Vascular remodelling in human skeletal muscle

2011 ◽  
Vol 39 (6) ◽  
pp. 1628-1632 ◽  
Author(s):  
Thomas Gustafsson
Keyword(s):  
Skeletal Muscle ◽  
Cell Types ◽  
Model Systems ◽  
Limited Information ◽  
Muscle Adaptation ◽  
Multiple Systems ◽  
Sprouting Angiogenesis ◽  
Capillary Growth ◽  
Ecm Extracellular Matrix ◽  
Exercise Induced

Exercise-induced angiogenesis in skeletal muscle involves both non-sprouting and sprouting angiogenesis and results from the integrated responses of multiple systems and stimuli. VEGF-A (vascular endothelial growth factor A) levels are increased in exercised muscle and have been demonstrated to be critical for exercise-induced capillary growth. Only limited information is available regarding the role of other angiogenic and angiostatic factors in exercise, but changes in the angiopoietin family following repetitive bouts of exercise occur in a pattern that is favourable for angiogenesis. Results from other angiogenic model systems, indicate that miRNAs (microRNAs) are important factors in the regulation of angiogenesis and thus to explore their role as regulators of exercise induced angiogenesis will be an important avenue of study in the future. ECM (extracellular matrix) remodelling and activation of MMPs (matrix metalloproteinases) are, to some extent, overlooked players in skeletal muscle adaptation. Degradation of ECM proteins liberates angiogenic factors from immobilized matrix stores and make cell migration possible. In fact, it is known that MMPs become activated by a single bout of exercise in humans, rapid interstitial changes occur long before any changes in gene transcription could result in protein synthesis and inhibition of MMP activity completely abolishes sprouting angiogenesis. A growing body of evidence suggests that circulating and resident progenitor cells, in addition to other cell types located in skeletal muscle tissue, participate in skeletal muscle angiogenesis by various mechanisms. However, more studies are needed before these can be confirmed as mechanisms of exercise-induced capillary growth.

scholarly journals Effects of Exercise-Induced ROS on the Pathophysiological Functions of Skeletal Muscle

2021 ◽  
Vol 2021 ◽  
pp. 1-5
Author(s):  
Fan Wang ◽  
Xin Wang ◽  
Yiping Liu ◽  
Zhenghong Zhang
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Acute Exercise ◽  
Redox System ◽  
The Body ◽  
Muscle Adaptation ◽  
Exercise Induced ◽  
And Function ◽  
Stress Fatigue

Oxidative stress is the imbalance of the redox system in the body, which produces excessive reactive oxygen species, leads to multiple cellular damages, and closely relates to some pathological conditions, such as insulin resistance and inflammation. Meanwhile, exercise as an external stimulus of oxidative stress causes the changes of pathophysiological functions in the tissues and organs, including skeletal muscle. Exercise-induced oxidative stress is considered to have different effects on the structure and function of skeletal muscle. Long-term regular or moderate exercise-induced oxidative stress is closely related to the formation of muscle adaptation, while excessive free radicals produced by strenuous or acute exercise can cause muscle oxidative stress fatigue and damage, which impacts exercise capacity and damages the body’s health. The present review systematically summarizes the relationship between exercise-induced oxidative stress and the adaptions, damage, and fatigue in skeletal muscle, in order to clarify the effects of exercise-induced oxidative stress on the pathophysiological functions of skeletal muscle.

Hormetic modulation of angiogenic factors by exercise-induced mechanical and metabolic stress in human skeletal muscle

2020 ◽  
Vol 319 (4) ◽  
pp. H824-H834
Author(s):  
M. Fiorenza ◽  
L. Gliemann ◽  
N. Brandt ◽  
J. Bangsbo
Keyword(s):  
Skeletal Muscle ◽  
Muscle Activity ◽  
Human Skeletal Muscle ◽  
Metabolic Stress ◽  
Angiogenic Factors ◽  
Capillary Growth ◽  
Exercise Induced ◽  
Molecular Signals

Skeletal muscle capillary growth is orchestrated by angiogenic factors sensitive to mechanical and metabolic signals. In this study, we employed an integrative exercise model to synergistically target, yet to different extents and for different durations, the mechanical and metabolic components of muscle activity that promote angiogenesis. Our results suggest that the magnitude of the myocellular perturbations incurred during exercise determines the amplitude of the angiogenic molecular signals, implying hormetic modulation of skeletal muscle angiogenesis by exercise-induced mechanical and metabolic stress.

scholarly journals REDD1 induction regulates the skeletal muscle gene expression signature following acute aerobic exercise

2017 ◽  
Vol 313 (6) ◽  
pp. E737-E747 ◽  
Author(s):  
Bradley S. Gordon ◽  
Jennifer L. Steiner ◽  
Michael L. Rossetti ◽  
Shuxi Qiao ◽  
Leif W. Ellisen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Aerobic Exercise ◽  
Acute Exercise ◽  
Gene Expression Signature ◽  
Model Systems ◽  
Expression Signature ◽  
Altered Gene Expression ◽  
Altered Gene ◽  
Exercise Induced

