Static stretch increases c-Jun NH2-terminal kinase activity and p38 phosphorylation in rat skeletal muscle

2001 ◽  
Vol 280 (2) ◽  
pp. C352-C358 ◽  
Author(s):  
Marni D. Boppart ◽  
Michael F. Hirshman ◽  
Kei Sakamoto ◽  
Roger A. Fielding ◽  
Laurie J. Goodyear
Keyword(s):  
Skeletal Muscle ◽  
Muscle Contraction ◽  
Protein Kinases ◽  
Human Skeletal Muscle ◽  
Fiber Type ◽  
Eccentric Contractions ◽  
Sprague Dawley ◽  
Static Stretch

Physical exercise and contraction increase c-Jun NH2-terminal kinase (JNK) activity in rat and human skeletal muscle, and eccentric contractions activate JNK to a greater extent than concentric contractions in human skeletal muscle. Because eccentric contractions include a lengthening or stretch component, we compared the effects of isometric contraction and static stretch on JNK and p38, the stress-activated protein kinases. Soleus and extensor digitorum longus (EDL) muscles dissected from 50- to 90-g male Sprague-Dawley rats were subjected to 10 min of electrical stimulation that produced contractions and/or to 10 min of stretch (0.24 N tension, 20–25% increase in length) in vitro. In the soleus muscle, contraction resulted in a small, but significant, increase in JNK activity (1.8-fold above basal) and p38 phosphorylation (4-fold). Static stretch had a much more profound effect on the stress-activated protein kinases, increasing JNK activity 19-fold and p38 phosphorylation 21-fold. Increases in JNK activation and p38 phosphorylation in response to static stretch were fiber-type dependent, with greater increases occurring in the soleus than in the EDL. Immunohistochemistry performed with a phosphospecific antibody revealed that activation of JNK occurred within the muscle fibers. These studies suggest that the stretch component of a muscle contraction may be a major contributor to the increases in JNK activity and p38 phosphorylation observed after exercise in vivo.

scholarly journals FGF-2–dependent signaling activated in aged human skeletal muscle promotes intramuscular adipogenesis

2021 ◽  
Vol 118 (37) ◽  
pp. e2021013118 ◽  
Author(s):  
Sebastian Mathes ◽  
Alexandra Fahrner ◽  
Umesh Ghoshdastider ◽  
Hannes A. Rüdiger ◽  
Michael Leunig ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Transcriptional Activation ◽  
Human Skeletal Muscle ◽  
Muscle Growth ◽  
Muscle Cells ◽  
Adeno Associated Virus ◽  
Adult Skeletal Muscle

Aged skeletal muscle is markedly affected by fatty muscle infiltration, and strategies to reduce the occurrence of intramuscular adipocytes are urgently needed. Here, we show that fibroblast growth factor-2 (FGF-2) not only stimulates muscle growth but also promotes intramuscular adipogenesis. Using multiple screening assays upstream and downstream of microRNA (miR)-29a signaling, we located the secreted protein and adipogenic inhibitor SPARC to an FGF-2 signaling pathway that is conserved between skeletal muscle cells from mice and humans and that is activated in skeletal muscle of aged mice and humans. FGF-2 induces the miR-29a/SPARC axis through transcriptional activation of FRA-1, which binds and activates an evolutionary conserved AP-1 site element proximal in the miR-29a promoter. Genetic deletions in muscle cells and adeno-associated virus–mediated overexpression of FGF-2 or SPARC in mouse skeletal muscle revealed that this axis regulates differentiation of fibro/adipogenic progenitors in vitro and intramuscular adipose tissue (IMAT) formation in vivo. Skeletal muscle from human donors aged >75 y versus <55 y showed activation of FGF-2–dependent signaling and increased IMAT. Thus, our data highlights a disparate role of FGF-2 in adult skeletal muscle and reveals a pathway to combat fat accumulation in aged human skeletal muscle.

scholarly journals Microdialysis of skeletal muscle at rest

1999 ◽  
Vol 58 (4) ◽  
pp. 919-923 ◽  
Author(s):  
Jan Henriksson
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Human Skeletal Muscle ◽  
Human Metabolism ◽  
High Expectations ◽  
Perfusate Flow ◽  
Muscle Research ◽  
Interstitial Glucose

