scholarly journals The Impact of N-Acetyl Cysteine and Coenzyme Q10 Supplementation on Skeletal Muscle Antioxidants and Proteome in Fit Thoroughbred Horses

Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1739
Author(s):  
Marisa L. Henry ◽  
Deborah Velez-Irizarry ◽  
Joe D. Pagan ◽  
Lorraine Sordillo ◽  
Jeff Gandy ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Coenzyme Q10 ◽  
Maximal Exercise ◽  
Citrate Synthase ◽  
Tca Cycle ◽  
Redox Status ◽  
Thoroughbred Horses ◽  
Redox Capacity ◽  
Acetyl Cysteine ◽  
The Impact

Horses have one of the highest skeletal muscle oxidative capacities amongst mammals, which, combined with a high glycolytic capacity, could perturb redox status during maximal exercise. We determined the effect of 30 d of oral coenzyme Q10 and N-acetyl-cysteine supplementation (NACQ) on muscle glutathione (GSH), cysteine, ROS, and coenzyme Q10 concentrations, and the muscle proteome, in seven maximally exercising Thoroughbred horses using a placebo and randomized cross-over design. Gluteal muscle biopsies were obtained the day before and 1 h after maximal exercise. Concentrations of GSH, cysteine, coenzyme Q10, and ROS were measured, and citrate synthase, glutathione peroxidase, and superoxide dismutase activities analyzed. GSH increased significantly 1 h post-exercise in the NACQ group (p = 0.022), whereas other antioxidant concentrations/activities were unchanged. TMT proteomic analysis revealed 40 differentially expressed proteins with NACQ out of 387 identified, including upregulation of 13 mitochondrial proteins (TCA cycle and NADPH production), 4 Z-disc proteins, and down regulation of 9 glycolytic proteins. NACQ supplementation significantly impacted muscle redox capacity after intense exercise by enhancing muscle glutathione concentrations and increasing expression of proteins involved in the uptake of glutathione into mitochondria and the NAPDH-associated reduction of oxidized glutathione, without any evident detrimental effects on performance.

241 Skeletal Muscle Mitochondrial Capacities Are Impacted by Breed and Temperament in Young Angus and Brahman Steers

2021 ◽  
Vol 99 (Supplement_3) ◽  
pp. 127-127
Author(s):  
Chloey P Guy ◽  
Lauren T Wesolowski ◽  
Audrey L Earnhardt ◽  
Dustin Law ◽  
Don A Neuendorff ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fixed Effects ◽  
Linear Models ◽  
Citrate Synthase ◽  
Volume Density ◽  
Skeletal Muscle Mitochondria ◽  
Mitochondrial Volume ◽  
Mitochondrial Volume Density ◽  
Brahman Steers ◽  
The Impact

Abstract Temperament impacts skeletal muscle mitochondria in Brahman heifers, but this has not been investigated in steers or between cattle breeds. We hypothesized mitochondrial measures would be greater in Angus than Brahman, temperamental than calm steers, and the trapezius (TRAP) than the longissimus thoracis (LT) muscle. Samples from calm (n = 13 per breed), intermediate (n = 12 per breed), and temperamental (n=13 per breed) Angus and Brahman steers (mean±SD 10.0±0.8 mo) were evaluated for mitochondrial enzyme activities via colorimetry. Calm and temperamental LT samples were evaluated for oxidative phosphorylation (P) and electron transfer (E) capacities by high-resolution respirometry. Data were analyzed using linear models with fixed effects of breed, muscle, temperament, and all interactions. Brahman tended to have greater mitochondrial volume density (citrate synthase activity; CS) than Angus (P = 0.08), while intrinsic (relative to CS) mitochondrial function (cytochrome c oxidase activity) was greater in Angus than Brahman (P = 0.001) and greater in TRAP than LT (P = 0.008). Angus exhibited greater integrative (per mg tissue) and intrinsic P with complex I (PCI), P with complexes I+II (PCI+II), maximum noncoupled E, and E with complex II (ECII; P ≤ 0.04) and tended to have greater intrinsic leak (P = 0.1) than Brahman. Contribution of PCI to total E was greater in Angus than Brahman (P = 0.01), while contribution of ECII to total E was greater in Brahman than Angus (P = 0.05). A trend for the interaction of breed and temperament (P = 0.07) indicated calm Angus had the greatest intrinsic ECII (P ≤ 0.03) while intrinsic ECII was similar between temperamental Angus and calm and temperamental Brahman. Integrative PCI+II and ECII, and the contribution of PCI and PCI+II to overall E tended to be greater in temperamental than calm steers (P ≤ 0.09), while intrinsic ECII tended to be greater in calm than temperamental steers (P = 0.07). The impact of these mitochondrial differences on meat quality measures remains to be determined.