The metabolic stress placed on skeletal muscle by aerobic exercise promotes acute and long-term health benefits in part through changes in gene expression. However, the transducers that mediate altered gene expression signatures have not been completely elucidated. Regulated in development and DNA damage 1 (REDD1) is a stress-induced protein whose expression is transiently increased in skeletal muscle following acute aerobic exercise. However, the role of this induction remains unclear. Because REDD1 altered gene expression in other model systems, we sought to determine whether REDD1 induction following acute exercise altered the gene expression signature in muscle. To do this, wild-type and REDD1-null mice were randomized to remain sedentary or undergo a bout of acute treadmill exercise. Exercised mice recovered for 1, 3, or 6 h before euthanization. Acute exercise induced a transient increase in REDD1 protein expression within the plantaris only at 1 h postexercise, and the induction occurred in both cytosolic and nuclear fractions. At this time point, global changes in gene expression were surveyed using microarray. REDD1 induction was required for the exercise-induced change in expression of 24 genes. Validation by RT-PCR confirmed that the exercise-mediated changes in genes related to exercise capacity, muscle protein metabolism, neuromuscular junction remodeling, and Metformin action were negated in REDD1-null mice. Finally, the exercise-mediated induction of REDD1 was partially dependent upon glucocorticoid receptor activation. In all, these data show that REDD1 induction regulates the exercise-mediated change in a distinct set of genes within skeletal muscle.

scholarly journals Early potential effects of resveratrol supplementation on skeletal muscle adaptation involved in exercise-induced weight loss in obese mice

BMB Reports ◽  
2018 ◽  
Vol 51 (4) ◽  
pp. 200-205 ◽  
Author(s):  
Jingyu Sun ◽  
Chen Zhang ◽  
MinJeong Kim ◽  
Yajuan Su ◽  
Lili Qin ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Weight Loss ◽  
Obese Mice ◽  
Muscle Adaptation ◽  
Exercise Induced

scholarly journals Serum Cardiac and Skeletal Muscle Marker Changes in Repetitive Breath-hold Diving

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Danilo Cialoni ◽  
Andrea Brizzolari ◽  
Nicola Sponsiello ◽  
Valentina Lancellotti ◽  
Cesare Lori ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Creatine Kinase ◽  
Troponin I ◽  
Environmental Changes ◽  
Acute Hypoxia ◽  
Training Session ◽  
Breath Hold ◽  
Muscle Adaptation ◽  
Cardiac Muscles ◽  
Exercise Induced

Abstract Background Breath-hold diving (BH-diving) is associated to extreme environmental conditions, prolonged physical activity, and complex adaptation mechanisms to supply enough O2 to vital organs. Consequently, one of the biggest effects could be an increased exercise-induced muscle fatigue, in both skeletal and cardiac muscles that can induce an increase of muscles injury markers including creatine kinase (CK), aspartate transferase (AST), and alanine transferase (ALT) when concerning the skeletal muscle, cardiac creatine kinase isoenzyme (CK-MBm) and cardiac troponin I (cTnI) when concerning the cardiac muscle, and lactate dehydrogenase (LDH) as index of muscle stress. The aim of this study is to investigate serum cardiac and skeletal muscle markers before and after a BH-diving training session. Results We found statistically significant increases of CK (T0: 136.1% p < 0.0001; T1: 138.5%, p < 0.0001), CK-MBm (T0: 145.1%, p < 0.0001; T1: 153.2%, p < 0.0001) LDH (T0: 110.4%, p < 0.0003; T1: 110.1%, p < 0.0013) in both T0 and T1 blood samples, as compared to basal value. AST showed a statistically significant increase only at T0 (106.8%, p < 0.0007) while ALT did not exhibit statistically significant changes. We did not find any changes in cTnI levels between pre-dive and post-dive samples. Conclusions Our data seem to indicate that during a BH-diving training session, skeletal and cardiac muscles react to physical effort releasing stress-related substances. Although the peculiar nature of BH-diving makes it difficult to understand if our results are related only to exercise induced muscle adaptation or whether acute hypoxia or a response to environmental changes (pressure) play a role to explain the observed changes, further studies are needed to better understand if these biomarker changes are linked to physical exercise or to acute hypoxia, or if both conditions play a role.

