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.

scholarly journals The Role of the Skeletal Muscle Secretome in Mediating Endurance and Resistance Training Adaptations

2021 ◽  
Vol 12 ◽  
Author(s):  
Aurel B. Leuchtmann ◽  
Volkan Adak ◽  
Sedat Dilbaz ◽  
Christoph Handschin
Keyword(s):  
Skeletal Muscle ◽  
Resistance Training ◽  
Acute Exercise ◽  
Current Knowledge ◽  
Liver Fat ◽  
Training Adaptations ◽  
Exercise Induced ◽  
And Function

Exercise, in the form of endurance or resistance training, leads to specific molecular and cellular adaptions not only in skeletal muscles, but also in many other organs such as the brain, liver, fat or bone. In addition to direct effects of exercise on these organs, the production and release of a plethora of different signaling molecules from skeletal muscle are a centerpiece of systemic plasticity. Most studies have so far focused on the regulation and function of such myokines in acute exercise bouts. In contrast, the secretome of long-term training adaptation remains less well understood, and the contribution of non-myokine factors, including metabolites, enzymes, microRNAs or mitochondrial DNA transported in extracellular vesicles or by other means, is underappreciated. In this review, we therefore provide an overview on the current knowledge of endurance and resistance exercise-induced factors of the skeletal muscle secretome that mediate muscular and systemic adaptations to long-term training. Targeting these factors and leveraging their functions could not only have broad implications for athletic performance, but also for the prevention and therapy in diseased and elderly populations.

Skeletal muscle adaptations to exercise are not influenced by metformin treatment in humans: secondary analyses of two randomised, clinical trials.

2021 ◽  
Author(s):  
Nanna Skytt Pilmark ◽  
Laura Oberholzer ◽  
Jens Frey Halling ◽  
Jonas M. Kristensen ◽  
Christina Pedersen Bønding ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Exercise Training ◽  
Human Skeletal Muscle ◽  
Acute Exercise ◽  
Metformin Treatment ◽  
Ampk Activation ◽  
Double Blind ◽  
Parallel Group ◽  
Exercise Induced

Metformin and exercise both improve glycemic control, but in vitro studies have indicated that an interaction between metformin and exercise occurs in skeletal muscle, suggesting a blunting effect of metformin on exercise training adaptations. Two studies (a double-blind, parallel-group, randomized clinical trial conducted in 29 glucose-intolerant individuals and a double-blind, cross-over trial conducted in 15 healthy lean males) were included in this paper. In both studies, the effect of acute exercise +/- metformin treatment on different skeletal muscle variables, previously suggested to be involved in a pharmaco-physiological interaction between metformin and exercise, was assessed. Furthermore, in the parallel-group trial, the effect of 12 weeks of exercise training was assessed. Skeletal muscle biopsies were obtained before and after acute exercise and 12 weeks of exercise training, and mitochondrial respiration, oxidative stress and AMPK activation was determined. Metformin did not significantly affect the effects of acute exercise or exercise training on mitochondrial respiration, oxidative stress or AMPK activation, indicating that the response to acute exercise and exercise training adaptations in skeletal muscle is not affected by metformin treatment. Further studies are needed to investigate whether an interaction between metformin and exercise is present in other tissues, e.g. the gut. Trial registration: ClinicalTrials.gov (NCT03316690 and NCT02951260). Novelty bullets • Metformin does not affect exercise-induced alterations in mitochondrial respiratory capacity in human skeletal muscle • Metformin does not affect exercise-induced alterations in systemic levels of oxidative stress nor emission of reactive oxygen species from human skeletal muscle • Metformin does not affect exercise-induced AMPK activation in human skeletal muscle

scholarly journals Mitochondria-targeted antioxidant supplementation augments acute exercise-induced increases in muscle PGC1α mRNA and improves training-induced increases in peak power independent of mitochondrial content and function in untrained middle-aged men

2021 ◽  
Author(s):  
S. C. Broome ◽  
T. Pham ◽  
A. J. Braakhuis ◽  
R. Narang ◽  
H. W. Wang ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Mitochondrial Biogenesis ◽  
High Intensity ◽  
Peak Power ◽  
Acute Exercise ◽  
Mitochondrial Content ◽  
High Intensity Interval ◽  
Exercise Induced ◽  
And Function

