Modeling of Muscle Atrophy and Exercise Induced Hypertrophy

2017 ◽  
pp. 116-127
Author(s):  
Xianlian Zhou ◽  
Paulien E. Roos ◽  
Xinyu Chen
Keyword(s):  
Muscle Atrophy ◽  
Exercise Induced

GLUCOCORTICOID CYTOSOL BINDING IN EXERCISE-INDUCED SPARING OF MUSCLE ATROPHY

1985 ◽  
Vol 17 (2) ◽  
pp. 261 ◽  
Author(s):  
T. T. Kurowski ◽  
G. H. Andrews ◽  
J. A. Capaccio ◽  
R. T. Chatterton ◽  
R. C. Hickson
Keyword(s):  
Muscle Atrophy ◽  
Exercise Induced

scholarly journals A mini review: Proteomics approaches to understand disused vs. exercised human skeletal muscle

2018 ◽  
Vol 50 (9) ◽  
pp. 746-757 ◽  
Author(s):  
Yoshitake Cho ◽  
Robert S. Ross
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Muscle Atrophy ◽  
Human Skeletal Muscle ◽  
Molecular Mechanisms ◽  
Bed Rest ◽  
Skeletal Muscle Atrophy ◽  
Direct Result ◽  
Muscle Disorders ◽  
Exercise Induced

Immobilization, bed rest, or denervation leads to muscle disuse and subsequent skeletal muscle atrophy. Muscle atrophy can also occur as a component of various chronic diseases such as cancer, AIDS, sepsis, diabetes, and chronic heart failure or as a direct result of genetic muscle disorders. In addition to this atrophic loss of muscle mass, metabolic deregulation of muscle also occurs. In contrast, physical exercise plays a beneficial role in counteracting disuse-induced atrophy by increasing muscle mass and strength. Along with this, exercise can also reduce mitochondrial dysfunction and metabolic deregulation. Still, while exercise causes valuable metabolic and functional adaptations in skeletal muscle, the mechanisms and effectors that lead to these changes such as increased mitochondria content or enhanced protein synthesis are not fully understood. Therefore, mechanistic insights may ultimately provide novel ways to treat disuse induced atrophy and metabolic deregulation. Mass spectrometry (MS)-based proteomics offers enormous promise for investigating the molecular mechanisms underlying disuse and exercise-induced changes in skeletal muscle. This review will focus on initial findings uncovered by using proteomics approaches with human skeletal muscle specimens and discuss their potential for the future study.

Androgen cytosol binding in exercise-induced sparing of muscle atrophy

1984 ◽  
Vol 247 (5) ◽  
pp. E597-E603
Author(s):  
R. C. Hickson ◽  
T. T. Kurowski ◽  
J. A. Capaccio ◽  
R. T. Chatterton
Keyword(s):  
Muscle Atrophy ◽  
Specific Binding ◽  
Exercise Group ◽  
Treadmill Running ◽  
Female Rats ◽  
Binding Model ◽  
Subcutaneous Injections ◽  
Treatment Groups ◽  
Exercise Induced ◽  
Gastrocnemius Muscles

This study was undertaken to determine whether the exercise-induced sparing of glucocorticoid-induced muscle atrophy is related to increased androgen cytosol binding. Female rats were divided into a sedentary or an exercise group that was trained by treadmill running 100 min/day for 13-15 wk. During the last 12 days of training, each of these groups was further subdivided into groups that received daily subcutaneous injections of cortisone acetate (CA) (100 mg/kg body wt) or the vehicle 1% carboxymethyl cellulose. Exercise prevented 30-40% of the weight loss due to CA treatment in gastrocnemius and plantaris muscles. Scatchard analyses of specific binding of [3H]methyltrienolone (R1881), a synthetic androgen that binds to androgen receptors, were nonlinear in muscles from vehicle-treated sedentary and trained rats and were resolved by a two-component binding model. The lower affinity component, which was attributed to a glucocorticoid receptor, disappeared in muscles of glucocorticoid-treated animals as evidenced by linear Scatchard plots. Receptor concentrations of the androgenic component of [3H]methyltrienolone binding were similar in gastrocnemius and plantaris muscles in all treatment groups. In binding specificity studies of gastrocnemius muscles, the relatively high competition by various glucocorticoids and progesterone for [3H]methyltrienolone binding in the vehicle-treated groups was reduced by CA treatment. The lack of change in androgen cytosol receptor levels suggests that this is not a mechanism by which exercise protects against glucocorticoid-induced muscle atrophy.

scholarly journals Maintenance of type 2 glycolytic myofibers with age by Mib1-Actn3 axis

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Ji-Yun Seo ◽  
Jong-Seol Kang ◽  
Ye Lynne Kim ◽  
Young-Woo Jo ◽  
Ji-Hoon Kim ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Atrophy ◽  
Muscle Function ◽  
Therapeutic Potential ◽  
Chronic Exercise ◽  
Skeletal Muscle Function ◽  
Age Related ◽  
Underlying Mechanisms ◽  
Exercise Induced

AbstractAge-associated muscle atrophy is a debilitating condition associated with loss of muscle mass and function with age that contributes to limitation of mobility and locomotion. However, the underlying mechanisms of how intrinsic muscle changes with age are largely unknown. Here we report that, with age, Mind bomb-1 (Mib1) plays important role in skeletal muscle maintenance via proteasomal degradation-dependent regulation of α-actinin 3 (Actn3). The disruption of Mib1 in myofibers (Mib1ΔMF) results in alteration of type 2 glycolytic myofibers, muscle atrophy, impaired muscle function, and Actn3 accumulation. After chronic exercise, Mib1ΔMF mice show muscle atrophy even at young age. However, when Actn3 level is downregulated, chronic exercise-induced muscle atrophy is ameliorated. Importantly, the Mib1 and Actn3 levels show clinical relevance in human skeletal muscles accompanied by decrease in skeletal muscle function with age. Together, these findings reveal the significance of the Mib1-Actn3 axis in skeletal muscle maintenance with age and suggest the therapeutic potential for the treatment or amelioration of age-related muscle atrophy.