scholarly journals The redox-dependent regulation of satellite cells following aseptic muscle trauma (SpEED): Study protocol for a randomized controlled trial

2019 ◽  
Author(s):  
Konstantinos Papanikolaou ◽  
Dimitrios Draganidis ◽  
Athanasios Chatzinikolaou ◽  
Vassiliki C. Laschou ◽  
Kalliopi Georgakouli ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cells ◽  
Muscle Regeneration ◽  
Repeated Measures ◽  
Controlled Trial ◽  
Redox Status ◽  
Muscle Performance ◽  
Repeated Measures Design ◽  
Muscle Trauma ◽  
The Impact

Abstract Background Muscle satellite cells (SCs) are crucial for muscle regeneration following muscle trauma. Acute skeletal muscle damage results in inflammation and production of reactive oxygen species (ROS) which may be implicated in SCs activation. Protection of these cells from oxidative damage is essential to ensure sufficient muscle regeneration. The aim of this study is to determine whether SCs activity under conditions of aseptic skeletal muscle trauma induced by exercise is redox-dependent. Methods/design Based on their SCs content in their vastus lateralis skeletal muscle, participants will be classified as either high or low respondents. In a randomized, double-blind, crossover, repeated measures design, participants will then receive either Placebo or N-acetylcysteine (alters redox potential in muscle) during a preliminary 7-day loading phase, and for 8 consecutive days following a single bout of intense muscle-damaging exercise. In both trials, blood samples and muscle biopsies will be collected, and muscle performance and soreness will be measured at baseline, pre-exercise, 2- and 8-days post-exercise. Biological samples will be analyzed for redox status and SCs activity. Between trials, a 4-week washout period will be implemented. Discussion This study is designed to investigate the impact of redox status on SCs mobilization and thus skeletal muscle potential for regeneration under conditions of aseptic inflammation induced by exercise. Findings of this trial will provide insight into i) molecular pathways involved in SCs recruitment and muscle healing under conditions of aseptic skeletal muscle trauma present in numerous catabolic conditions and ii) if skeletal muscle’s potential for regeneration depends on its basal SCs content.

Tricarboxylic acid cycle intermediate pool size and estimated cycle flux in human muscle during exercise

1998 ◽  
Vol 275 (2) ◽  
pp. E235-E242 ◽  
Author(s):  
Martin J. Gibala ◽  
Dave A. MacLean ◽  
Terry E. Graham ◽  
Bengt Saltin
Keyword(s):  
Skeletal Muscle ◽  
Maximal Exercise ◽  
Tricarboxylic Acid Cycle ◽  
Tca Cycle ◽  
Tricarboxylic Acid ◽  
Pool Size ◽  
Intense Exercise ◽  
The Tca Cycle ◽  
Small Change ◽  
The Relationship

We examined the relationship between tricarboxylic acid (TCA) cycle intermediate (TCAI) pool size, TCA cycle flux (calculated from leg O2uptake), and pyruvate dehydrogenase activity (PDHa) in human skeletal muscle. Six males performed moderate leg extensor exercise for 10 min, followed immediately by intense exercise until exhaustion (3.8 ± 0.5 min). The sum of seven measured TCAI (ΣTCAI) increased ( P ≤ 0.05) from 1.39 ± 0.11 at rest to 2.88 ± 0.31 after 10 min and to 5.38 ± 0.31 mmol/kg dry wt at exhaustion. TCA cycle flux increased ∼70-fold during submaximal exercise and was ∼100-fold higher than rest at exhaustion. PDHa corresponded to 77 and 90% of TCA cycle flux during submaximal and maximal exercise, respectively. The present data demonstrate that a tremendous increase in TCA cycle flux can occur in skeletal muscle despite a relatively small change in TCAI pool size. It is suggested that the increase in ΣTCAI during exercise may primarily reflect an imbalance between the rate of pyruvate production and its rate of oxidation in the TCA cycle.

scholarly journals The redox-dependent regulation of satellite cells following aseptic muscle trauma (SpEED): Study protocol for a randomized controlled trial