ABSTRACTThe role of mitochondrial ROS production and signalling in muscle adaptations to exercise training has not been explored in detail. Here we investigated the effect of supplementation with the mitochondria-targeted antioxidant MitoQ on a) the skeletal muscle mitochondrial and antioxidant gene transcriptional response to acute high-intensity exercise and b) skeletal muscle mitochondrial content and function following exercise training. In a randomised, double-blind, placebo-controlled, parallel design study, 23 untrained men (age: 44 ± 7 years, VO2peak: 39.6 ± 7.9 ml/kg/min) were randomised to receive either MitoQ (20 mg/d) or a placebo for 10 days before completing a bout of high-intensity interval exercise (cycle ergometer, 10 × 60 s at VO2peak workload with 75 s rest). Blood samples and vastus lateralis muscle biopsies were collected before exercise and immediately and 3 hours after exercise. Participants then completed high-intensity interval training (HIIT; 3 sessions per week for 3 weeks) and another blood sample and muscle biopsy were collected. MitoQ supplementation augmented acute exercise-induced increases in skeletal muscle mRNA expression of the major regulator of proteins involved in mitochondrial biogenesis peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1-α). Despite this, training-induced increases in skeletal muscle mitochondrial content were unaffected by MitoQ supplementation. HIIT-induced increases in VO2peak and 20 km time trial performance were also unaffected by MitoQ while MitoQ augmented training-induced increases in peak power achieved during the VO2peak test. These data suggest that MitoQ supplementation enhances the effect of training on peak power, which may be related to the augmentation of skeletal muscle PGC1α expression following acute exercise. However, this effect does not appear to be related to an effect of MitoQ supplementation on HIIT-induced mitochondrial biogenesis in skeletal muscle and may therefore be the result of other adaptations mediated by PGC1α.

Stanozolol treatment decreases the mitochondrial ROS generation and oxidative stress induced by acute exercise in rat skeletal muscle

2011 ◽  
Vol 110 (3) ◽  
pp. 661-669 ◽  
Author(s):  
Ana Saborido ◽  
Alba Naudí ◽  
Manuel Portero-Otín ◽  
Reinald Pamplona ◽  
Alicia Megías
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Fatty Acid Composition ◽  
Mitochondrial Membrane ◽  
Acute Exercise ◽  
Ros Generation ◽  
Ros Production ◽  
Rat Skeletal Muscle ◽  
Mitochondrial Ros ◽  
Exercise Induced

Anabolic androgenic steroids are used in the sport context to enhance muscle mass and strength and to increase muscle fatigue resistance. Since muscle fatigue has been related to oxidative stress caused by an exercise-linked reactive oxygen species (ROS) production, we investigated the potential effects of a treatment with the anabolic androgenic steroid stanozolol against oxidative damage induced on rat skeletal muscle mitochondria by an acute bout of exhaustive exercise. Mitochondrial ROS generation with complex I- and complex II-linked substrates was increased in exercised control rats, whereas it remained unchanged in the steroid-treated animals. Stanozolol treatment markedly reduced the extent of exercise-induced oxidative damage to mitochondrial proteins, as indicated by the lower levels of the specific markers of protein oxidation, glycoxidation, and lipoxidation, and the preservation of the activity of the superoxide-sensitive enzyme aconitase. This effect was not due to an enhancement of antioxidant enzyme activities. Acute exercise provoked changes in mitochondrial membrane fatty acid composition characterized by an increased content in docosahexaenoic acid. In contrast, the postexercise mitochondrial fatty acid composition was not altered in stanozolol-treated rats. Our results suggest that stanozolol protects against acute exercise-induced oxidative stress by reducing mitochondrial ROS production, in association with a preservation of mitochondrial membrane properties.

scholarly journals Endurance training reduces the contraction-induced interleukin-6 mRNA expression in human skeletal muscle

2004 ◽  
Vol 287 (6) ◽  
pp. E1189-E1194 ◽  
Author(s):  
Christian P. Fischer ◽  
Peter Plomgaard ◽  
Anne K. Hansen ◽  
Henriette Pilegaard ◽  
Bengt Saltin ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Mrna Expression ◽  
Muscle Glycogen ◽  
Human Skeletal Muscle ◽  
Acute Exercise ◽  
Glycogen Content ◽  
Knee Extensor ◽  
Exercise Induced ◽  
Response To Exercise ◽  
Resting Muscle

Contracting skeletal muscle expresses large amounts of IL-6. Because 1) IL-6 mRNA expression in contracting skeletal muscle is enhanced by low muscle glycogen content, and 2) IL-6 increases lipolysis and oxidation of fatty acids, we hypothesized that regular exercise training, associated with increased levels of resting muscle glycogen and enhanced capacity to oxidize fatty acids, would lead to a less-pronounced increase of skeletal muscle IL-6 mRNA in response to acute exercise. Thus, before and after 10 wk of knee extensor endurance training, skeletal muscle IL-6 mRNA expression was determined in young healthy men ( n = 7) in response to 3 h of dynamic knee extensor exercise, using the same relative workload. Maximal power output, time to exhaustion during submaximal exercise, resting muscle glycogen content, and citrate synthase and 3-hydroxyacyl-CoA dehydrogenase enzyme activity were all significantly enhanced by training. IL-6 mRNA expression in resting skeletal muscle did not change in response to training. However, although absolute workload during acute exercise was 44% higher ( P < 0.05) after the training period, skeletal muscle IL-6 mRNA content increased 76-fold ( P < 0.05) in response to exercise before the training period, but only 8-fold ( P < 0.05, relative to rest and pretraining) in response to exercise after training. Furthermore, the exercise-induced increase of plasma IL-6 ( P < 0.05, pre- and posttraining) was not higher after training despite higher absolute work intensity. In conclusion, the magnitude of the exercise-induced IL-6 mRNA expression in contracting human skeletal muscle was markedly reduced by 10 wk of training.

