scholarly journals Resistance exercise training influences skeletal muscle immune activation: a microarray analysis

2012 ◽  
Vol 112 (3) ◽  
pp. 443-453 ◽  
Author(s):  
Paul M. Gordon ◽  
Dongmei Liu ◽  
Maureen A. Sartor ◽  
Heidi B. IglayReger ◽  
Emidio E. Pistilli ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Resistance Exercise ◽  
Immune Activation ◽  
Biceps Brachii ◽  
Training Session ◽  
Protective Role ◽  
Acute Bout ◽  
Expression Of Genes ◽  
Molecular Events

The primary aim of this investigation was to evaluate the effect of training on the immune activation in skeletal muscle in response to an acute bout of resistance exercise (RE). Seven young healthy men and women underwent a 12-wk supervised progressive unilateral arm RE training program. One week after the last training session, subjects performed an acute bout of bilateral RE in which the trained and the untrained arm exercised at the same relative intensity. Muscle biopsies were obtained 4 h postexercise from the biceps brachii of both arms and assessed for global transcriptom using Affymetrix U133 plus 2.0 microarrays. Significantly regulated biological processes and gene groups were analyzed using a logistic regression-based method following differential (trained vs. untrained) gene expression testing via an intensity-based Bayesian moderated t-test. The results from the present study suggest that training blunts the transcriptional upregulation of immune activation by minimizing expression of genes involved in monocyte recruitment and enhancing gene expression involved in macrophage anti-inflammatory polarization. Additionally, our data suggest that training blunts the transcriptional upregulation of the stress response and the downregulation of glucose metabolism, mitochondrial structure, and oxidative phosphorylation, and it enhances the transcriptional upregulation of the extracellular matrix and cytoskeleton development and organization and the downregulation of gene transcription and muscle contraction. This study provides novel insight into the molecular processes involved in the adaptive response of skeletal muscle following RE training and the cellular and molecular events implicating the protective role of training on muscle stress and damage inflicted by acute mechanical loading.

scholarly journals Acute bout of resistance exercise increases vitamin D receptor protein expression in rat skeletal muscle

2015 ◽  
Vol 100 (10) ◽  
pp. 1168-1176 ◽  
Author(s):  
Yuhei Makanae ◽  
Riki Ogasawara ◽  
Koji Sato ◽  
Yusuke Takamura ◽  
Kenji Matsutani ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Vitamin D ◽  
Protein Expression ◽  
Resistance Exercise ◽  
Vitamin D Receptor ◽  
Receptor Protein ◽  
Rat Skeletal Muscle ◽  
Acute Bout

scholarly journals Losartan has no additive effect on the response to heavy-resistance exercise in human elderly skeletal muscle

2018 ◽  
Vol 125 (5) ◽  
pp. 1536-1554 ◽  
Author(s):  
Mette Flindt Heisterberg ◽  
Jesper L. Andersen ◽  
Peter Schjerling ◽  
Alberte Lund ◽  
Simone Dalskov ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Angiotensin Ii ◽  
Resistance Training ◽  
Resistance Exercise ◽  
Satellite Cells ◽  
Type I ◽  
Elderly Men ◽  
Fiber Area ◽  
Heavy Resistance Exercise