Techniques in human skeletal muscle research are by necessity predominantly 'descriptive'.Microdialysis has raised high expectations that it could meet the demand for a method that allows 'mechanistic' investigations to be performed in human skeletal muscle. In the present review, some views are given on how well the initial expectations on the use of the microdialysis technique in skeletal muscle have been fulfilled, and the areas in which additional work is needed in order to validate microdialysis as an important metabolic technique in this tissue. The microdialysis catheter has been equated to an artificial blood vessel, which is introduced into the tissue. By means of this 'vessel' the concentrations of compounds in the interstitial space can be monitored. The concentration of substances in the collected samples is dependent on the rate of perfusate flow. When perfusate flow is slow enough to allow complete equilibration between interstitial and perfusate fluids, the concentration in the perfusate is maximal and identical to the interstitial concentration. Microdialysis data may be influenced by changes in blood flow, especially in instances where the tissue diffusivity limits the recovery in vivo, i.e. when recovery in vitro is 100 %, whereas the recovery in vivo is less than 100 %. Microdialysis data indicate that a significant arterial-interstitial glucose concentration gradient exists in skeletal muscle but not in adipose tissue at rest. While the concentrations of glucose and lactate in the dialysate from skeletal muscle are close to the expected values, the glycerol values obtained for muscle are still puzzling. Ethanol added to the perfusate will be cleared by the tissue at a rate that is determined by the nutritive blood flow (the microdialysis ethanol technique). It is concluded that microdialysis of skeletal muscle has become an important technique for mechanistic studies in human metabolism and nutrition.

Carbohydrate metabolism in human skeletal muscle during exercise is not regulated by G-1,6-P2

1988 ◽  
Vol 65 (1) ◽  
pp. 487-489 ◽  
Author(s):  
A. Katz ◽  
K. Sahlin ◽  
J. Henriksson
Keyword(s):  
Skeletal Muscle ◽  
Human Skeletal Muscle ◽  
Work Load ◽  
Short Term ◽  
Catalytic Function ◽  
Muscle Ph ◽  
Induced Changes ◽  
Femoris Muscle

Glucose 1,6-bisphosphate (G-1,6-P2) is a potent activator of phosphofructokinase (PFK) and an inhibitor of hexokinase in vitro. It has been suggested that increases in G-1,6-P2 are a main means by which PFK can achieve significant catalytic function in vivo despite falling pH and that increases in G-1,6-P2 will inhibit hexokinase in vivo. The purpose of the present study was to determine whether contraction-induced changes in flux through PFK and hexokinase are associated with changes in G-1,6-P2 in skeletal muscle. Ten men performed bicycle exercise for 10 min at 40 and 75% of maximal O2 uptake (VO2max) and to fatigue [4.8 +/- 0.6 (SE) min] at 100% VO2max. Biopsies were obtained from the quadriceps femoris muscle at rest and after each work load and analyzed for G-1,6-P2. G-1,6-P2 averaged 111 +/- 13 mumol/kg dry wt at rest and 121 +/- 16, 123 +/- 15, and 123 +/- 11 mumol/kg dry wt after the low-, moderate-, and high-intensity exercise bouts, respectively (P less than 0.05 for all means vs. rest). Flux through PFK was estimated to increase exponentially as the exercise intensity increased and muscle pH decreased at the higher work loads, whereas flux through hexokinase was estimated to increase during exercise at 40 and 75% VO2max but decrease sharply at 100% VO2max. These data demonstrate that flux through neither PFK nor hexokinase is mediated by changes in G-1,6-P2 in human skeletal muscle during short-term dynamic exercise.

Enhanced skeletal muscle arteriolar reactivity to ANG II after recovery from ischemic acute renal failure

2005 ◽  
Vol 289 (6) ◽  
pp. R1770-R1776 ◽  
Author(s):  
David P. Basile ◽  
Deborah L. Donohoe ◽  
Shane A. Phillips ◽  
Jefferson C. Frisbee
Keyword(s):  
Skeletal Muscle ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Pressor Response ◽  
Gracilis Muscle ◽  
Ang Ii ◽  
Sprague Dawley

