition as well as growth.

scholarly journals lncRNA-Six1 Is a Target of miR-1611 that Functions as a ceRNA to Regulate Six1 Protein Expression and Fiber Type Switching in Chicken Myogenesis

Cells ◽  
2018 ◽  
Vol 7 (12) ◽  
pp. 243 ◽  
Author(s):  
Manting Ma ◽  
Bolin Cai ◽  
Liang Jiang ◽  
Bahareldin Ali Abdalla ◽  
Zhenhui Li ◽  
...  
Keyword(s):  
Fiber Type ◽  
Muscle Fibers ◽  
Muscle Fiber Types ◽  
Fiber Types ◽  
Proliferation And Differentiation ◽  
Slow Twitch Muscle ◽  
Fast Twitch Muscle ◽  
Slow Twitch ◽  
Slow Twitch Fibers ◽  
Fast Twitch

Emerging studies indicate important roles for non-coding RNAs (ncRNAs) as essential regulators in myogenesis, but relatively less is known about their function. In our previous study, we found that lncRNA-Six1 can regulate Six1 in cis to participate in myogenesis. Here, we studied a microRNA (miRNA) that is specifically expressed in chickens (miR-1611). Interestingly, miR-1611 was found to contain potential binding sites for both lncRNA-Six1 and Six1, and it can interact with lncRNA-Six1 to regulate Six1 expression. Overexpression of miR-1611 represses the proliferation and differentiation of myoblasts. Moreover, miR-1611 is highly expressed in slow-twitch fibers, and it drives the transformation of fast-twitch muscle fibers to slow-twitch muscle fibers. Together, these data demonstrate that miR-1611 can mediate the regulation of Six1 by lncRNA-Six1, thereby affecting proliferation and differentiation of myoblasts and transformation of muscle fiber types.

Gene Polymorphisms and Fiber-Type Composition of Human Skeletal Muscle

2012 ◽  
Vol 22 (4) ◽  
pp. 292-303 ◽  
Author(s):  
Ildus I. Ahmetov ◽  
Olga L. Vinogradova ◽  
Alun G. Williams
Keyword(s):  
Skeletal Muscle ◽  
Muscle Fiber ◽  
Human Skeletal Muscle ◽  
Fiber Type ◽  
Vastus Lateralis Muscle ◽  
Type I ◽  
Fiber Types ◽  
Fiber Type Composition ◽  
Type Composition ◽  
Type I Fibers

The ability to perform aerobic or anaerobic exercise varies widely among individuals, partially depending on their muscle-fiber composition. Variability in the proportion of skeletal-muscle fiber types may also explain marked differences in aspects of certain chronic disease states including obesity, insulin resistance, and hypertension. In untrained individuals, the proportion of slow-twitch (Type I) fibers in the vastus lateralis muscle is typically around 50% (range 5–90%), and it is unusual for them to undergo conversion to fast-twitch fibers. It has been suggested that the genetic component for the observed variability in the proportion of Type I fibers in human muscles is on the order of 40–50%, indicating that muscle fiber-type composition is determined by both genotype and environment. This article briefly reviews current progress in the understanding of genetic determinism of fiber-type proportion in human skeletal muscle. Several polymorphisms of genes involved in the calcineurin–NFAT pathway, mitochondrial biogenesis, glucose and lipid metabolism, cytoskeletal function, hypoxia and angiogenesis, and circulatory homeostasis have been associated with fiber-type composition. As muscle is a major contributor to metabolism and physical strength and can readily adapt, it is not surprising that many of these gene variants have been associated with physical performance and athlete status, as well as metabolic and cardiovascular diseases. Genetic variants associated with fiber-type proportions have important implications for our understanding of muscle function in both health and disease.

In vitro O2 uptake and histochemical fiber type of resting hamster muscles

1984 ◽  
Vol 57 (1) ◽  
pp. 246-253 ◽  
Author(s):  
S. M. Sullivan ◽  
R. N. Pittman
Keyword(s):  
Surface Area ◽  
Fiber Type ◽  
Oxidative Capacity ◽  
Histochemical Staining ◽  
Striated Muscles ◽  
Type Composition ◽  
Slow Twitch ◽  
Pattern Number ◽  
Fast Twitch

