CONCENTRATION AND TURNOVER OF CYTOCHROMEcIN SKELETAL MUSCLES OF WARM- AND COLD-ACCLIMATED RATS

1966 ◽  
Vol 44 (6) ◽  
pp. 875-880 ◽  
Author(s):  
Florent Depocas
Keyword(s):  
Skeletal Muscle ◽  
Cytochrome C ◽  
Muscle Mass ◽  
Half Life ◽  
Skeletal Muscles ◽  
Gastrocnemius Muscle ◽  
Average Concentration ◽  
Abdominal Muscles ◽  
A Value ◽  
Total Muscle

Cytochrome c concentration in ventrolateral abdominal muscles of cold-acclimated rats was significantly higher than in corresponding muscles of warm-acclimated rats, but concentration of this protein in gastrocnemius muscle was similar in both groups of animals. Average concentration of cytochrome c in all skeletal muscles was higher in cold- than in warm-acclimated rats. Total amount of skeletal muscle cytochrome c per rat, calculated as the product of estimated total muscle mass and average concentration of cytochrome c, was similar in both groups. The fractional rates of turnover of skeletal muscle cytochrome c, labelled by administration of 1-14C-acetate to warm- and cold-acclimated rats, were, respectively −0.050 ± 0.003 and −0.047 ± 0.005 per day, corresponding to half-lives of 13.8 and 14.8 days. The rate of turnover of cytochrome c was 0.5 mg cytochrome c per rat per day at both acclimation temperatures. A value of 14 days for the half-life of sarcosomes is suggested.

Change in skeletal muscle index and its prognostic significance in conversion therapy for initially unresectable colorectal cancer.

2021 ◽  
Vol 39 (3_suppl) ◽  
pp. 56-56
Author(s):  
Hiroaki Nozawa ◽  
Shigenobu Emoto ◽  
Koji Murono ◽  
Yasutaka Shuno ◽  
Soichiro Ishihara
Keyword(s):  
Colorectal Cancer ◽  
Skeletal Muscle ◽  
Muscle Mass ◽  
Skeletal Muscles ◽  
Systemic Chemotherapy ◽  
Stage Iv ◽  
The Body ◽  
Pharmacological Intervention ◽  
Conversion Therapy ◽  
Skeletal Muscle Index

56 Background: Systemic chemotherapy can cause loss of skeletal muscle mass in colorectal cancer (CRC) patients in the neoadjuvant and palliative settings. However, it is largely unknown how the body composition is changed by chemotherapy rendering unresectable CRC to resectable disease or how it affects the prognosis. This study aimed at elucidating the effects of systemic chemotherapy on skeletal muscles and survival in stage IV CRC patients who underwent conversion therapy. Methods: We reviewed 98 stage IV CRC patients who received systemic chemotherapy in our hospital. According to the treatment setting, patients were divided into the ‘Conversion’, ‘Neoadjuvant chemotherapy (NAC)’, and ‘Palliation’ groups. The cross-sectional area of skeletal muscles at the third lumbar level and changes in the skeletal muscle index (SMI), defined as the area divided by height squared, during chemotherapy were compared among patient groups. The effects of these parameters on prognosis were analyzed in the Conversion group. Results: The mean SMI increased by 8.0% during chemotherapy in the Conversion group (n = 38), whereas it decreased by 6.2% in the NAC group (n = 18) and 3.7% in the Palliation group (n = 42, p < 0.0001). Moreover, patients with increased SMI during chemotherapy had a better overall survival (OS) than those whose SMI decreased in the Conversion group (p = 0.021). The increase in SMI was an independent predictor of favorable OS on multivariate analysis (hazard ratio: 0.26). Conclusions: Stage IV CRC patients who underwent conversion to resection often had an increased SMI. As such an increase in SMI further conveys a survival benefit in conversion therapy, it may be important to make efforts to preserve muscle mass by meticulous approaches, such as nutritional support, muscle exercise programs, and pharmacological intervention even during chemotherapy in patients with metastatic CRC.