2019 ◽  
Author(s):  
Konstantinos Papanikolaou ◽  
Dimitrios Draganidis ◽  
Athanasios Chatzinikolaou ◽  
Vassiliki C. Laschou ◽  
Kalliopi Georgakouli ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cells ◽  
Muscle Regeneration ◽  
Repeated Measures ◽  
Controlled Trial ◽  
Redox Status ◽  
Muscle Performance ◽  
Repeated Measures Design ◽  
Muscle Trauma ◽  
The Impact

Abstract Background Muscle satellite cells (SCs) are crucial for muscle regeneration following muscle trauma. Acute skeletal muscle damage results in inflammation and production of reactive oxygen species (ROS) which may be implicated in SCs activation. Protection of these cells from oxidative damage is essential to ensure sufficient muscle regeneration. The aim of this study is to determine whether SCs activity under conditions of aseptic skeletal muscle trauma induced by exercise is redox-dependent. Methods/design Based on their SCs content in their vastus lateralis skeletal muscle, participants will be classified as either high or low respondents. In a randomized, double-blind, crossover, repeated measures design, participants will then receive either Placebo or N-acetylcysteine (alters redox potential in muscle) during a preliminary 7-day loading phase, and for 8 consecutive days following a single bout of intense muscle-damaging exercise. In both trials, blood samples and muscle biopsies will be collected, and muscle performance and soreness will be measured at baseline, pre-exercise, 2- and 8-days post-exercise. Biological samples will be analyzed for redox status and SCs activity. Between trials, a 4-week washout period will be implemented. Discussion This study is designed to investigate the impact of redox status on SCs mobilization and thus skeletal muscle potential for regeneration under conditions of aseptic inflammation induced by exercise. Findings of this trial will provide insight into i) molecular pathways involved in SCs recruitment and muscle healing under conditions of aseptic skeletal muscle trauma present in numerous catabolic conditions and ii) if skeletal muscle’s potential for regeneration depends on its basal SCs content.

scholarly journals The redox-dependent regulation of satellite cells following aseptic muscle trauma (SpEED): Study protocol for a randomized controlled trial

2019 ◽  
Author(s):  
Konstantinos Papanikolaou ◽  
Dimitrios Draganidis ◽  
Athanasios Chatzinikolaou ◽  
Vassiliki C. Laschou ◽  
Kalliopi Georgakouli ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cells ◽  
Muscle Regeneration ◽  
Repeated Measures ◽  
Controlled Trial ◽  
Redox Status ◽  
Muscle Performance ◽  
Repeated Measures Design ◽  
Muscle Trauma ◽  
The Impact

Abstract Background Muscle satellite cells (SCs) are crucial for muscle regeneration following muscle trauma. Acute skeletal muscle damage results in inflammation and production of reactive oxygen species (ROS) which may be implicated in SCs activation. Protection of these cells from oxidative damage is essential to ensure sufficient muscle regeneration. The aim of this study is to determine whether SCs activity under conditions of aseptic skeletal muscle trauma induced by exercise is redox-dependent. Methods/design Based on their SCs content in their vastus lateralis skeletal muscle, participants will be classified as either high or low respondents. In a randomized, double-blind, crossover, repeated measures design, participants will then receive either Placebo or N-acetylcysteine (alters redox potential in muscle) during a preliminary 7-day loading phase, and for 8 consecutive days following a single bout of intense muscle-damaging exercise. In both trials, blood samples and muscle biopsies will be collected, and muscle performance and soreness will be measured at baseline, pre-exercise, 2- and 8-days post-exercise. Biological samples will be analyzed for redox status and SCs activity. Between trials, a 4-week washout period will be implemented. Discussion This study is designed to investigate the impact of redox status on SCs mobilization and thus skeletal muscle potential for regeneration under conditions of aseptic inflammation induced by exercise. Findings of this trial will provide insight into i) molecular pathways involved in SCs recruitment and muscle healing under conditions of aseptic skeletal muscle trauma present in numerous catabolic conditions and ii) if skeletal muscle’s potential for regeneration depends on its basal SCs content.