In vitro oxygen consumption (VO2), histochemical fiber type, capillary arrangement, and muscle fiber geometry were measured in three hamster striated muscles. These muscles varied markedly in their histochemical fiber type composition (% by number): retractor (70% FG, fast-twitch, glycolytic; 16% FOG, fast-twitch, oxidative-glycolytic; 14% SO, slow-twitch, oxidative); soleus (57% FOG, 43% SO), and sartorius (98% FG, 2% FOG). Sartorius VO2 [0.80 +/- 0.034 (SE) ml O2 X min-1 X 100 g-1] was significantly different (P less than 0.01) from VO2 of retractor (0.89 +/- 0.038) and soleus (1.00 +/- 0.048).The number of capillaries around a fiber and the surface area/volume were greater for FOG and SO fibers than for FG fibers. Fibers of all types appeared to be roughly elliptical in shape. Capillaries were uniformly distributed around fibers in the soleus, but they were located more toward the ends of the major diameter in the retractor and sartorius. The results suggest a relationship among a fiber's oxidative capacity (based on its histochemical staining pattern), number of surrounding capillaries and surface area/volume. Furthermore, results suggest that VO2 and capillary spacing around a fiber may depend on fiber type.

scholarly journals Comparative analysis of the transcriptomes of EDL, psoas, and soleus muscles from mice

BMC Genomics ◽  
2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Pabodha Hettige ◽  
Uzma Tahir ◽  
Kiisa C. Nishikawa ◽  
Matthew J. Gage
Keyword(s):  
Skeletal Muscles ◽  
Striated Muscle ◽  
Fiber Type ◽  
Expression Patterns ◽  
Fiber Types ◽  
Muscle Adaptation ◽  
Myosin Heavy Chain Isoform ◽  
Genes Encoding ◽  
Slow Twitch ◽  
Fast Twitch

Abstract Background Individual skeletal muscles have evolved to perform specific tasks based on their molecular composition. In general, muscle fibers are characterized as either fast-twitch or slow-twitch based on their myosin heavy chain isoform profiles. This approach made sense in the early days of muscle studies when SDS-PAGE was the primary tool for mapping fiber type. However, Next Generation Sequencing tools permit analysis of the entire muscle transcriptome in a single sample, which allows for more precise characterization of differences among fiber types, including distinguishing between different isoforms of specific proteins. We demonstrate the power of this approach by comparing the differential gene expression patterns of extensor digitorum longus (EDL), psoas, and soleus from mice using high throughput RNA sequencing. Results EDL and psoas are typically classified as fast-twitch muscles based on their myosin expression pattern, while soleus is considered a slow-twitch muscle. The majority of the transcriptomic variability aligns with the fast-twitch and slow-twitch characterization. However, psoas and EDL exhibit unique expression patterns associated with the genes coding for extracellular matrix, myofibril, transcription, translation, striated muscle adaptation, mitochondrion distribution, and metabolism. Furthermore, significant expression differences between psoas and EDL were observed in genes coding for myosin light chain, troponin, tropomyosin isoforms, and several genes encoding the constituents of the Z-disk. Conclusions The observations highlight the intricate molecular nature of skeletal muscles and demonstrate the importance of utilizing transcriptomic information as a tool for skeletal muscle characterization.

Cardioprotection induced by cardiac-specific overexpression of fibroblast growth factor-2 is mediated by the MAPK cascade

2005 ◽  
Vol 289 (5) ◽  
pp. H2167-H2175 ◽  
Author(s):  
Stacey L. House ◽  
Kevin Branch ◽  
Gilbert Newman ◽  
Thomas Doetschman ◽  
Jo El J. Schultz
Keyword(s):  
Infarct Size ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Contractile Function ◽  
Ischemia Reperfusion ◽  
Mapk Signaling ◽  
Low Flow ◽  
Wild Type ◽  
Erk Inhibition ◽  
Sb 203580