Structural and functional remodeling of skeletal muscle microvasculature is induced by simulated microgravity

2000 ◽  
Vol 278 (6) ◽  
pp. H1866-H1873 ◽  
Author(s):  
Michael D. Delp ◽  
Patrick N. Colleran ◽  
M. Keith Wilkerson ◽  
Matthew R. McCurdy ◽  
Judy Muller-Delp
Keyword(s):  
Skeletal Muscle ◽  
Soleus Muscle ◽  
Skeletal Muscles ◽  
Gastrocnemius Muscle ◽  
Fluid Pressure ◽  
Hindlimb Unloading ◽  
Cross Sectional ◽  
Luminal Diameter ◽  
Structural Remodeling

Hindlimb unloading of rats results in a diminished ability of skeletal muscle arterioles to constrict in vitro and elevate vascular resistance in vivo. The purpose of the present study was to determine whether alterations in the mechanical environment (i.e., reduced fluid pressure and blood flow) of the vasculature in hindlimb skeletal muscles from 2-wk hindlimb-unloaded (HU) rats induces a structural remodeling of arterial microvessels that may account for these observations. Transverse cross sections were used to determine media cross-sectional area (CSA), wall thickness, outer perimeter, number of media nuclei, and vessel luminal diameter of feed arteries and first-order (1A) arterioles from soleus and the superficial portion of gastrocnemius muscles. Endothelium-dependent dilation (ACh) was also determined. Media CSA of resistance arteries was diminished by hindlimb unloading as a result of decreased media thickness (gastrocnemius muscle) or reduced vessel diameter (soleus muscle). ACh-induced dilation was diminished by 2 wk of hindlimb unloading in soleus 1A arterioles, but not in gastrocnemius 1A arterioles. These results indicate that structural remodeling and functional adaptations of the arterial microvasculature occur in skeletal muscles of the HU rat; the data suggest that these alterations may be induced by reductions in transmural pressure (gastrocnemius muscle) and wall shear stress (soleus muscle).

scholarly journals Two Weeks of Smoking Cessation Reverse Cigarette Smoke-Induced Skeletal Muscle Atrophy and Mitochondrial Dysfunction in Mice

2020 ◽  
Author(s):  
Tom Tanjeko Ajime ◽  
Jef Serré ◽  
Rob C I Wüst ◽  
Guy Anselme Mpaka Messa ◽  
Chiel Poffé ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Smoking Cessation ◽  
Mitochondrial Dysfunction ◽  
Muscle Mass ◽  
Muscle Atrophy ◽  
Skeletal Muscles ◽  
Skeletal Muscle Atrophy ◽  
Limb Muscle ◽  
Male Mice ◽  
And Function

Abstract Introduction Apart from its adverse effects on the respiratory system, cigarette smoking also induces skeletal muscle atrophy and dysfunction. Whether short-term smoking cessation can restore muscle mass and function is unknown. We, therefore, studied the impact of 1- and 2-week smoking cessation on skeletal muscles in a mouse model. Methods Male mice were divided into four groups: Air-exposed (14 weeks); cigarette smoke (CS)-exposed (14 weeks); CS-exposed (13 weeks) followed by 1-week cessation; CS-exposed (12 weeks) followed by 2 weeks cessation to examine exercise capacity, physical activity levels, body composition, muscle function, capillarization, mitochondrial function and protein expression in the soleus, plantaris, and diaphragm muscles. Results CS-induced loss of body and muscle mass was significantly improved within 1 week of cessation due to increased lean and fat mass. Mitochondrial respiration and protein levels of the respiratory complexes in the soleus were lower in CS-exposed mice, but similar to control values after 2 weeks of cessation. Exposing isolated soleus muscles to CS extracts reduced mitochondrial respiration that was reversed after removing the extract. While physical activity was reduced in all groups, exercise capacity, limb muscle force, fatigue resistance, fiber size and capillarization, and diaphragm cytoplasmic HIF-1α were unaltered by CS-exposure. However, CS-induced diaphragm atrophy and increased capillary density were not seen after 2 weeks of smoking cessation. Conclusion In male mice, 2 weeks of smoking cessation reversed smoking-induced mitochondrial dysfunction, limb muscle mass loss, and diaphragm muscle atrophy, highlighting immediate benefits of cessation on skeletal muscles. Implications Our study demonstrates that CS-induced skeletal muscle mitochondrial dysfunction and atrophy are significantly improved by 2 weeks of cessation in male mice. We show for the first time that smoking cessation as short as 1 to 2 weeks is associated with immediate beneficial effects on skeletal muscle structure and function with the diaphragm being particularly sensitive to CS-exposure and cessation. This could help motivate smokers to quit smoking as early as possible. The knowledge that smoking cessation has potential positive extrapulmonary effects is particularly relevant for patients referred to rehabilitation programs and those admitted to hospitals suffering from acute or chronic muscle deterioration yet struggling with smoking cessation.