Our purpose here was to investigate the potential of blocking the angiotensin II type I receptor (AT1R) on the hypertrophy response of elderly human skeletal muscle to 4 mo of heavy-resistance exercise training. Fifty-eight healthy elderly men (+65 yr) were randomized into three groups, consuming either AT1R blocker (losartan, 100 mg/day) or placebo for 4 mo. Two groups performed resistance training (RT) and were treated with either losartan or placebo, and one group did not train but was treated with losartan. Quadriceps muscle biopsies, MR scans, and strength tests were performed at baseline and after 8 and 16 wk. Biopsies were sectioned for immunohistochemistry to determine the number of satellite cells, capillaries, fiber type distribution, and fiber area. Gene expression levels of myostatin, connective tissue, and myogenic signaling pathways were determined by real-time RT-PCR. Four months of heavy-resistance training led in both training groups to expected improvements in quadriceps (∼3–4%) and vastus lateralis (∼5–6%), cross-sectional area, and type II fiber area (∼10–18%), as well as dynamic (∼13%) and isometric (∼19%) quadriceps peak force, but with absolutely no effect of losartan on these outcomes. Furthermore, no changes were seen in satellite cell number with training, and most gene targets failed to show any changes induced by training or losartan treatment. We conclude that there does not appear to be any effect of AT1R blocking in elderly men during 4 mo of resistance training. Therefore, we do not find any support for using AT1R blockers for promoting muscle adaptation to training in humans. NEW & NOTEWORTHY Animal studies have suggested that blocking angiotensin II type I receptor (AT1R) enhances muscle regeneration and prevents disuse atrophy, but studies in humans are limited. Focusing on hypertrophy, satellite cells, and gene expression, we found that AT1R blocking did not result in any greater responses with 4 mo of resistance training. These results do not support previous findings and question the value of blocking AT1R in the context of preserving aging human muscle.

scholarly journals PO-306 The effect of four weeks hypoxic resistance training on myostatin and follistatin expression in skeletal muscle of rats

2018 ◽  
Vol 1 (5) ◽  
Author(s):  
Xuecheng Bai Bai ◽  
Yang Hu ◽  
Yanchun Li
Keyword(s):  
Skeletal Muscle ◽  
Resistance Training ◽  
Resistance Exercise ◽  
Mrna Expression ◽  
Muscle Atrophy ◽  
Biceps Brachii ◽  
Skeletal Muscle Atrophy ◽  
Significant Difference ◽  
Wet Weight ◽  
Hypoxic Resistance

Objective Loss of skeletal muscle weight is a common phenomenon in hypoxic environment. It has been recognized that resistance training can reduce hypoxia-induced skeletal muscle atrophy, but its molecular mechanism is still unclear. Myostatin is a major factor that inhibits muscle growth and differentiation, and Follistatin can inhibit Myostatin. Therefore, this study is to clarify the effect of 4-week hypoxic resistance exercise on Myostatin and Follistatin gene expression in skeletal muscle of rats. Methods Twenty four 8-week-old male SD rats were randomly divided into normoxic control group (group C: 6 rats), normoxic exercise group (group R: 6 rats), hypoxic control group (group H: 6 rats) and hypoxic exercise group (group HR: 6 rats). Rats in each hypoxic group were fed in a hypoxic chamber (atmospheric hypoxia) with oxygen concentration of 12.7% (simulated 4000m altitude). Rats in each exercise group were trained according to the rat's resistance training program developed in our laboratory. After all the intervention, DEXA was used to analyze the body composition. The soleus, extensor digitorum longus and biceps brachii muscles of rats were taken and the wet weight of individual muscles was measured. The data were processed by SPSS17.0 statistical software. The expression level of skeletal muscle mRNA was expressed as "median (25-75%)" and the data of body composition and muscle wet weight were expressed as"mean±standard deviation". The differences between the groups were evaluated using a one-way analysis of variance (ANOVA) test. The significance level for the study was less than 0.05. Results Body composition analysis after 4 weeks of hypoxic intervention showed that the body weight of rats in group H decreased significantly (p=0.012), and the muscle mass decreased more significantly (p<0.001). But resistance exercises obviously reduced the muscle atrophy (p<0.01) caused by hypoxia. After analyzing the changes of the wet weight of individual muscles, it was found that the wet weight of biceps brachii in HR group was significantly higher than that in H group (p=0.048). After 4 weeks of hypoxic intervention and hypoxic resistance exercise, the expression of Myostatin mRNA in individual muscles of each group changed differently. The expression of Myostatin mRNA in soleus muscle of H group was significantly higher than that of C group (371.2%) after 4 weeks of hypoxia intervention. Myostatin mRNA expression in soleus and biceps brachii of HR group was significantly lower than that of H group (591.1% and 478.4% respectively). However, there was no significant difference in the expression level of Myostatin mRNA in the extensor digitorum longus between each group (p=0.259). The change of Follistatin mRNA expression in different groups also showed a different trend. The expression of Follistatin mRNA in soleus muscle and biceps brachii muscle was significantly different among groups (p=0.003, p=0.004, respectively). However, there was no significant difference in the expression level of Follistatin mRNA in the extensor digitorum longus between each group (p=0.734). Myostatin mRNA/Follistatin mRNA ratio (M/F) showed a more significant difference. The M/F ratio of soleus muscle in group H was significantly lower than that in group C (p<0.001), but the M/F ratio in group HR was significantly higher than that in group H (p<0.001). The M/F ratio of biceps brachii in group H was significantly lower than that in group C (p<0.001), but the M/F ratio in group HR showed a higher trend than that in group H (p=0.051). Conclusions Hypoxic exposure results in an increase in Myostatin mRNA expression in skeletal muscle, but hypoxic resistance exercise reduces such an increase. On the contrary, the level of Follistatin mRNA expression in skeletal muscle decreased after hypoxic exposure, and hypoxic resistance exercise could slow down the decline. As a result, rat resistance exercise significantly slowed down hypoxia-induced muscle atrophy. In conclusion, the mutual restriction between Myostatin and Follistatin is one of the main links of resistance exercise to reduce hypoxia-induced skeletal muscle atrophy. However, the process of resistance training to reduce the hypoxia-induced skeletal muscle atrophy is very complex. There are many molecular signaling pathways involved, which need further study.

