Treadmill running and static stretching improve long-lasting hyperalgesia, joint limitation, and muscle atrophy induced by cast immobilization in rats

2013 ◽  
Vol 534 ◽  
pp. 295-300 ◽  
Author(s):  
Atsuko Morimoto ◽  
Handriadi Winaga ◽  
Hiroki Sakurai ◽  
Mika Ohmichi ◽  
Takahiko Yoshimoto ◽  
...  
Keyword(s):  
Muscle Atrophy ◽  
Treadmill Running ◽  
Static Stretching ◽  
Cast Immobilization ◽  
Joint Limitation

scholarly journals Effect of short-term hindlimb immobilization on skeletal muscle atrophy and the transcriptome in a low compared with high responder to endurance training model

PLoS ONE ◽  
2022 ◽  
Vol 17 (1) ◽  
pp. e0261723
Author(s):  
Jamie-Lee M. Thompson ◽  
Daniel W. D. West ◽  
Thomas M. Doering ◽  
Boris P. Budiono ◽  
Sarah J. Lessard ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Endurance Training ◽  
Muscle Atrophy ◽  
Female Rats ◽  
Skeletal Muscle Atrophy ◽  
Biological Processes ◽  
Short Term ◽  
Cast Immobilization ◽  
Protein Ubiquitination ◽  
Differential Gene

Skeletal muscle atrophy is a physiological response to disuse, aging, and disease. We compared changes in muscle mass and the transcriptome profile after short-term immobilization in a divergent model of high and low responders to endurance training to identify biological processes associated with the early atrophy response. Female rats selectively bred for high response to endurance training (HRT) and low response to endurance training (LRT; n = 6/group; generation 19) underwent 3 day hindlimb cast immobilization to compare atrophy of plantaris and soleus muscles with line-matched controls (n = 6/group). RNA sequencing was utilized to identify Gene Ontology Biological Processes with differential gene set enrichment. Aerobic training performed prior to the intervention showed HRT improved running distance (+60.6 ± 29.6%), while LRT were unchanged (-0.3 ± 13.3%). Soleus atrophy was greater in LRT vs. HRT (-9.0 ±8.8 vs. 6.2 ±8.2%; P<0.05) and there was a similar trend in plantaris (-16.4 ±5.6% vs. -8.5 ±7.4%; P = 0.064). A total of 140 and 118 biological processes were differentially enriched in plantaris and soleus muscles, respectively. Soleus muscle exhibited divergent LRT and HRT responses in processes including autophagy and immune response. In plantaris, processes associated with protein ubiquitination, as well as the atrogenes (Trim63 and Fbxo32), were more positively enriched in LRT. Overall, LRT demonstrate exacerbated atrophy compared to HRT, associated with differential gene enrichments of biological processes. This indicates that genetic factors that result in divergent adaptations to endurance exercise, may also regulate biological processes associated with short-term muscle unloading.

Exercise interrupts ongoing glucocorticoid-induced muscle atrophy and glutamine synthetase induction

1992 ◽  
Vol 263 (6) ◽  
pp. E1157-E1163 ◽  
Author(s):  
M. T. Falduto ◽  
A. P. Young ◽  
R. C. Hickson
Keyword(s):  
Enzyme Activity ◽  
Glutamine Synthetase ◽  
Muscle Atrophy ◽  
Contractile Activity ◽  
Hormone Treatment ◽  
Quadriceps Muscle ◽  
Treadmill Running ◽  
Female Rats ◽  
Glucocorticoid Treatment ◽  
Fast Twitch