scholarly journals Differential distribution of ryanodine receptor type 3 (RyR3) gene product in mammalian skeletal muscles

1996 ◽  
Vol 316 (1) ◽  
pp. 19-23 ◽  
Author(s):  
Antonio CONTI ◽  
L. GORZA ◽  
Vincenzo SORRENTINO
Keyword(s):  
Skeletal Muscle ◽  
Muscle Contraction ◽  
Gene Product ◽  
Skeletal Muscles ◽  
Mammalian Species ◽  
Diaphragm Muscle ◽  
Muscle Fibres ◽  
Abdominal Muscles ◽  
Mammalian Skeletal Muscle ◽  
Specific Subset

Activation of intracellular Ca2+-release channels/ryanodine receptors (RyRs) is a fundamental step in the regulation of muscle contraction. In mammalian skeletal muscle, Ca2+-release channels containing the type 1 isoform of RyR (RyR1) open to release Ca2+ from the sarcoplasmic reticulum (SR) upon stimulation by the voltage-activated dihydropyridine receptor on the T-tubule/plasma membrane. In addition to RyR1, low levels of the mRNA of the RyR3 isoform have been recently detected in mammalian skeletal muscles. Here we report data on the distribution of the RyR3 gene product in mammalian skeletal muscles. Western-blot analysis of SR of individual muscles indicated that, at variance with the even distribution of the RyR1 isoform, the RyR3 content varies among different muscles, with relatively higher amounts being detected in diaphragm and soleus, and lower levels in abdominal muscles and tibialis anterior. In these muscles RyR3 was localized in the terminal cisternae of the SR. No detectable levels of RyR3 were observed in the extensor digitorum longus. Preferential high content of RyR3 in the diaphragm muscle was observed in several mammalian species. In situ hybridization analysis demonstrated that RyR3 transcripts are not restricted to a specific subset of skeletal-muscle fibres. Differential utilization of the RyR3 isoform in skeletal muscle may be relevant to the modulation of Ca2+ release with respect to specific muscle-contraction properties.

scholarly journals Passive repetitive stretching increases skeletal muscle mass and myofiber cross-sectional area in senescence-accelerated model mouse

2021 ◽  
Author(s):  
Yumin Wang ◽  
Satoshi Ikeda ◽  
Katsunori Ikoma
Keyword(s):  
Skeletal Muscle ◽  
Mrna Expression ◽  
Signaling Pathways ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Gastrocnemius Muscle ◽  
Cross Sectional Area ◽  
Sectional Area ◽  
Cross Sectional ◽  
Passive Stretching