scholarly journals Chronic Alcohol Dysregulates Skeletal Muscle Myogenic Gene Expression after Hind Limb Immobilization in Female Rats

Biomolecules ◽  
2020 ◽  
Vol 10 (3) ◽  
pp. 441
Author(s):  
Danielle E. Levitt ◽  
Alice Y. Yeh ◽  
Matthew J. Prendergast ◽  
Ronald G. Budnar, Jr. ◽  
Katherine A. Adler ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Muscle Regeneration ◽  
Hind Limb ◽  
Female Rats ◽  
Skeletal Muscle Regeneration ◽  
Skeletal Muscle Atrophy ◽  
Expression Of Genes ◽  
Risk Factors For Falls ◽  
Limb Immobilization

Alcohol use and aging are risk factors for falls requiring immobilization and leading to skeletal muscle atrophy. Skeletal muscle regeneration is integral to post-immobilization recovery. This study aimed to elucidate the effects of alcohol and ovarian hormone loss on the expression of genes implicated in muscle regeneration. Three-month-old female rats received an ovariectomy or a sham surgery, consumed an alcohol-containing or control diet for 10 weeks, were subjected to unilateral hind limb immobilization for seven days, and finally were allowed a three (3d)- or 14 (14d)-day recovery. Immobilization decreased the quadriceps weight at 3d and 14d, and alcohol decreased the quadriceps weight at 14d in the nonimmobilized hind limb (NI). At 3d, alcohol decreased gene expression of myoblast determination protein (MyoD) in the immobilized hind limb (IMM) and myocyte enhancer factor (Mef)2C and tumor necrosis factor (TNF)α in NI, and ovariectomy increased MyoD and decreased TNFα expression in NI. At 14d, alcohol increased the gene expression of Mef2C, MyoD, TNFα, and transforming growth factor (TFG)β in IMM and decreased monocyte chemoattractant protein (MCP)1 expression in NI; ovariectomy increased TNFα expression in NI, and alcohol and ovariectomy together increased Mef2C expression in NI. Despite increased TGFβ expression, there was no concomitant alcohol-mediated increase in collagen in IMM at 14d. Overall, these data indicate that alcohol dysregulated the post-immobilization alteration in the expression of genes implicated in regeneration. Whether alcohol-mediated molecular changes correspond with post-immobilization functional alterations remains to be determined.