scholarly journals Role of PGC-1α during acute exercise-induced autophagy and mitophagy in skeletal muscle

2015 ◽  
Vol 308 (9) ◽  
pp. C710-C719 ◽  
Author(s):  
Anna Vainshtein ◽  
Liam D. Tryon ◽  
Marion Pauly ◽  
David A. Hood
Keyword(s):  
Skeletal Muscle ◽  
Acute Exercise ◽  
Transmembrane Protein ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Lipid Trafficking ◽  
Mitochondrial Transcription Factor ◽  
Energy Demands ◽  
Niemann Pick ◽  
Exercise Induced

Regular exercise leads to systemic metabolic benefits, which require remodeling of energy resources in skeletal muscle. During acute exercise, the increase in energy demands initiate mitochondrial biogenesis, orchestrated by the transcriptional coactivator peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α). Much less is known about the degradation of mitochondria following exercise, although new evidence implicates a cellular recycling mechanism, autophagy/mitophagy, in exercise-induced adaptations. How mitophagy is activated and what role PGC-1α plays in this process during exercise have yet to be evaluated. Thus we investigated autophagy/mitophagy in muscle immediately following an acute bout of exercise or 90 min following exercise in wild-type (WT) and PGC-1α knockout (KO) animals. Deletion of PGC-1α resulted in a 40% decrease in mitochondrial content, as well as a 25% decline in running performance, which was accompanied by severe acidosis in KO animals, indicating metabolic distress. Exercise induced significant increases in gene transcripts of various mitochondrial (e.g., cytochrome oxidase subunit IV and mitochondrial transcription factor A) and autophagy-related (e.g., p62 and light chain 3) genes in WT, but not KO, animals. Exercise also resulted in enhanced targeting of mitochondria for mitophagy, as well as increased autophagy and mitophagy flux, in WT animals. This effect was attenuated in the absence of PGC-1α. We also identified Niemann-Pick C1, a transmembrane protein involved in lysosomal lipid trafficking, as a target of PGC-1α that is induced with exercise. These results suggest that mitochondrial turnover is increased following exercise and that this effect is at least in part coordinated by PGC-1α. Anna Vainshtein received the AJP-Cell 2015 Paper of the Year award. Listen to a podcast with Anna Vainshtein and coauthor David A. Hood at http://ajpcell.podbean.com/e/ajp-cell-paper-of-the-year-2015-award-podcast/ .

scholarly journals The Recent Understanding of the Neurotrophin's Role in Skeletal Muscle Adaptation

2011 ◽  
Vol 2011 ◽  
pp. 1-12 ◽  
Author(s):  
Kunihiro Sakuma ◽  
Akihiko Yamaguchi
Keyword(s):  
Skeletal Muscle ◽  
Neuromuscular Disorders ◽  
Muscle Fibers ◽  
Brain Disorders ◽  
Muscle Adaptation ◽  
Bdnf Mrna ◽  
Pathological Conditions ◽  
Development And Differentiation ◽  
And Function

This paper summarizes the various effects of neurotrophins in skeletal muscle and how these proteins act as potential regulators of the maintenance, function, and regeneration of skeletal muscle fibers. Increasing evidence suggests that this family of neurotrophic factors influence not only the survival and function of innervating motoneurons but also the development and differentiation of myoblasts and muscle fibers. Muscle contractions (e.g., exercise) produce BDNF mRNA and protein in skeletal muscle, and the BDNF seems to play a role in enhancing glucose metabolism and may act for myokine to improve various brain disorders (e.g., Alzheimer's disease and major depression). In adults with neuromuscular disorders, variations in neurotrophin expression are found, and the role of neurotrophins under such conditions is beginning to be elucidated. This paper provides a basis for a better understanding of the role of these factors under such pathological conditions and for treatment of human neuromuscular disease.

scholarly journals Exercise-Induced Oxidative Stress, Nitric Oxide and Plasma Amino Acid Profile in Recreational Runners with Vegetarian and Non-Vegetarian Dietary Patterns