Abstract Mechanical stimulation has benefits for muscle mass and function. Passive stretching is widely performed in clinical rehabilitation medicine. However, the hypertrophic effects of passive repetitive stretching on senescent skeletal muscles against muscle atrophy remain unknown. We used senescence-accelerated model SAM-P8 mice. The gastrocnemius muscle was passively repetitive stretched by manual ankle dorsiflexion for 15 min, 5 days a week for 2 weeks under deep anesthesia. We examined the effects of passive stretching on muscle mass, myofiber cross-sectional area, muscle fiber type and composition, satellite cell content, mRNA expression of the signaling pathways involved in muscle protein synthesis, muscle-specific ubiquitin ligases, and myogenic regulatory factors. The gastrocnemius muscle weight of the stretched side increased compared with that of the unstretched side. In addition to the increase in muscle mass, muscle fiber cross-sectional area of the stretched side was greater than that of the unstretched side. Passive repetitive stretching significantly increased the mRNA expression level of Akt, p70S6K, 4E-BP1, Myf5, myogenin, MuRF1. Passive repetitive stretching promoted skeletal muscle mass and myofiber cross-sectional area in SAM-P8 mice. These hypertrophic observations are attributable to the stretch-activated signaling pathways involved in protein turnover. These findings are applicable to clinical muscle strengthening and sarcopenia prevention.

scholarly journals REDD1 deletion prevents dexamethasone-induced skeletal muscle atrophy

2014 ◽  
Vol 307 (11) ◽  
pp. E983-E993 ◽  
Author(s):  
Florian A. Britto ◽  
Gwenaelle Begue ◽  
Bernadette Rossano ◽  
Aurélie Docquier ◽  
Barbara Vernus ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Synthesis ◽  
Muscle Mass ◽  
Tibialis Anterior ◽  
Skeletal Muscle Mass ◽  
Gastrocnemius Muscle ◽  
Mtorc1 Signaling ◽  
Inhibition Of Protein Synthesis ◽  
Stress Dependent

REDD1 (regulated in development and DNA damage response 1) has been proposed to inhibit the mechanistic target of rapamycin complex 1 (mTORC1) during in vitro hypoxia. REDD1 expression is low under basal conditions but is highly increased in response to several catabolic stresses, like hypoxia and glucocorticoids. However, REDD1 function seems to be tissue and stress dependent, and its role in skeletal muscle in vivo has been poorly characterized. Here, we investigated the effect of REDD1 deletion on skeletal muscle mass, protein synthesis, proteolysis, and mTORC1 signaling pathway under basal conditions and after glucocorticoid administration. Whereas skeletal muscle mass and typology were unchanged between wild-type (WT) and REDD1-null mice, oral gavage with dexamethasone (DEX) for 7 days reduced tibialis anterior and gastrocnemius muscle weights as well as tibialis anterior fiber size only in WT. Similarly, REDD1 deletion prevented the inhibition of protein synthesis and mTORC1 activity (assessed by S6, 4E-BP1, and ULK1 phosphorylation) observed in gastrocnemius muscle of WT mice following single DEX administration for 5 h. However, our results suggest that REDD1-mediated inhibition of mTORC1 in skeletal muscle is not related to the modulation of the binding between TSC2 and 14-3-3. In contrast, our data highlight a new mechanism involved in mTORC1 inhibition linking REDD1, Akt, and PRAS40. Altogether, these results demonstrated in vivo that REDD1 is required for glucocorticoid-induced inhibition of protein synthesis via mTORC1 downregulation. Inhibition of REDD1 may thus be a strategy to limit muscle loss in glucocorticoid-mediated atrophy.