Lack of myostatin alters intermyofibrillar mitochondria activity, unbalances redox status, and impairs tolerance to chronic repetitive contractions in muscle

2012 ◽  
Vol 302 (8) ◽  
pp. E1000-E1008 ◽  
Author(s):  
Claire Ploquin ◽  
Béatrice Chabi ◽  
Gilles Fouret ◽  
Barbara Vernus ◽  
Christine Feillet-Coudray ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Citrate Synthase ◽  
Redox Homeostasis ◽  
Force Production ◽  
Redox Status ◽  
Wild Type ◽  
Endurance Test ◽  
Mitochondrial Content ◽  
Functional Consequences ◽  
Deficient Mice

Loss of myostatin (mstn) function leads to a decrease in mitochondrial content, a reduced expression of cytochrome c oxidase, and a lower citrate synthase activity in skeletal muscle. These data suggest functional or ultrastructural mitochondrial abnormalities that can impact on muscle endurance characteristics in such phenotype. To address this issue, we investigated subsarcolemmal and intermyofibrillar (IMF) mitochondrial activities, skeletal muscle redox homeostasis, and muscle fiber endurance quality in mstn-deficient mice [mstn knockout (KO)]. We report that lack of mstn induced a decrease in the coupling of IMF mitochondria respiration, with significantly higher basal oxygen consumption. No lysis of mitochondrial cristae or excessive swelling were observed in mstn KO mice compared with wild-type (WT) mice. Concerning redox status, mstn KO gastrocnemius exhibited a significant decrease in lipid peroxidation levels (−56%; P < 0.01 vs. WT) together with a significant upregulation of the antioxidant glutathione system. In contrast, superoxide dismutase and catalase activities were altered in mstn KO, gastrocnemius and soleus with a reduction of up to 80% compared with WT animals. The force production observed after contractile endurance test was significantly lower in extensor digitorum longus and soleus muscles of mstn KO mice compared with the controls (17 ± 3 and 36 ± 5% vs. 28 ± 4 and 56 ± 5%, respectively, P < 0.05). Together, these findings indicate that, besides an increased skeletal muscle mass, genetic mstn inhibition has differential effects on redox homeostasis and mitochondrial function that would have functional consequences on muscle response to endurance exercise.

scholarly journals The redox-dependent regulation of satelite cells following aseptic muscle trauma (SpEED): Study protocol for a randomized controlled trial

2019 ◽  
Author(s):  
Konstantinos Papanikolaou ◽  
Athanasios Z. Jamurtas ◽  
Dimitrios Draganidis ◽  
Athanasios Chatzinikolaou ◽  
Vassiliki C. Laschou ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Redox Potential ◽  
Muscle Regeneration ◽  
Repeated Measures ◽  
Controlled Trial ◽  
Redox Status ◽  
Muscle Performance ◽  
Repeated Measures Design ◽  
Muscle Trauma ◽  
The Impact

Abstract Background: Muscle satellite cells (SCs) are crucial for muscle regeneration following muscle trauma. Acute skeletal muscle damage results in inflammation and production of reactive oxygen species (ROS) which may be implicated in SCs activation. Protection of these cells from oxidative damage is essential to ensure sufficient muscle regeneration. The aim of this study is to determine whether SCs activity under conditions of aseptic skeletal muscle trauma induced by exercise is redox-dependent. Methods: Based on their SCs content in their vastus lateralis skeletal muscle, participants will be classified as either high or low respondents. In a randomized, double-blind, crossover, repeated measures design, participants will then receive either Placebo or N-acetylcysteine (alters redox potential in muscle) during a preliminary 7-day loading phase, and for 8 consecutive days following a single bout of intense muscle-damaging exercise. In both trials, blood samples and muscle biopsies will be collected, and muscle performance and soreness will be measured at baseline, pre-exercise, 2- and 8-days post-exercise. Biological samples will be analyzed for redox status and SCs activity. Between trials, a 4-week washout period will be implemented. Discussion: This study is designed to investigate the impact of redox status on SCs mobilization and thus skeletal muscle potential for regeneration under conditions of aseptic inflammation induced by exercise. Findings of this trial will provide insight into i) molecular pathways involved in SCs recruitment and muscle healing under conditions of aseptic skeletal muscle trauma present in numerous catabolic conditions and ii) if skeletal muscle’s potential for regeneration depends on its basal SCs content. Trial registration: ClinicalTrials.gov, NCT03711838; Registered on 10/19/2018. Keywords: Muscle stem cells, cell signaling, antioxidants, redox potential, tissue regeneration.

