scholarly journals Relationship between intermuscular adipose tissue infiltration and myostatin before and after aerobic exercise training

2018 ◽  
Vol 315 (3) ◽  
pp. R461-R468 ◽  
Author(s):  
Adam R. Konopka ◽  
Christopher A. Wolff ◽  
Miranda K. Suer ◽  
Matthew P. Harber
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Exercise Training ◽  
Aerobic Exercise ◽  
Exercise Capacity ◽  
Muscle Function ◽  
Aerobic Exercise Training ◽  
Skeletal Muscle Function ◽  
Intermuscular Adipose Tissue ◽  
Before And After

Intermuscular adipose tissue (IMAT) is associated with impaired skeletal muscle contractile and metabolic function. Myostatin and downstream signaling proteins such as cyclin-dependent kinase 2 (CDK2) contribute to the regulation of adipose and skeletal muscle mass in cell culture and animals models, but this relationship remains incompletely understood in humans. The purpose of this study was to determine if the infiltration of IMAT was associated with skeletal muscle myostatin and downstream proteins before and after 12 wk of aerobic exercise training (AET) in healthy older women (OW; 69 ± 2 yr), older men (OM; 74 ± 3 yr), and young men (YM; 20 ± 1 yr). We found that the infiltration of IMAT was correlated with myostatin and phosphorylated CDK2 at tyrosine 15 [P-CDK2(Tyr15)]. IMAT infiltration was greater in the older subjects and was associated with lower skeletal muscle function and exercise capacity. After 12 wk of AET, there was no change in body weight. Myostatin and P-CDK2(Tyr15) were both decreased after AET, and the reduction in myostatin was associated with decreased IMAT infiltration. The decrease in myostatin and IMAT occurred concomitantly with increased exercise capacity, skeletal muscle size, and function after AET. These findings demonstrate that the reduction in IMAT infiltration after AET in weight stable individuals was accompanied by improvements in skeletal muscle function and exercise capacity. Moreover, the association between myostatin and IMAT was present in the untrained state and in response to exercise training, strengthening the potential regulatory role of myostatin on IMAT.

Aerobic exercise training improves skeletal muscle function and Ca2+ handling-related protein expression in sympathetic hyperactivity-induced heart failure

2010 ◽  
Vol 109 (3) ◽  
pp. 702-709 ◽  
Author(s):  
C. R. Bueno ◽  
J. C. B. Ferreira ◽  
M. G. Pereira ◽  
A. V. N. Bacurau ◽  
P. C. Brum
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Protein Expression ◽  
Aerobic Exercise ◽  
Muscle Function ◽  
Exercise Tolerance ◽  
Aerobic Exercise Training ◽  
Related Protein ◽  
Skeletal Muscle Function ◽  
Related Proteins

The cellular mechanisms of positive effects associated with aerobic exercise training on overall intrinsic skeletal muscle changes in heart failure (HF) remain unclear. We investigated potential Ca2+ abnormalities in skeletal muscles comprising different fiber compositions and investigated whether aerobic exercise training would improve muscle function in a genetic model of sympathetic hyperactivity-induced HF. A cohort of male 5-mo-old wild-type (WT) and congenic α2A/α2C adrenoceptor knockout (ARKO) mice in a C57BL/6J genetic background were randomly assigned into untrained and trained groups. Exercise training consisted of a 8-wk running session of 60 min, 5 days/wk (from 5 to 7 mo of age). After completion of the exercise training protocol, exercise tolerance was determined by graded treadmill exercise test, muscle function test by Rotarod, ambulation and resistance to inclination tests, cardiac function by echocardiography, and Ca2+ handling-related protein expression by Western blot. α2A/α2CARKO mice displayed decreased ventricular function, exercise intolerance, and muscle weakness paralleled by decreased expression of sarcoplasmic Ca2+ release-related proteins [α1-, α2-, and β1-subunits of dihydropyridine receptor (DHPR) and ryanodine receptor (RyR)] and Ca2+ reuptake-related proteins [sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA)1/2 and Na+/Ca2+ exchanger (NCX)] in soleus and plantaris. Aerobic exercise training significantly improved exercise tolerance and muscle function and reestablished the expression of proteins involved in sarcoplasmic Ca2+ handling toward WT levels. We provide evidence that Ca2+ handling-related protein expression is decreased in this HF model and that exercise training improves skeletal muscle function associated with changes in the net balance of skeletal muscle Ca2+ handling proteins.