CHANGES IN THE RELATIVE AMOUNTS OF ASCORBIC ACID AND GLYCOGEN IN DENERVATED RAT GASTROCNEMIUS MUSCLE

1965 ◽  
Vol 43 (6) ◽  
pp. 705-710 ◽  
Author(s):  
G. L. A. Graff ◽  
A. J. Hudson ◽  
K. P. Strickland
Keyword(s):  
Ascorbic Acid ◽  
Muscle Mass ◽  
Gastrocnemius Muscle ◽  
Glycogen Content ◽  
Ascorbic Acid Content ◽  
Relative Increase ◽  
Unit Weight ◽  
Contributory Factor ◽  
Denervated Muscle ◽  
A Value

In this investigation both ascorbic acid and glycogen were determined in rat gastrocnemius muscle after denervation for times ranging from 12 hours to 60 days. To assess more correctly the changes due to denervation, concentrations per unit weight and content per whole muscle were expressed as a percentage of the corresponding value obtained from the contralateral control. The concentrations of ascorbic acid and glycogen in the normal rat gastrocnemius were, respectively, 2.7 ± 0.1 μg (S.E.M. for 51 animals) and 355 (as a glucose equivalent) ± 15 μg (S.E.M. for 52 animals) per 100 mg wet weight. The concentration of ascorbic acid per unit weight showed significant increase (+ 27%) 36 hours after neurotomy and reached five times the control value 60 days after the denervation. The ascorbic acid content of the whole denervated muscle gradually accumulated to a value of 195% of control at 5 days and then declined to a value of 78% at 15 days and 65% at 60 days. In the later stages of atrophy the losses in ascorbic acid were always less than the losses in muscle mass. The glycogen concentration per unit weight remained essentially unchanged for the first 36–48 hours after neurotomy; it then dropped abruptly to 39% of the original value on the 3rd day and stayed at about this level until the 60th day after denervation. In the first 12 hours there appeared to be a slight rise in the glycogen content of the whole denervated muscle. Subsequently, there was a rapid loss of glycogen from 116% of normal at 24 hours to 35% at 3 days; during the same period of time the loss in muscle mass was only 16%. The loss in glycogen content after 60 days represented 94% of the original amount.The observed initial accumulation of ascorbic acid after denervation may reflect a relative increase in active transport (or in situ synthesis) over breakdown mechanisms. The results reported rule out the possibility that a local deficiency in ascorbic acid per unit weight of muscle is a contributory factor to denervation atrophy and show that there is a continuous local accumulation of ascorbic acid.

scholarly journals Muscle oxidative capacity during IL-6-dependent cancer cachexia

2011 ◽  
Vol 300 (2) ◽  
pp. R201-R211 ◽  
Author(s):  
James P. White ◽  
Kristen A. Baltgalvis ◽  
Melissa J. Puppa ◽  
Shuichi Sato ◽  
John W. Baynes ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cytochrome C ◽  
Muscle Mass ◽  
Gastrocnemius Muscle ◽  
Cancer Cachexia ◽  
Muscle Wasting ◽  
Muscle Protein ◽  
Oxidative Capacity ◽  
Muscle Oxidative Capacity ◽  
Markers Of Oxidative Stress

Many diseases are associated with catabolic conditions that induce skeletal muscle wasting. These various catabolic states may have similar and distinct mechanisms for inducing muscle protein loss. Mechanisms related to muscle wasting may also be related to muscle metabolism since glycolytic muscle fibers have greater wasting susceptibility with several diseases. The purpose of this study was to determine the relationship between muscle oxidative capacity and muscle mass loss in red and white hindlimb muscles during cancer cachexia development in the Apc Min/+ mouse. Gastrocnemius and soleus muscles were excised from Apc Min/+ mice at 20 wk of age. The gastrocnemius muscle was partitioned into red and white portions. Body mass (−20%), gastrocnemius muscle mass (−41%), soleus muscle mass (−34%), and epididymal fat pad (−100%) were significantly reduced in severely cachectic mice ( n = 8) compared with mildly cachectic mice ( n = 6). Circulating IL-6 was fivefold higher in severely cachectic mice. Cachexia significantly reduced the mitochondrial DNA-to-nuclear DNA ratio in both red and white portions of the gastrocnemius. Cytochrome c and cytochrome- c oxidase complex subunit IV (Cox IV) protein were reduced in all three muscles with severe cachexia. Changes in muscle oxidative capacity were not associated with altered myosin heavy chain expression. PGC-1α expression was suppressed by cachexia in the red and white gastrocnemius and soleus muscles. Cachexia reduced Mfn1 and Mfn2 mRNA expression and markers of oxidative stress, while Fis1 mRNA was increased by cachexia in all muscle types. Muscle oxidative capacity, mitochondria dynamics, and markers of oxidative stress are reduced in both oxidative and glycolytic muscle with severe wasting that is associated with increased circulating IL-6 levels.