Skeletal muscle adaptation in response to mechanical stress in p130cas−/− mice

2013 ◽  
Vol 304 (6) ◽  
pp. C541-C547 ◽  
Author(s):  
Takayuki Akimoto ◽  
Kanako Okuhira ◽  
Katsuji Aizawa ◽  
Shogo Wada ◽  
Hiroaki Honda ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Mechanical Stress ◽  
P38 Mapk ◽  
Fiber Type ◽  
Cellular Signaling ◽  
Mapk Signaling ◽  
Muscle Adaptation ◽  
Type Transformation ◽  
Exercise Induced ◽  
Specific Deletion

Mammalian skeletal muscles undergo adaptation in response to changes in the functional demands upon them, involving mechanical-stress-induced cellular signaling called “mechanotransduction.” We hypothesized that p130Cas, which is reported to act as a mechanosensor that transduces mechanical extension into cellular signaling, plays an important role in maintaining and promoting skeletal muscle adaptation in response to mechanical stress via the p38 MAPK signaling pathway. We demonstrate that muscle-specific p130Cas−/− mice express the contractile proteins normally in skeletal muscle. Furthermore, muscle-specific p130Cas−/− mice show normal mechanical-stress-induced muscle adaptation, including exercise-induced IIb-to-IIa muscle fiber type transformation and hypertrophy. Finally, we provide evidence that exercise-induced p38 MAPK signaling is not impaired by the muscle-specific deletion of p130Cas. We conclude that p130Cas plays a limited role in mechanical-stress-induced skeletal muscle adaptation.

scholarly journals Exercise Serum Alters Genes Related Mitochondria in Cardiomyocyte Culture Cell

2020 ◽  
Vol 5 (2) ◽  
Author(s):  
Ronny Lesmana ◽  
Wibowo Budi Prasetyo ◽  
Hamidie Ronald Daniel Ray ◽  
Vita Murniati Tarawan ◽  
Hanna Goenawan ◽  
...  
Keyword(s):  
Genetic Regulation ◽  
Specific Protein ◽  
Culture Cell ◽  
Limited Information ◽  
Muscle Adaptation ◽  
Rat Cardiomyocytes ◽  
Selective Degradation ◽  
Specific Protocol ◽  
Male Wistar Rats ◽  
Exercise Induced

Exercise-induced hearth muscle adaptation is important for physiological process after exercise. This adaptation will ensure basal mitochondrial homeostasis and as a part of the mitochondria quality control. This process is reflected by equal level of biogenesis stimulation and as well as the selective degradation of old and undesirable mitochondria through fusion or fission cycle and Mitophagy. There is limited information about genetic regulation stimulated by training in cardiomyocytes. We believe there is a specific myokines or protein release in the serum and initiate cardiac muscle adaptation process. In the present study, twelve male wistar rats were appointed to two group: sedentary control and aerobic-intensity (AE, 15m/minute). Rats were trained for running with specific protocol as follows: 30 minutes/day with a 5 times/week interval for 8 weeks. On the last day, serum form control and exercise groups were taken via retro-orbital sinus. Then, 3.105  H9C2 cells (Rat cardiomyocytes cell line)  were cultured and incubated by this serum for 24 hours. After treatment, cell were extracted using trisure for RNA purification and continue with reverse transcriptase PCR. Our data showed that expression of the Pgc-1α, Mfn1, Mfn2, Opa1, Drp1, Pink, and Parkin genes were altered and modulated. Specifically, Mfn1, Mfn2, and Opa1 gene expression levels significantly increased. Interestingly, we did not find significant modulation for  Pgc-1α, Drp1, Pink, and Parkin. Taken together, serum of exercise rats might be contained with myokines or specific protein which was released during training and it altered mitochondrial genes expression in cardiomyocytes culture cell. We believe that myokines release in the serum had a contribution in cardiacmyocyte adaptation.

scholarly journals Myonuclear accretion is a determinant of exercise-induced remodeling in skeletal muscle

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Qingnian Goh ◽  
Taejeong Song ◽  
Michael J Petrany ◽  
Alyssa AW Cramer ◽  
Chengyi Sun ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Interval Training ◽  
Physiological Model ◽  
Exercise Intolerance ◽  
Muscle Repair ◽  
Muscle Adaptation ◽  
Adaptive Responses ◽  
Hypertrophic Growth ◽  
High Intensity Interval ◽  
Exercise Induced

Skeletal muscle adapts to external stimuli such as increased work. Muscle progenitors (MPs) control muscle repair due to severe damage, but the role of MP fusion and associated myonuclear accretion during exercise are unclear. While we previously demonstrated that MP fusion is required for growth using a supra-physiological model (Goh and Millay, 2017), questions remained about the need for myonuclear accrual during muscle adaptation in a physiological setting. Here, we developed an 8 week high-intensity interval training (HIIT) protocol and assessed the importance of MP fusion. In 8 month-old mice, HIIT led to progressive myonuclear accretion throughout the protocol, and functional muscle hypertrophy. Abrogation of MP fusion at the onset of HIIT resulted in exercise intolerance and fibrosis. In contrast, ablation of MP fusion 4 weeks into HIIT, preserved exercise tolerance but attenuated hypertrophy. We conclude that myonuclear accretion is required for different facets of exercise-induced adaptive responses, impacting both muscle repair and hypertrophic growth.

Sign in / Sign up

Export Citation Format

Share Document