This study was undertaken to determine whether regular endurance exercise is a deterrent to a developing state of muscle atrophy from glucocorticoids and to evaluate whether the contractile activity antagonizes the hormonal actions on glutamine synthetase, alanine aminotransferase, and cytosolic aspartate aminotransferase (cAspAT). Adult female rats were administered cortisol acetate (CA, 100 mg/kg body wt) or an equal volume of the vehicle solution for up to 15 days. Exercise (treadmill running at 31 m/min, 10% grade, 90 min/day) was introduced after 4 days of CA treatment, at which time plantaris and quadriceps muscle mass had been reduced to 90% of control levels. Running for 11 consecutive days prevented 40 mg of the 90-mg loss and 227 mg of the 808-mg loss that were subsequently observed in plantaris and quadriceps muscles, respectively, in the sedentary animals. Glutamine synthetase mRNA and enzyme activity were elevated threefold by glucocorticoid treatment in the deep quadriceps (fast-twitch red) muscles after 4 days. Initiating exercise completely interfered with the further hormonal induction (to approximately 5-fold) of this enzyme and, after 11 consecutive days of the exercise regimen, glutamine synthetase mRNA and enzyme activity were 58 and 68% of values from CA-treated sedentary animals. In vehicle-treated groups, basal levels of glutamine synthetase expression were also diminished by exercise to approximately 40% of the values in sedentary controls. Hormone treatment did not alter either aminotransferase enzyme activity but reduced cAspAT mRNA in fast-twitch red muscles by 50%. Exercise abolished the glucocorticoid effect on cAspAT mRNA.(ABSTRACT TRUNCATED AT 250 WORDS)

THE EFFECTS OF CREATINE ON CAST IMMOBILIZATION INDUCED MUSCLE ATROPHY AND DETRAINING

2003 ◽  
Vol 35 (Supplement 1) ◽  
pp. S401
Author(s):  
A W. Johnston ◽  
D G. Burke ◽  
L G. MacNeil
Keyword(s):  
Muscle Atrophy ◽  
Cast Immobilization

A model of muscle atrophy using cast immobilization in mice

2005 ◽  
Vol 32 (5) ◽  
pp. 672-674 ◽  
Author(s):  
Tiffany N. Frimel ◽  
Fatema Kapadia ◽  
Gabriel S. Gaidosh ◽  
Ye Li ◽  
Glenn A. Walter ◽  
...  
Keyword(s):  
Muscle Atrophy ◽  
Cast Immobilization

scholarly journals TLR4-defective (C3H/HeJ) mice are not protected from cast immobilization-induced muscle atrophy

2017 ◽  
Vol 5 (8) ◽  
pp. e13255 ◽  
Author(s):  
Noriaki Kawanishi ◽  
Risa Nozaki ◽  
Hisashi Naito ◽  
Shuichi Machida
Keyword(s):  
Muscle Atrophy ◽  
Cast Immobilization

Partial prevention of glucocorticoid-induced muscle atrophy by endurance training

1981 ◽  
Vol 241 (3) ◽  
pp. E226-E232 ◽  
Author(s):  
R. C. Hickson ◽  
J. R. Davis
Keyword(s):  
Muscle Atrophy ◽  
Protein Concentration ◽  
Gastrocnemius Muscle ◽  
Citrate Synthase ◽  
Treadmill Running ◽  
Male Rats ◽  
Total Protein Concentration ◽  
Muscle Weight ◽  
Subcutaneous Injections ◽  
Fast Twitch

Male rats were either sham-operated (N) or castrated (C) at 65 days of age. They were further subdivided into sedentary or exercise groups that were trained by treadmill running 5 days/wk for 12 wk. During the last 10 days of training, the animals received daily subcutaneous injections of cortisone acetate (CA) (100 mg/kg) or 1% carboxymethylcellulose. Body weight decreased approximately 25% in all groups that received CA. The fast-twitch plantaris and gastrocnemius muscle weights were approximately 35% lower in CA-treated versus cortisone-free N and C sedentary animals. Exercise prevented from one-fourth to one-half of the muscle weight loss in N and C runners when compared to their respective pair weight controls. Muscle weights of the CA-treated freely eating N controls were significantly less than that of N runners that received CA. In plantaris muscles of both N and C animals that received CA, total protein concentration and citrate synthase activity, a mitochondrial marker, remained constant, but their amounts per muscle decreased in proportion to the atrophy. However, myoglobin concentration increased in plantaris muscles of CA-treated animals, although total myoglobin per muscle was reduced slightly. Myoglobin levels were increased in plantaris muscles both as a result of training and CA, but citrate synthase activity was increased only as a result of the exercise. These results show that exercise can retard the glucocorticoid-induced muscle atrophy.

scholarly journals Essential Amino Acid-Enriched Diet Alleviates Dexamethasone-Induced Loss of Muscle Mass and Function through Stimulation of Myofibrillar Protein Synthesis and Improves Glucose Metabolism in Mice