scholarly journals Glucose disposal by skeletal muscle in response to re-feeding after progressive starvation

1991 ◽  
Vol 277 (2) ◽  
pp. 429-433 ◽  
Author(s):  
M J Holness ◽  
M C Sugden
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Glucose Intolerance ◽  
Skeletal Muscles ◽  
Glucose Utilization ◽  
Strong Relationship ◽  
Glucose Disposal ◽  
Prolonged Starvation ◽  
Glucose Clearance ◽  
Glycogen Deposition

We investigated the extent to which increases in glucose utilization indices (GUIs) in individual skeletal muscles during chow re-feeding after 6 h, 24 h or 48 h starvation are related to the antecedent duration of starvation. Chow re-feeding after either acute or prolonged starvation led to an increase in glucose disposal by the muscle mass. Glucose intolerance after prolonged starvation was not associated with lower values of GUI in skeletal muscle. In both working and non-working muscles, the increment in GUI during the first 2 h of re-feeding was less after acute than after prolonged starvation. In non-working muscles the differential responses to re-feeding were due to higher GUI values after re-feeding rather than lower pre-prandial GUI values. Therefore the contribution of non-working muscles to glucose clearance is higher as the antecedent period of starvation is extended. Rates of glycogen deposition in non-working muscles after refeeding were similar to absolute values of GUI, and a strong relationship existed between measured GUI values and rates of glycogen deposition.

Role of autophagy in COPD skeletal muscle dysfunction

2013 ◽  
Vol 114 (9) ◽  
pp. 1273-1281 ◽  
Author(s):  
Sabah N. A. Hussain ◽  
Marco Sandri
Keyword(s):  
Skeletal Muscle ◽  
Protein Degradation ◽  
Muscle Mass ◽  
Skeletal Muscles ◽  
Airflow Limitation ◽  
Muscle Dysfunction ◽  
Skeletal Muscle Dysfunction ◽  
Copd Patients ◽  
Lung Dysfunction

Chronic obstructive pulmonary disease (COPD) is a debilitating disease caused by parenchymal damage and irreversible airflow limitation. In addition to lung dysfunction, patients with COPD develop weight loss, malnutrition, poor exercise performance, and skeletal muscle atrophy. The latter has been attributed to an imbalance between muscle protein synthesis and protein degradation. Several reports have confirmed that enhanced protein degradation and atrophy of limb muscles of COPD patient is mediated in part through activation of the ubiquitin-proteasome pathway and that this activation is triggered by enhanced production of reactive oxygen species. Until recently, the importance of the autophagy-lysosome pathway in protein degradation of skeletal muscles has been largely ignored, however, recent evidence suggests that this pathway is actively involved in recycling of cytosolic proteins, organelles, and protein aggregates in normal skeletal muscles. The protective role of autophagy in the regulation of muscle mass has recently been uncovered in mice with muscle-specific suppression of autophagy. These mice develop severe muscle weakness, atrophy, and decreased muscle contractility. No information is yet available about the involvement of the autophagy in the regulation of skeletal muscle mass in COPD patients. Pilot experiments on vastus lateralis muscle samples suggest that the autophagy-lysosome system is induced in COPD patients compared with control subjects. In this review, we summarize recent progress related to molecular structure, regulation, and roles of the autophagy-lysosome pathway in normal and diseased skeletal muscles. We also speculate about regulation and functional importance of this system in skeletal muscle dysfunction in COPD patients.

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