Effects of streptozotocin-induced diabetes and physical training on gene expression of titin-based stretch-sensing complexes in mouse striated muscle

2007 ◽  
Vol 292 (2) ◽  
pp. E533-E542 ◽  
Author(s):  
T. Maarit Lehti ◽  
Mika Silvennoinen ◽  
Riikka Kivelä ◽  
Heikki Kainulainen ◽  
Jyrki Komulainen
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Cardiac Muscle ◽  
Physical Training ◽  
Striated Muscle ◽  
Fiber Type ◽  
Training Session ◽  
Mrna Levels ◽  
Strain Sensing ◽  
Induced Changes

In striated muscle, a sarcomeric noncontractile protein, titin, is proposed to form the backbone of the stress- and strain-sensing structures. We investigated the effects of diabetes, physical training, and their combination on the gene expression of proteins of putative titin stretch-sensing complexes in skeletal and cardiac muscle. Mice were divided into control (C), training (T), streptozotocin-induced diabetic (D), and diabetic training (DT) groups. Training groups performed for 1, 3, or 5 wk of endurance training on a motor-driven treadmill. Muscle samples from T and DT groups together with respective controls were collected 24 h after the last training session. Gene expression of calf muscles (soleus, gastrocnemius, and plantaris) and cardiac muscle were analyzed using microarray and quantitative PCR. Diabetes induced changes in mRNA expression of the proteins of titin stretch-sensing complexes in Z-disc (MLP, myostatin), I-band (CARP, Ankrd2), and M-line (titin kinase signaling). Training alleviated diabetes-induced changes in most affected mRNA levels in skeletal muscle but only one change in cardiac muscle. In conclusion, we showed diabetes-induced changes in mRNA levels of several fiber-type-biased proteins (MLP, myostatin, Ankrd2) in skeletal muscle. These results are consistent with previous observations of diabetes-induced atrophy leading to slower fiber type composition. The ability of exercise to alleviate diabetes-induced changes may indicate slower transition of fiber type.

scholarly journals Expression of genes involved in key metabolic processes during winter flounder (Pseudopleuronectes americanus) metamorphosis

2013 ◽  
Vol 91 (3) ◽  
pp. 156-163 ◽  
Author(s):  
Marie Vagner ◽  
Benjamin de Montgolfier ◽  
Jean-Marie Sévigny ◽  
Réjean Tremblay ◽  
Céline Audet
Keyword(s):  
Gene Expression ◽  
Expression Patterns ◽  
Pentose Phosphate ◽  
Winter Flounder ◽  
Benthic Habitat ◽  
Pseudopleuronectes Americanus ◽  
Metabolic Processes ◽  
Expression Of Genes ◽  
Molecular Events ◽  
Gh Gene

The aim of this study was to better understand the molecular events governing ontogeny in winter flounder (Pseudopleuronectes americanus (Walbaum, 1792)). The expression of seven genes involved in key metabolic processes during metamorphosis were measured at settlement (S0), at 15 (S15), and 30 (S30) days after settlement and compared with those in pelagic larvae prior to settlement (PL). Two critical stages were identified: (1) larval transit from the pelagic to the benthic habitat (from PL to S0) and (2) metamorphosis maturation, when the larvae stay settled without growth (from S0 to S30). Growth hormone (gh) gene expression significantly increased at S0. At S30, an increase in cytochrome oxidase (cox) gene expression occurred with a second surge of gh gene expression, suggesting that enhanced aerobic capacity was supporting growth before the temperature decrease in the fall. Expression patterns of pyruvate kinase (pk), glucose-6-phosphate dehydrogenase (g6pd), and bile salt activated lipase (bal) genes indicated that energy synthesis may be mainly supplied through glycolysis in PL, through the pentose–phosphate pathway at settlement, and through lipid metabolism at S30. The expression of the heat-shock protein 70 (hsp70), superoxide dismutase (sod), cox, and peroxiredoxin-6 (prx6) genes revealed that oxidative stress and the consequent development of antioxidative protection were limited during the PL stage, reinforced at settlement, and very high at S30, certainly owing to the higher growth rate observed at this period.

