scholarly journals Increased 1,25(OH)2-Vitamin D Concentrations after Energy Restriction Are Associated with Changes in Skeletal Muscle Phenotype

Nutrients ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 607
Author(s):  
Angela Vidal ◽  
Rafael Rios ◽  
Carmen Pineda ◽  
Ignacio Lopez ◽  
Ana I. Raya ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Vitamin D ◽  
Muscle Mass ◽  
Fiber Type ◽  
Control Diet ◽  
Energy Restriction ◽  
Plasma Vitamin ◽  
Type I ◽  
Vitamin D Metabolites ◽  
Muscle Weight

The influence of energy restriction (ER) on muscle is controversial, and the mechanisms are not well understood. To study the effect of ER on skeletal muscle phenotype and the influence of vitamin D, rats (n = 34) were fed a control diet or an ER diet. Muscle mass, muscle somatic index (MSI), fiber-type composition, fiber size, and metabolic activity were studied in tibialis cranialis (TC) and soleus (SOL) muscles. Plasma vitamin D metabolites and renal expression of enzymes involved in vitamin D metabolism were measured. In the ER group, muscle weight was unchanged in TC and decreased by 12% in SOL, but MSI increased in both muscles (p < 0.0001) by 55% and 36%, respectively. Histomorphometric studies showed 14% increase in the percentage of type IIA fibers and 13% reduction in type IIX fibers in TC of ER rats. Decreased size of type I fibers and reduced oxidative activity was identified in SOL of ER rats. An increase in plasma 1,25(OH)2-vitamin D (169.7 ± 6.8 vs. 85.4 ± 11.5 pg/mL, p < 0.0001) with kidney up-regulation of CYP27b1 and down-regulation of CYP24a1 was observed in ER rats. Plasma vitamin D correlated with MSI in both muscles (p < 0.001), with the percentages of type IIA and type IIX fibers in TC and with the oxidative profile in SOL. In conclusion, ER preserves skeletal muscle mass, improves contractile phenotype in phasic muscles (TC), and reduces energy expenditure in antigravity muscles (SOL). These beneficial effects are closely related to the increases in vitamin D secondary to ER.

Skeletal muscle myostatin mRNA expression is fiber-type specific and increases during hindlimb unloading

1999 ◽  
Vol 277 (2) ◽  
pp. R601-R606 ◽  
Author(s):  
Christian J. Carlson ◽  
Frank W. Booth ◽  
Scott E. Gordon
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Soleus Muscle ◽  
Fiber Type ◽  
Weight Bearing ◽  
Mrna Abundance ◽  
Hindlimb Unloading ◽  
Negative Regulator ◽  
Type I ◽  
Mrna Levels

Transgenic mice lacking a functional myostatin (MSTN) gene demonstrate greater skeletal muscle mass resulting from muscle fiber hypertrophy and hyperplasia (McPherron, A. C., A. M. Lawler, and S.-J. Lee. Nature 387: 83–90, 1997). Therefore, we hypothesized that, in normal mice, MSTN may act as a negative regulator of muscle mass. Specifically, we hypothesized that the predominately slow (type I) soleus muscle, which demonstrates greater atrophy than the fast (type II) gastrocnemius-plantaris complex (Gast/PLT), would show more elevation in MSTN mRNA abundance during hindlimb unloading (HU). Surprisingly, MSTN mRNA was not detectable in weight-bearing or HU soleus muscle, which atrophied 42% by the 7th day of HU in female ICR mice. In contrast, MSTN mRNA was present in weight-bearing Gast/PLT muscle and was significantly elevated (67%) at 1 day but not at 3 or 7 days of HU. However, the Gast/PLT muscle had only atrophied 17% by the 7th day of HU. Because the soleus is composed only of type I and IIa fibers, whereas the Gast/PLT expresses type IId/x and IIb in addition to type I and IIa, it was necessary to perform a more careful analysis of the relationship between MSTN mRNA levels and myosin heavy-chain (MHC) isoform expression (as a marker of fiber type). A significant correlation ( r = 0.725, P < 0.0005) was noted between the percentage of MHC isoform IIb expression and MSTN mRNA abundance in several muscles of the mouse hindlimb. These results indicate that MSTN expression is not strongly associated with muscle atrophy induced by HU; however, it is strongly associated with MHC isoform IIb expression in normal muscle.