Nutrients ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 1875 ◽  
Author(s):  
Josefine Nebl ◽  
Kathrin Drabert ◽  
Sven Haufe ◽  
Paulina Wasserfurth ◽  
Julian Eigendorf ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Amino Acid ◽  
Acute Exercise ◽  
Amino Acid Profile ◽  
Post Exercise ◽  
Stable Isotope Dilution ◽  
Amino Acid Profiles ◽  
Recreational Runners ◽  
Exercise Induced

This study investigated the exercise-induced changes in oxidative stress, nitric oxide (NO) metabolism and amino acid profile in plasma of omnivorous (OMN, n = 25), lacto-ovo-vegetarian (LOV, n = 25) and vegan (VEG, n = 23) recreational runners. Oxidative stress was measured as malondialdehyde (MDA), NO as nitrite and nitrate, and various amino acids, including homoarginine and guanidinoacetate, the precursor of creatine. All analytes were measured by validated stable-isotope dilution gas chromatographic-mass spectrometric methods. Pre-exercise, VEG had the highest MDA and nitrate concentrations, whereas nitrite concentration was highest in LOV. Amino acid profiles differed between the groups, with guanidinoacetate being highest in OMN. Upon acute exercise, MDA increased in the LOV and VEG group, whereas nitrate, nitrite and creatinine did not change. Amino acid profiles changed post-exercise in all groups, with the greatest changes being observed for alanine (+28% in OMN, +21% in LOV and +28% in VEG). Pre-exercise, OMN, LOV and VEG recreational runners differ with respect to oxidative stress, NO metabolism and amino acid profiles, in part due to their different dietary pattern. Exercise elicited different changes in oxidative stress with no changes in NO metabolism and closely comparable elevations in alanine. Guanidinoacetate seems to be differently utilized in OMN, LOV and VEG, pre- and post-exercise.

scholarly journals PO-055 Changes of trace elements in skeletal muscle and serum of rats after exercise-induced injury

2018 ◽  
Vol 1 (3) ◽  
Author(s):  
Jingyun Liu ◽  
Qun Zuo
Keyword(s):  
Skeletal Muscle ◽  
Trace Elements ◽  
Nitric Acid ◽  
Vena Cava ◽  
The Body ◽  
Emission Spectrometry ◽  
Control Group ◽  
Exercise Induced ◽  
And Control ◽  
Cu And Zn

Objective This study is to investigate the changes of trace elements (Cu, Fe, Zn, Se, Mg) in serum and skeletal muscle of rats after skeletal muscle injury induced by downhill running, and to find out the change regularity of trace elements in the body after exercise injury. To provide experimental basis for how to use trace elements supplements reasonably. Methods Fifty-four healthy male Sprague-Dawley rats aged 8 weeks were randomly divided into two groups: control group (C, N=6) and exercise group (E, N=48, include: 0 h group, 6 h group, 12 h group, 24 h group, 48 h group, 72 h group, 1- week group and 2- week group). The rats in exercise groups run down a 16°incline at 16m/min for 90 minutes. At the end of the exercise, the rats were killed at 0 h, 6 h, 12 h, 24 h, 48 h, 72 h, 1 week and 2 weeks, respectively. The serum was got from the inferior vena cava blood and diluted by 1% nitric acid. The muscle was got from the right side of the rat's sural which were digested by concentrated nitric acid and 30% hydrogen peroxide in 75℃water bath for 20mins. The content of trace elements in muscle and serum were measured by inductively coupled plasma atomic emission spectrometry (ICP-MS). All the data are analyzed and processed by SPSS22.0 statistical software. Results (1) The contents of trace elements in serum showed: Cu, Zn, Mg, Se decreased immediately after exercise, but the Cu still increased to reach a peak at 24h after decreasing, and after 2 weeks the content of Cu was slightly lower than pre-exercise level. However, the content of Zn did not elevate again, it continued declined to the lowest at 24h which was significantly lower than control group (P < 0.05). And after 2 weeks, Zn did not return to the pre-exercise level. The changes of Mg, Se in serum was not statistically significant. There is no difference between 0h and control groups in content of Fe, after that Fe decreased continually and appeared the least value at 24h, the differences between immediate group and control group were statistically significant (P < 0.05). Fe returned to the pre-exercise level after 2 weeks. (2) The contents of trace elements in muscle showed: Most of trace elements increased to the maximum level at 6 h, after that Mg, Fe, Cu decreased to the lowest value at 72 h which were significant lower than 0h group or 6h group (P < 0. 05). ALL the trace elements were lower than pre-exercise level. There was no statistical difference in the content of Se in muscle. Conclusions (1) The different changes of trace elements in skeletal muscle and serum after exercise injury may be due to the redistribution of trace elements caused by the body adaptability. (2) The most obviously changes of trace element in serum and muscle are Cu and Zn. Both of them did not return to the pre-exercise level after 2 weeks, it suggests that the supplement include Cu and Zn may play an important role in recovering after exercise-induced injury.

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