Effects of Antioxidant Supplementation and Exercise Training on Erythrocyte Antioxidant Enzymes

2006 ◽  
Vol 76 (5) ◽  
pp. 324-331 ◽  
Author(s):  
Marsh ◽  
Laursen ◽  
Coombes
Keyword(s):  
Antioxidant Enzymes ◽  
Exercise Training ◽  
Endurance Training ◽  
Young Male ◽  
Antioxidant Defenses ◽  
Antioxidant Enzyme Activities ◽  
Antioxidant Supplementation ◽  
Male Wistar Rats ◽  
Exercise Induced ◽  
Antioxidant Supplements

Erythrocytes transport oxygen to tissues and exercise-induced oxidative stress increases erythrocyte damage and turnover. Increased use of antioxidant supplements may alter protective erythrocyte antioxidant mechanisms during training. Aim of study: To examine the effects of antioxidant supplementation (α-lipoic acid and α-tocopherol) and/or endurance training on the antioxidant defenses of erythrocytes. Methods: Young male Wistar rats were assigned to (1) sedentary; (2) sedentary and antioxidant-supplemented; (3) endurance-trained; or (4) endurance-trained and antioxidant-supplemented groups for 14 weeks. Erythrocyte superoxide dismutase (SOD), glutathione peroxidase (GPX), and catalase (CAT) activities, and plasma malondialdehyde (MDA) were then measured. Results: Antioxidant supplementation had no significant effect (p > 0.05) on activities of antioxidant enzymes in sedentary animals. Similarly, endurance training alone also had no effect (p > 0.05). GPX (125.9 ± 2.8 vs. 121.5 ± 3.0 U.gHb–1, p < 0.05) and CAT (6.1 ± 0.2 vs. 5.6 ± 0.2 U.mgHb–1, p < 0.05) activities were increased in supplemented trained animals compared to non-supplemented sedentary animals whereas SOD (61.8 ± 4.3 vs. 52.0 ± 5.2 U.mgHb–1, p < 0.05) activity was decreased. Plasma MDA was not different among groups (p > 0.05). Conclusions: In a rat model, the combination of exercise training and antioxidant supplementation increased antioxidant enzyme activities (GPX, CAT) compared with each individual intervention.

Trans-resveratrol supplement lowers lipid peroxidation responses of exercise in male Wistar rats

2020 ◽  
pp. 1-6 ◽  
Author(s):  
Masoud Nasiri ◽  
Saja Ahmadizad ◽  
Mehdi Hedayati ◽  
Tayebe Zarekar ◽  
Mehdi Seydyousefi ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Antioxidant Capacity ◽  
Total Antioxidant Capacity ◽  
Wistar Rats ◽  
Enzymatic Antioxidants ◽  
Acute Response ◽  
Total Antioxidant ◽  
Male Wistar Rats ◽  
Exercise Induced ◽  
And Control

Abstract. Physical exercise increases free radicals production; antioxidant supplementation may improve the muscle fiber’s ability to scavenge ROS and protect muscles against exercise-induced oxidative damage. This study was designed to examine the effects of all-trans resveratrol supplementation as an antioxidant to mediate anti-oxidation and lipid per-oxidation responses to exercise in male Wistar rats. Sixty-four male Wistar rats were randomly divided into four equal number (n = 16) including training + supplement (TS), training (T), supplement (S) and control (C) group. The rats in TS and S groups received a dose of 10 mg/kg resveratrol per day via gavage. The training groups ran on a rodent treadmill 5 times per week at the speed of 10 m/min for 10 min; the speed gradually increased to 30 m/min for 60 minutes at the end of 12th week. The acute phase of exercise protocol included a speed of 25 m/min set to an inclination of 10° to the exhaustion point. Superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) activity, non-enzymatic antioxidants bilirubin, uric acid, lipid peroxidation levels (MDA) and the total antioxidant capacity (TAC) were measured after the exercise termination. The data were analyzed by using one-way ANOVA. The result showed that endurance training caused a significant increase in MDA level [4.5 ± 0.75 (C group) vs. 5.9 ± 0.41 nmol/l (T group)] whereas it decreased the total antioxidant capacity [8.5 ± 1.35 (C group) vs. 7.1 ± 0.55 mmol/l (T group)] (p = 0.001). In addition, GPx and CAT decreased but not significantly (p > 0.05). The training and t-resveratrol supplementation had no significant effect on the acute response of all variables except MDA [4.3 ± 1.4 (C group) vs. 4.0 ± 0.90 nmol/l (TS group)] (p = 0.001) and TAC [8.5 ± 0.90 (C group) vs. 6.6 ± 0.80 mmol/l (TS group)] (p = 0.004). It was concluded that resveratrol supplementation may prevent exercise-induced oxidative stress by preventing lipid peroxidation.

Exercise-induced Anaphylaxis to Cabbage and Mustard

2003 ◽  
Vol 15 (04) ◽  
pp. 181-183 ◽  
Author(s):  
Anja Lingelbach ◽  
Jürgen Rakoski ◽  
Johannes Ring
Keyword(s):  
Exercise Induced
Sign in / Sign up

Export Citation Format

Share Document