Metabolites ◽  
2022 ◽  
Vol 12 (1) ◽  
pp. 84
Author(s):  
Yeongmin Kim ◽  
Sanghee Park ◽  
Jinseok Lee ◽  
Jiwoong Jang ◽  
Jiyeon Jung ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Glucose Metabolism ◽  
Muscle Mass ◽  
Muscle Atrophy ◽  
Myofibrillar Protein ◽  
Treadmill Running ◽  
Synthesis Rate ◽  
Protein Synthesis Rate ◽  
Myofibrillar Protein Synthesis ◽  
Stimulation Of

Dexamethasone (DEX) induces dysregulation of protein turnover, leading to muscle atrophy and impairment of glucose metabolism. Positive protein balance, i.e., rate of protein synthesis exceeding rate of protein degradation, can be induced by dietary essential amino acids (EAAs). In this study, we investigated the roles of an EAA-enriched diet in the regulation of muscle proteostasis and its impact on glucose metabolism in the DEX-induced muscle atrophy model. Mice were fed normal chow or EAA-enriched chow and were given daily injections of DEX over 10 days. We determined muscle mass and functions using treadmill running and ladder climbing exercises, protein kinetics using the D2O labeling method, molecular signaling using immunoblot analysis, and glucose metabolism using a U-13C6 glucose tracer during oral glucose tolerance test (OGTT). The EAA-enriched diet increased muscle mass, strength, and myofibrillar protein synthesis rate, concurrent with improved glucose metabolism (i.e., reduced plasma insulin concentrations and increased insulin sensitivity) during the OGTT. The U-13C6 glucose tracing revealed that the EAA-enriched diet increased glucose uptake and subsequent glycolytic flux. In sum, our results demonstrate a vital role for the EAA-enriched diet in alleviating the DEX-induced muscle atrophy through stimulation of myofibrillar proteins synthesis, which was associated with improved glucose metabolism.

Exercise interrupts ongoing glucocorticoid-induced muscle atrophy and glutamine synthetase induction

2006 ◽  
Vol 263 (6) ◽  
pp. E1157-E1163
Author(s):  
M. T. Falduto ◽  
A. P. Young ◽  
R. C. Hickson
Keyword(s):  
Enzyme Activity ◽  
Glutamine Synthetase ◽  
Muscle Atrophy ◽  
Contractile Activity ◽  
Hormone Treatment ◽  
Quadriceps Muscle ◽  
Treadmill Running ◽  
Female Rats ◽  
Glucocorticoid Treatment ◽  
Fast Twitch

This study was undertaken to determine whether regular endurance exercise is a deterrent to a developing state of muscle atrophy from glucocorticoids and to evaluate whether the contractile activity antagonizes the hormonal actions on glutamine synthetase, alanine aminotransferase, and cytosolic aspartate aminotransferase (cAspAT). Adult female rats were administered cortisol acetate (CA, 100 mg/kg body wt) or an equal volume of the vehicle solution for up to 15 days. Exercise (treadmill running at 31 m/min, 10% grade, 90 min/day) was introduced after 4 days of CA treatment, at which time plantaris and quadriceps muscle mass had been reduced to 90% of control levels. Running for 11 consecutive days prevented 40 mg of the 90-mg loss and 227 mg of the 808-mg loss that were subsequently observed in plantaris and quadriceps muscles, respectively, in the sedentary animals. Glutamine synthetase mRNA and enzyme activity were elevated threefold by glucocorticoid treatment in the deep quadriceps (fast-twitch red) muscles after 4 days. Initiating exercise completely interfered with the further hormonal induction (to approximately 5-fold) of this enzyme and, after 11 consecutive days of the exercise regimen, glutamine synthetase mRNA and enzyme activity were 58 and 68% of values from CA-treated sedentary animals. In vehicle-treated groups, basal levels of glutamine synthetase expression were also diminished by exercise to approximately 40% of the values in sedentary controls. Hormone treatment did not alter either aminotransferase enzyme activity but reduced cAspAT mRNA in fast-twitch red muscles by 50%. Exercise abolished the glucocorticoid effect on cAspAT mRNA.(ABSTRACT TRUNCATED AT 250 WORDS)

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