In addition to the long-term renal complications, previous studies suggested that after acute renal failure (ARF), rats manifest an increased pressor response to an overnight infusion of ANG II. The present study tested whether recovery from ARF results in alterations in sensitivity to the peripheral vasculature. ARF was induced in Sprague-Dawley rats by 45 min of bilateral renal ischemia and reperfusion. Animals were allowed to recover renal structure and function for 5–8 wk, after which the acute pressor responses to ANG II were evaluated either in vivo in in situ skeletal muscle arterioles or in isolated gracilis muscle arteries in vitro. Baseline arterial pressure was not different in ARF rats vs. sham-operated controls, although ARF rats exhibited an enhanced pressor response to bolus ANG II infusion compared with control rats. Steady-state plasma ANG II concentration and plasma renin activity were similar between ARF and control rats. Constrictor reactivity of in situ cremasteric arterioles from ARF rats was enhanced in response to increasing concentrations of ANG II; however, no difference was observed in arteriolar responses to elevated Po2, norepinephrine, acetylcholine, or sodium nitroprusside. Isolated gracilis muscle arteries from ARF rats also showed increased vasoconstriction in response to ANG II but not norepinephrine. In conclusion, recovery from ischemic ARF is not associated with hypertension but is associated with increased arteriolar constrictor reactivity to ANG II. Although the mechanisms of this altered responsiveness are unclear, such changes may relate, in part, to cardiovascular complications in patients with ARF and/or after renal transplant.

scholarly journals PO-252 Effect of acupuncture intervention on the changes of cytoplasmic and mitochondrial Ca2+ concentration following eccentric contractions in rat skeletal muscle

2018 ◽  
Vol 1 (5) ◽  
Author(s):  
Aishan Liu ◽  
Fangming Liu ◽  
Xuelin Zhang ◽  
Yarong Wang ◽  
Mei Kong ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Electrical Stimulation ◽  
Fluorescent Imaging ◽  
Eccentric Contractions ◽  
Rat Skeletal Muscle ◽  
Tetanic Force ◽  
Acupuncture Intervention ◽  
Stimulation Group

  Objective The purpose of this study was to evaluate the effect of acupuncture intervention on the changes of cytoplasmic and mitochondrial Ca2+ concentration following eccentric contractions (ECC) in rat skeletal muscle. Methods 24 healthy male Wistar rats were randomly divided into 4 groups: control group (C, n=6)、electrical stimulation group (E, n=6)、electrical stimulation group with acupuncture intervention (EA, n=6)、electrical stimulation group with acupuncture +TRP channel inhibitor Gd3+ (EAI, n=6). The animal model of eccentric induced skeletal muscle injury was established by electrical stimulation on spinotrapezius muscle of anaesthetised rats in vivo, that is to say, the intact spinotrapezius muscle of adult Wistar rats was exteriorized, and tetanic eccentric contractions (100 Hz, 10 sets of 50 contractions) were elicited by electrical stimulation during synchronized muscle stretch of 10% resting muscle length. Cytoplasmic Ca2+ accumulation were determined by loading the muscle with fura 4-AM using fluorescent imaging in vivo, and mitochondrial Ca2+ concentration were determined by loading the muscle with fura 2-AM using fluorescent imaging in vitro, and recorded changes of muscle maximum tetanic force. Results (1) In vivo, compared with the C , cytoplasmic Ca2+ accumulation increased more rapidly during ECC in the E (P < 0.001). Acupuncture intervention significantly reduced cytosolic Ca2+ accumulation in the EA compared with the E (P < 0.01), and we discovered that muscle deformation generated by acupuncture intervention induced a robust Ca2+ spark response confined in close spatial proximity to the sarcolemmal membrane in intact muscle fibers. Although no significant differences between the EA and EAI, Gd3+ abolished the majority of cytoplasmic Ca2+ accumulation decrease during ECC in the EAI and a robust Ca2+ spark response disappeared compared with the EA. (2) In vitro, compared with the C, mitochondrial Ca2+ concentration did not elevations in MCC in the E. EA cytoplasmic Ca2+ increased rapidly above the C and E (P < 0.01), respectively, but EAI significantly attenuated the increases in  mitochondrial Ca2+ concentration compared with the EA (P < 0.01). (3). Compared with the C , maximum tetanic force was significantly lower in the E after ECC (P < 0.01). EA maximum tetanic force increased rapidly compared with the E after ECC (P < 0.05), but EAL abolished the majority maximum tetanic force increase after ECC (P < 0.05). Conclusions (1)Eccentric contraction caused cytoplasmic Ca2+ accumulation, but  mitochondrial Ca2+ concentration decrease. (2)Acupuncture can effectively reduce cytosolic Ca2+ overload, following by mitochondrial Ca2+ concentration increase , which in turn abnormally high cytoplasmic Ca2+ levels are buffed by the mitochondria, and improved muscle function, and the effect was associated to the TRP channels.  