Aerobic exercise training improves Ca2+ handling and redox status of skeletal muscle in mice

2010 ◽  
Vol 235 (4) ◽  
pp. 497-505 ◽  
Author(s):  
Julio C B Ferreira ◽  
Aline V Bacurau ◽  
Carlos R Bueno ◽  
Telma C Cunha ◽  
Leonardo Y Tanaka ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Muscle Fiber ◽  
Citrate Synthase ◽  
Fiber Type ◽  
Redox Status ◽  
Related Protein ◽  
Cellular Redox ◽  
Running Performance ◽  
Protein Levels

Exercise training is known to promote relevant changes in the properties of skeletal muscle contractility toward powerful fibers. However, there are few studies showing the effect of a well-established exercise training protocol on Ca2+ handling and redox status in skeletal muscles with different fiber-type compositions. We have previously standardized a valid and reliable protocol to improve endurance exercise capacity in mice based on maximal lactate steady-state workload (MLSSw). The aim of this study was to investigate the effect of exercise training, performed at MLSSw, on the skeletal muscle Ca2+ handling-related protein levels and cellular redox status in soleus and plantaris. Male C57BL/6J mice performed treadmill training at MLSSw over a period of eight weeks. Muscle fiber-typing was determined by myosin ATPase histochemistry, citrate synthase activity by spectrophotometric assay, Ca2+ handling-related protein levels by Western blot and reduced to oxidized glutathione ratio (GSH:GSSG) by high-performance liquid chromatography. Trained mice displayed higher running performance and citrate synthase activity compared with untrained mice. Improved running performance in trained mice was paralleled by fast-to-slow fiber-type shift and increased capillary density in both plantaris and soleus. Exercise training increased dihydropyridine receptor (DHPR) α2 subunit, ryanodine receptor and Na+/Ca2+ exchanger levels in plantaris and soleus. Moreover, exercise training elevated DHPR β1 subunit and sarcoplasmic reticulum Ca2+-ATPase (SERCA) 1 levels in plantaris and SERCA2 levels in soleus of trained mice. Skeletal muscle GSH content and GSH:GSSG ratio was increased in plantaris and soleus of trained mice. Taken together, our findings indicate that MLSSw exercise-induced better running performance is, in part, due to increased levels of proteins involved in skeletal muscle Ca2+ handling, whereas this response is partially dependent on specificity of skeletal muscle fiber-type composition. Finally, we demonstrated an augmented cellular redox status and GSH antioxidant capacity in trained mice.

Xanthine oxidase inhibition attenuates skeletal muscle signaling following acute exercise but does not impair mitochondrial adaptations to endurance training

2013 ◽  
Vol 304 (8) ◽  
pp. E853-E862 ◽  
Author(s):  
G. D. Wadley ◽  
M. A. Nicolas ◽  
D. S. Hiam ◽  
G. K. McConell
Keyword(s):  
Skeletal Muscle ◽  
Uric Acid ◽  
Cell Signaling ◽  
Xanthine Oxidase ◽  
Endurance Training ◽  
Acute Exercise ◽  
Citrate Synthase ◽  
Treadmill Running ◽  
Mitochondrial Proteins ◽  
The Impact

The aim of this research was to examine the impact of the xanthine oxidase (XO) inhibitor allopurinol on the skeletal muscle activation of cell signaling kinases' and adaptations to mitochondrial proteins and antioxidant enzymes following acute endurance exercise and endurance training. Male Sprague-Dawley rats performed either acute exercise (60 min of treadmill running, 27 m/min, 5% incline) or 6 wk of endurance training (5 days/wk) while receiving allopurinol or vehicle. Allopurinol treatment reduced XO activity to 5% of the basal levels ( P < 0.05), with skeletal muscle uric acid levels being almost undetectable. Following acute exercise, skeletal muscle oxidized glutathione (GSSG) significantly increased in allopurinol- and vehicle-treated groups despite XO activity and uric acid levels being unaltered by acute exercise ( P < 0.05). This suggests that the source of ROS was not from XO. Surprisingly, muscle GSSG levels were significantly increased following allopurinol treatment. Following acute exercise, allopurinol treatment prevented the increase in p38 MAPK and ERK phosphorylation and attenuated the increase in mitochondrial transcription factor A (mtTFA) mRNA ( P < 0.05) but had no effect on the increase in peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α), nuclear respiratory factor-2, GLUT4, or superoxide dismutase mRNA. Allopurinol also had no impact on the endurance training-induced increases in PGC-1α, mtTFA, and mitochondrial proteins including cytochrome c, citrate synthase, and β-hydroxyacyl-CoA dehydrogenase. In conclusion, although allopurinol inhibits cell signaling pathways in response to acute exercise, the inhibitory effects of allopurinol appear unrelated to exercise-induced ROS production by XO. Allopurinol also has little effect on increases in mitochondrial proteins following endurance training.

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