scholarly journals Insulin-resistant subjects have normal angiogenic response to aerobic exercise training in skeletal muscle, but not in adipose tissue

2015 ◽  
Vol 3 (6) ◽  
pp. e12415 ◽  
Author(s):  
R. Grace Walton ◽  
Brian S. Finlin ◽  
Jyothi Mula ◽  
Douglas E. Long ◽  
Beibei Zhu ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Exercise Training ◽  
Aerobic Exercise ◽  
Aerobic Exercise Training ◽  
Angiogenic Response ◽  
Insulin Resistant

scholarly journals GREM1 is epigenetically reprogrammed in muscle cells after exercise training and controls myogenesis and metabolism

2020 ◽  
Author(s):  
Odile Fabre ◽  
Lorenzo Giordani ◽  
Alice Parisi ◽  
Pattarawan Pattamaprapanont ◽  
Danial Ahwazi ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Stem Cells ◽  
Exercise Training ◽  
Muscle Function ◽  
Negative Control ◽  
Epigenetic Mechanism ◽  
Differentially Methylated Region ◽  
Skeletal Muscle Function ◽  
Muscle Stem Cells ◽  
Before And After

AbstractExercise training improves skeletal muscle function, notably through tissue regeneration by muscle stem cells. Here, we hypothesized that exercise training reprograms the epigenome of muscle cell, which could account for better muscle function. Genome-wide DNA methylation of myotube cultures established from middle-aged obese men before and after endurance exercise training identified a differentially methylated region (DMR) located downstream of Gremlin 1 (GREM1), which was associated with increased GREM1 expression. GREM1 expression was lower in muscle satellite cells from obese, compared to lean mice, and exercise training restored GREM1 levels to those of control animals. We show that GREM1 regulates muscle differentiation through the negative control of satellite cell self-renewal, and that GREM1 controls muscle lineage commitment and lipid oxidation through the AMPK pathway. Our study identifies novel functions of GREM1 and reveals an epigenetic mechanism by which exercise training reprograms muscle stem cells to improve skeletal muscle function.

Exercise training favors increased insulin-stimulated glucose uptake in skeletal muscle in contrast to adipose tissue: a randomized study using FDG PET imaging

2013 ◽  
Vol 305 (4) ◽  
pp. E496-E506 ◽  
Author(s):  
M. H. Reichkendler ◽  
P. Auerbach ◽  
M. Rosenkilde ◽  
A. N. Christensen ◽  
S. Holm ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Exercise Training ◽  
Physical Exercise ◽  
Aerobic Exercise ◽  
Glucose Uptake ◽  
Fdg Pet ◽  
Aerobic Exercise Training ◽  
Femoral Muscle ◽  
Muscle Groups

Physical exercise increases peripheral insulin sensitivity, but regional differences are poorly elucidated in humans. We investigated the effect of aerobic exercise training on insulin-stimulated glucose uptake in five individual femoral muscle groups and four different adipose tissue regions, using dynamic (femoral region) and static (abdominal region) 2-deoxy-2-[18F]fluoro-d-glucose (FDG) PET/CT methodology during steady-state insulin infusion (40 mU·m−2·min−1). Body composition was measured by dual X-ray absorptiometry and MRI. Sixty-one healthy, sedentary [V̇o2max 36(5) ml·kg−1·min−1; mean(SD)], moderately overweight [BMI 28.1(1.8) kg/m2], young [age: 30(6) yr] men were randomized to sedentary living (CON; n = 17 completers) or moderate (MOD; 300 kcal/day, n = 18) or high (HIGH; 600 kcal/day, n = 18) dose physical exercise for 11 wk. At baseline, insulin-stimulated glucose uptake was highest in femoral skeletal muscle followed by intraperitoneal visceral adipose tissue (VAT), retroperitoneal VAT, abdominal (anterior + posterior) subcutaneous adipose tissue (SAT), and femoral SAT ( P < 0.0001 between tissues). Metabolic rate of glucose increased similarly (∼30%) in the two exercise groups in femoral skeletal muscle (MOD 24[9, 39] μmol·kg−1·min−1, P = 0.004; HIGH 22[9, 35] μmol·kg−1·min−1, P = 0.003) (mean[95% CI]) and in five individual femoral muscle groups but not in femoral SAT. Standardized uptake value of FDG decreased ∼24% in anterior abdominal SAT and ∼20% in posterior abdominal SAT compared with CON but not in either intra- or retroperitoneal VAT. Total adipose tissue mass decreased in both exercise groups, and the decrease was distributed equally among subcutaneous and intra-abdominal depots. In conclusion, aerobic exercise training increases insulin-stimulated glucose uptake in skeletal muscle but not in adipose tissue, which demonstrates some interregional differences.