Our laboratory showed previously that cardiac-specific overexpression of FGF-2 [FGF-2 transgenic (Tg)] results in increased recovery of contractile function and decreased infarct size after ischemia-reperfusion injury. MAPK signaling is downstream of FGF-2 and has been implicated in other models of cardioprotection. Treatment of FGF-2 Tg and wild-type hearts with U-0126, a MEK-ERK pathway inhibitor, significantly reduced recovery of contractile function after global low-flow ischemia-reperfusion injury in FGF-2 Tg (86 ± 2% vehicle vs. 66 ± 4% U-0126; P < 0.05) but not wild-type (61 ± 7% vehicle vs. 67 ± 7% U-0126) hearts. Similarly, MEK-ERK inhibition significantly increased myocardial infarct size in FGF-2 Tg (12 ± 3% vehicle vs. 31 ± 2% U-0126; P < 0.05) but not wild-type (30 ± 4% vehicle vs. 36 ± 7% U-0126) hearts. In contrast, treatment of FGF-2 Tg and wild-type hearts with SB-203580, a p38 inhibitor, did not abrogate FGF-2-induced cardioprotection from postischemic contractile dysfunction. Instead, inhibition of p38 resulted in decreased infarct size in wild-type hearts (30 ± 4% vehicle vs. 11 ± 2% SB-203580; P < 0.05) but did not alter infarct size in FGF-2 Tg hearts (12 ± 3% vehicle vs. 14 ± 1% SB-203580). Western blot analysis of ERK and p38 activation revealed signaling alterations in FGF-2 Tg and wild-type hearts during early ischemia or reperfusion injury. In addition, MEK-independent ERK inhibition by p38 was observed during early ischemic injury. Together these data suggest that activation of ERK and inhibition of p38 by FGF-2 is cardioprotective during ischemia-reperfusion injury.

Mechanisms of Erythropoietin-Mediated Cardioprotection during Ischemia-Reperfusion Injury: Role of Protein Kinase C Signaling.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 2907-2907
Author(s):  
Murat O. Arcasoy ◽  
Paul Hanlon ◽  
Ping Fu ◽  
Charles Steenbergen ◽  
Elizabeth Murphy
Keyword(s):  
Protein Kinase ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Contractile Function ◽  
Ischemia Reperfusion ◽  
Cardioprotective Effect ◽  
Isolated Perfused Heart ◽  
Perfused Heart ◽  
Biologic Effects

Abstract The biologic effects of erythropoietin (EPO) are mediated by its cellular receptor EPOR, a member of the cytokine receptor superfamily. EPOR expression in non-hematopoietic cells is associated with novel biologic effects for EPO in diverse organ systems. We recently demonstrated functional EPOR expression in adult rat cardiac myocytes and found that recombinant EPO exerts a rapid cardioprotective effect during ischemia-reperfusion injury of the isolated, perfused heart. Here we investigated the mechanisms of the cardioprotective effect of EPO using Langendorff-perfused rat hearts while left-ventricular-developed pressure (LVDP) was measured continuously to assess contractile function. Hearts were treated directly with EPO in the presence or absence of inhibitors of specific signal transduction pathways prior to normothermic global ischemia followed by reperfusion. Post-ischemic recovery of contractile function was determined by measuring LVDP at the end of reperfusion and expressed as a percentage of the baseline pre-treatment measurement. We investigated EPO-mediated activation of signal transduction pathways in the isolated, perfused heart and observed phosphorylation of p44/p42 MAP kinases ERK 1/2 (Thr202/Tyr204) and protein kinase B/Akt (Ser473), a downstream target of the phosphatidylinositol 3-kinase (PI3K) signaling pathway. Furthermore, EPO treatment of the isolated, perfused heart was associated with translocation of protein kinase C (PKC) ε and δ isoforms to the membrane fraction. We investigated the role of specific signaling pathways in EPO-mediated cardioprotection by employing inhibitors targeting PI3K, PKC and MAP kinase kinase (MEK1). PI3K inhibitors LY294002 and wortmannin attenuated EPO-induced phosphorylation of Akt but had no effect on EPO-mediated cardioprotection. MEK1 inhibitor U0126 had no effect on EPO-mediated cardioprotection. The PKC catalytic inhibitor chelerythrine (chel) significantly inhibited EPO-mediated improvement in post-ischemic recovery of LVDP (figure 1). Hearts pre-treated with EPO exhibited significantly improved post-ischemic recovery of LVDP compared to control hearts (mean±SE: 72±3 in EPO-treated versus 35±3% in control hearts, P<0.05 by ANOVA and Bonferroni post-hoc test, n=10 experiments each group) and the protective effect of EPO was significantly inhibited in chel-treated hearts (52±4% in EPO+chel versus 72±3% in EPO-treated hearts, P<0.05, n=10). As a control, treatment of the hearts with chelerythrine alone had no significant effect on LVDP (49±4%) compared to control hearts. These data demonstrate that EPO-mediated activation of the PKC signaling pathway is required for the cardioprotective effect of EPO during ischemia-reperfusion injury. Figure Figure

scholarly journals Obesity-induced discrepancy between contractile and metabolic phenotypes in slow- and fast-twitch skeletal muscles of female obese Zucker rats