Molecular Characteristics of Aged Muscle Reflect an Altered Ability to Respond to Exercise

2001 ◽  
Vol 11 (s1) ◽  
pp. S9-S15 ◽  
Author(s):  
Alison C. Jozsi ◽  
Esther E. Dupont-Versteegden ◽  
Jane M. Taylor-Jones ◽  
William J. Evans ◽  
Todd A. Trappe ◽  
...  
Keyword(s):  
Gene Expression ◽  
Resistance Exercise ◽  
Exercise Bout ◽  
Elderly Subjects ◽  
Molecular Characteristics ◽  
Older Individuals ◽  
Variable Response ◽  
Hypertrophic Response ◽  
Expression Of Genes ◽  
Elevated Expression

Studies have been performed in humans to identify changes in gene expression that may account for the relatively weak and variable response of aged muscle to resistance exercise. The gene expression profile of skeletal muscle from elderly (62–75 years old) compared to younger (20–30 years old) men demonstrated elevated expression of genes typical of a stress or damage response. The expression of the majority of these genes was unaffected by a single bout of high-intensity resistance exercise in elderly subjects but was altered acutely by exercise in younger subjects so as to approach the pre-exercise levels observed in older subjects. The inability of muscle from elderly subjects to respond to resistance exercise was also apparent in the expression of inflammatory response genes, which increased within 24 hours of the exercise bout only in younger subjects. Other genes with potentially important roles in the adaptation of muscle to exercise, showed a similar or even more robust response in older compared to younger subjects. Taken together, these results may help to explain the variable hypertrophic response of muscle from older individuals to resistance training.

scholarly journals Increased ceramide content and NFκB signaling may contribute to the attenuation of anabolic signaling after resistance exercise in aged males

2012 ◽  
Vol 113 (11) ◽  
pp. 1727-1736 ◽  
Author(s):  
Donato A. Rivas ◽  
Evan P. Morris ◽  
Prashanth H. Haran ◽  
Evan P. Pasha ◽  
Mauricio da Silva Morais ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Resistance Exercise ◽  
Muscle Mass ◽  
High Intensity ◽  
Muscle Growth ◽  
Older Individuals ◽  
Acute Bout ◽  
Ceramide Content ◽  
Cell Fractions ◽  
Older Males

One of the most fundamental adaptive physiological events is the response of skeletal muscle to high-intensity resistance exercise, resulting in increased protein synthesis and ultimately larger muscle mass. However, muscle growth in response to contraction is attenuated in older humans. Impaired contractile-induced muscle growth may contribute to sarcopenia: the age-associated loss of muscle mass and function that is manifested by loss of strength, contractile capacity, and endurance. We hypothesized that the storage of ceramide would be increased in older individuals and this would be associated with increases in NFκB signaling and a decreased anabolic response to exercise. To test this hypothesis we measured ceramides at rest and anabolic and NFκB signaling after an acute bout of high-intensity resistance exercise in young and older males. Using lipidomics analysis we show there was a 156% increase in the accumulation of C16:0-ceramide ( P < 0.05) and a 30% increase in C20:0-ceramide ( P < 0.05) in skeletal muscle with aging, although there was no observable difference in total ceramide. C16:0-ceramide content was negatively correlated ( P = 0.008) with lower leg lean mass. Aging was associated with a ∼60% increase in the phosphorylation of the proinflammatory transcription factor NFκB in the total and nuclear cell fractions ( P < 0.05). Furthermore, there was an attenuated activation of anabolic signaling molecules such as Akt ( P < 0.05), FOXO1 ( P < 0.05), and S6K1 ( P < 0.05) after an acute bout of high-intensity resistance exercise in older males. We conclude that ceramide may have a significant role in the attenuation of contractile-induced skeletal muscle adaptations and atrophy that is observed with aging.

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