scholarly journals In Vivo Fatigue Reduces In Vitro Performance In Human Skeletal Muscle Fibers

2021 ◽  
Vol 53 (8S) ◽  
pp. 110-111
Author(s):  
Austin W. Ricci ◽  
Scott J. Mongold ◽  
Grace E. Privett ◽  
Karen W. Needham ◽  
Damien M. Callahan
Keyword(s):  
Skeletal Muscle ◽  
Human Skeletal Muscle ◽  
Muscle Fibers ◽  
Skeletal Muscle Fibers ◽  
In Vitro Performance

Genetic variation at RAB3GAP2 and its role in exercise-related adaptation and recovery

2021 ◽  
Author(s):  
Kristoffer Ström ◽  
Nikolay Oskolkov ◽  
Tugce Karaderi ◽  
Sebastian Kalamajski ◽  
Ola Ekström ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
T Cell Activation ◽  
Cell Activation ◽  
Genome Wide Association Study ◽  
Fiber Type ◽  
Whole Body ◽  
Protein Subunit ◽  
A Genome

Abstract Skeletal muscle fiber composition and capillary density influence physical performance and whole-body metabolic properties. ~45% of the variance in fiber type is heritable, which motivated us to perform a genome-wide association study of skeletal muscle histology from 656 Swedish men. Four independent variants were associated (p < 5x10− 8) with proportion of type IIx fibers or capillary-to-fiber ratio (C:F). The strongest signal localized to the rs115660502 variant, where the G-allele corresponded with increased C:F and reduced skeletal muscle expression of the proximal gene, RAB3 GTPase Activating Non-Catalytic Protein Subunit 2 (RAB3GAP2). The G-allele was less frequent in elite short-track sprinters and more frequent in endurance athletes than in matched non-athlete (population) controls; RAB3GAP2 expression was reduced by high-intensity intermittent training. RAB3GAP2 protein was not uniformly expressed in muscle tissue but localized to the endothelium and capillaries. Experimental reduction of RAB3GAP2 in human endothelial cells led to increased tube formation in vitro, to regulation of secreted factors promoting angiogenesis and T-cell activation, to reduced intracellular levels of von Willebrand factor (VWF) and, post-implantation, to increased endothelial cell density in vivo in mice. The amount of RAB3GAP2 in skeletal muscle was positively associated with exercise-induced release of VWF in vivo in humans. By regulating the release of protein factors (VWF, CD70, TNC, TNXB, MCP1, IGFBP3, COL1A1, TFPI2 and tPA), RAB3GAP2 influences fitness adaptation after exercise by improving muscle healing and promotion of capillary formation.

scholarly journals Age and prior exercise in vivo determine the subsequent in vitro molecular profile of myoblasts and nonmyogenic cells derived from human skeletal muscle

2019 ◽  
Vol 316 (6) ◽  
pp. C898-C912 ◽  
Author(s):  
Cecilie J. L. Bechshøft ◽  
Simon M. Jensen ◽  
Peter Schjerling ◽  
Jesper L. Andersen ◽  
Rene B. Svensson ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Stem Cell ◽  
Human Skeletal Muscle ◽  
Cell Function ◽  
Myogenic Differentiation ◽  
Molecular Profile ◽  
Muscle Stem Cell ◽  
Myogenic Cells

The decline in skeletal muscle regenerative capacity with age is partly attributed to muscle stem cell (satellite cell) dysfunction. Recent evidence has pointed to a strong interaction between myoblasts and fibroblasts, but the influence of age on this interaction is unknown. Additionally, while the native tissue environment is known to determine the properties of myogenic cells in vitro, how the aging process alters this cell memory has not been established at the molecular level. We recruited 12 young and 12 elderly women, who performed a single bout of heavy resistance exercise with the knee extensor muscles of one leg. Five days later, muscle biopsies were collected from both legs, and myogenic cells and nonmyogenic cells were isolated for in vitro experiments with mixed or separated cells and analyzed by immunostaining and RT-PCR. A lower myogenic fusion index was detected in the cells from the old versus young women, in association with differences in gene expression levels of key myogenic regulatory factors and senescence, which were further altered by performing exercise before tissue sampling. Coculture with nonmyogenic cells from the elderly led to a higher myogenic differentiation index compared with nonmyogenic cells from the young. These findings show that the in vitro phenotype and molecular profile of human skeletal muscle myoblasts and fibroblasts is determined by the age and exercise state of the original in vivo environment and help explain how exercise can enhance muscle stem cell function in old age.

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