2017 ◽  
Vol 123 (1) ◽  
pp. 249-259 ◽  
Author(s):  
Luz M. Acevedo ◽  
Ana I. Raya ◽  
Rafael Ríos ◽  
Escolástico Aguilera-Tejero ◽  
José-Luis L. Rivero
Keyword(s):  
Muscle Mass ◽  
Skeletal Muscles ◽  
Fiber Type ◽  
Succinic Dehydrogenase ◽  
Zucker Rats ◽  
Fiber Types ◽  
Type Composition ◽  
Obese Zucker Rats ◽  
And Function ◽  
Fast Twitch

A clear picture of skeletal muscle adaptations to obesity and related comorbidities remains elusive. This study describes fiber-type characteristics (size, proportions, and oxidative enzyme activity) in two typical hindlimb muscles with opposite structure and function in an animal model of genetic obesity. Lesser fiber diameter, fiber-type composition, and histochemical succinic dehydrogenase activity (an oxidative marker) of muscle fiber types were assessed in slow (soleus)- and fast (tibialis cranialis)-twitch muscles of obese Zucker rats and compared with age (16 wk)- and sex (females)-matched lean Zucker rats ( n = 16/group). Muscle mass and lesser fiber diameter were lower in both muscle types of obese compared with lean animals even though body weights were increased in the obese cohort. A faster fiber-type phenotype also occurred in slow- and fast-twitch muscles of obese rats compared with lean rats. These adaptations were accompanied by a significant increment in histochemical succinic dehydrogenase activity of slow-twitch fibers in the soleus muscle and fast-twitch fiber types in the tibialis cranialis muscle. Obesity significantly increased plasma levels of proinflammatory cytokines but did not significantly affect protein levels of peroxisome proliferator-activated receptors PPARγ or PGC1α in either muscle. These data demonstrate that, in female Zucker rats, obesity induces a reduction of muscle mass in which skeletal muscles show a diminished fiber size and a faster and more oxidative phenotype. It was noteworthy that this discrepancy in muscle's contractile and metabolic features was of comparable nature and extent in muscles with different fiber-type composition and antagonist functions. NEW & NOTEWORTHY This study demonstrates a discrepancy between morphological (reduced muscle mass), contractile (shift toward a faster phenotype), and metabolic (increased mitochondrial oxidative enzyme activity) characteristics in skeletal muscles of female Zucker fatty rats. It is noteworthy that this inconsistency was comparable (in nature and extent) in muscles with different structure and function.

scholarly journals Calcineurin Is Necessary for the Maintenance but Not Embryonic Development of Slow Muscle Fibers

2005 ◽  
Vol 25 (15) ◽  
pp. 6629-6638 ◽  
Author(s):  
Misook Oh ◽  
Igor I. Rybkin ◽  
Victoria Copeland ◽  
Michael P. Czubryt ◽  
John M. Shelton ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fiber Type ◽  
Oxidative Capacity ◽  
Muscle Fiber Types ◽  
Fiber Types ◽  
Specific Expression ◽  
Interacting Protein ◽  
Type Composition ◽  
Slow Fiber ◽  
Fast Twitch

ABSTRACT Skeletal muscles are a mosaic of slow and fast twitch myofibers. During embryogenesis, patterns of fiber type composition are initiated that change postnatally to meet physiological demand. To examine the role of the protein phosphatase calcineurin in the initiation and maintenance of muscle fiber types, we used a “Flox-ON” approach to obtain muscle-specific overexpression of the modulatory calcineurin-interacting protein 1 (MCIP1/DSCR1), an inhibitor of calcineurin. Myo-Cre transgenic mice with early skeletal muscle-specific expression of Cre recombinase were used to activate the Flox-MCIP1 transgene. Contractile components unique to type 1 slow fibers were absent from skeletal muscle of adult Myo-Cre/Flox-MCIP1 mice, whereas oxidative capacity, myoglobin content, and mitochondrial abundance were unaltered. The soleus muscles of Myo-Cre/Flox-MCIP1 mice fatigued more rapidly than the wild type as a consequence of the replacement of the slow myosin heavy chain MyHC-1 with a fast isoform, MyHC-2A. MyHC-1 expression in Myo-Cre/Flox-MCIP1 embryos and early neonates was normal. These results demonstrate that developmental patterning of slow fibers is independent of calcineurin, while the maintenance of the slow-fiber phenotype in the adult requires calcineurin activity.

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