Combination of Exercise Training and Diet Restriction Normalizes Limited Exercise Capacity and Impaired Skeletal Muscle Function in Diet-Induced Diabetic Mice

Endocrinology ◽  
2014 ◽  
Vol 155 (1) ◽  
pp. 68-80 ◽  
Author(s):  
Tadashi Suga ◽  
Shintaro Kinugawa ◽  
Shingo Takada ◽  
Tomoyasu Kadoguchi ◽  
Arata Fukushima ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Exercise Training ◽  
Exercise Capacity ◽  
Muscle Function ◽  
Normal Diet ◽  
Diabetic Mice ◽  
Diet Restriction ◽  
Skeletal Muscle Function

Exercise training (EX) and diet restriction (DR) are essential for effective management of obesity and insulin resistance in diabetes mellitus. However, whether these interventions ameliorate the limited exercise capacity and impaired skeletal muscle function in diabetes patients remains unexplored. Therefore, we investigated the effects of EX and/or DR on exercise capacity and skeletal muscle function in diet-induced diabetic mice. Male C57BL/6J mice that were fed a high-fat diet (HFD) for 8 weeks were randomly assigned for an additional 4 weeks to 4 groups: control, EX, DR, and EX+DR. A lean group fed with a normal diet was also studied. Obesity and insulin resistance induced by a HFD were significantly but partially improved by EX or DR and completely reversed by EX+DR. Although exercise capacity decreased significantly with HFD compared with normal diet, it partially improved with EX and DR and completely reversed with EX+DR. In parallel, the impaired mitochondrial function and enhanced oxidative stress in the skeletal muscle caused by the HFD were normalized only by EX+DR. Although obesity and insulin resistance were completely reversed by DR with an insulin-sensitizing drug or a long-term intervention, the exercise capacity and skeletal muscle function could not be normalized. Therefore, improvement in impaired skeletal muscle function, rather than obesity and insulin resistance, may be an important therapeutic target for normalization of the limited exercise capacity in diabetes. In conclusion, a comprehensive lifestyle therapy of exercise and diet normalizes the limited exercise capacity and impaired muscle function in diabetes mellitus.

scholarly journals Dynamic changes in DICER levels in adipose tissue control metabolic adaptations to exercise

2020 ◽  
Vol 117 (38) ◽  
pp. 23932-23941
Author(s):  
Bruna B. Brandão ◽  
Søren Madsen ◽  
Atefeh Rabiee ◽  
Matteo Oliverio ◽  
Gabriel P. Ruiz ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Exercise Training ◽  
Aerobic Exercise ◽  
Metabolic Stress ◽  
Aerobic Exercise Training ◽  
Whole Body ◽  
Mirna Biogenesis ◽  
Skeletal Muscle Function ◽  
Metabolic Adaptations ◽  
Key Enzyme

DICER is a key enzyme in microRNA (miRNA) biogenesis. Here we show that aerobic exercise training up-regulates DICER in adipose tissue of mice and humans. This can be mimicked by infusion of serum from exercised mice into sedentary mice and depends on AMPK-mediated signaling in both muscle and adipocytes. Adipocyte DICER is required for whole-body metabolic adaptations to aerobic exercise training, in part, by allowing controlled substrate utilization in adipose tissue, which, in turn, supports skeletal muscle function. Exercise training increases overall miRNA expression in adipose tissue, and up-regulation of miR-203-3p limits glycolysis in adipose under conditions of metabolic stress. We propose that exercise training-induced DICER-miR-203-3p up-regulation in adipocytes is a key adaptive response that coordinates signals from working muscle to promote whole-body metabolic adaptations.

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