scholarly journals Gsα deficiency in skeletal muscle leads to reduced muscle mass, fiber-type switching, and glucose intolerance without insulin resistance or deficiency

2009 ◽  
Vol 296 (4) ◽  
pp. C930-C940 ◽  
Author(s):  
Min Chen ◽  
Han-Zhong Feng ◽  
Divakar Gupta ◽  
James Kelleher ◽  
Kathryn E. Dickerson ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Fiber Type ◽  
Oxidative Capacity ◽  
Whole Body ◽  
Kinetic Properties ◽  
Intracellular Camp ◽  
Type I ◽  
Muscle Adaptation ◽  
Α Subunit

The ubiquitously expressed G protein α-subunit Gsα is required for receptor-stimulated intracellular cAMP responses and is an important regulator of energy and glucose metabolism. We have generated skeletal muscle-specific Gsα-knockout (KO) mice (MGsKO) by mating Gsα-floxed mice with muscle creatine kinase-cre transgenic mice. MGsKO mice had normal body weight and composition, and their serum glucose, insulin, free fatty acid, and triglyceride levels were similar to that of controls. However, MGsKO mice were glucose intolerant despite the fact that insulin sensitivity and glucose-stimulated insulin secretion were normal, suggesting an insulin-independent mechanism. Isolated muscles from MGsKO mice had increased basal glucose uptake and normal responses to a stimulator of AMP-activated protein kinase (AMPK), which indicates that AMPK and its downstream pathways are intact. Compared with control mice, MGsKO mice had reduced muscle mass with decreased cross-sectional area and force production. In addition, adult MGsKO mice showed an increased proportion of type I (slow-twitch, oxidative) fibers based on kinetic properties and myosin heavy chain isoforms, despite the fact that these muscles had reduced expression of peroxisome proliferator-activated receptor coactivator protein-1α (PGC-1α) and reduced mitochondrial content and oxidative capacity. Therefore Gsα deficiency led to fast-to-slow fiber-type switching, which appeared to be dissociated from the expected change in oxidative capacity. MGsKO mice are a valuable model for future studies of the role of Gsα signaling pathways in skeletal muscle adaptation and their effects on whole body metabolism.

scholarly journals AMPK Mediates Muscle Mass Change But Not the Transition of Myosin Heavy Chain Isoforms during Unloading and Reloading of Skeletal Muscles in Mice

2018 ◽  
Vol 19 (10) ◽  
pp. 2954 ◽  
Author(s):  
Tatsuro Egawa ◽  
Yoshitaka Ohno ◽  
Ayumi Goto ◽  
Shingo Yokoyama ◽  
Tatsuya Hayashi ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Myosin Heavy Chain ◽  
Muscle Mass ◽  
Heavy Chain ◽  
Fiber Type ◽  
Dominant Negative ◽  
Hindlimb Unloading ◽  
Mass Change ◽  
Muscle Weight ◽  
Myhc Isoforms

5′AMP-activated protein kinase (AMPK) plays an important role in the regulation of skeletal muscle mass and fiber-type distribution. However, it is unclear whether AMPK is involved in muscle mass change or transition of myosin heavy chain (MyHC) isoforms in response to unloading or increased loading. Here, we checked whether AMPK controls muscle mass change and transition of MyHC isoforms during unloading and reloading using mice expressing a skeletal-muscle-specific dominant-negative AMPKα1 (AMPK-DN). Fourteen days of hindlimb unloading reduced the soleus muscle weight in wild-type and AMPK-DN mice, but reduction in the muscle mass was partly attenuated in AMPK-DN mice. There was no difference in the regrown muscle weight between the mice after 7 days of reloading, and there was concomitantly reduced AMPKα2 activity, however it was higher in AMPK-DN mice after 14 days reloading. No difference was observed between the mice in relation to the levels of slow-type MyHC I, fast-type MyHC IIa/x, and MyHC IIb isoforms following unloading and reloading. The levels of 72-kDa heat-shock protein, which preserves muscle mass, increased in AMPK-DN-mice. Our results indicate that AMPK mediates the progress of atrophy during unloading and regrowth of atrophied muscles following reloading, but it does not influence the transition of MyHC isoforms.

Diabetic myopathy differs betweenIns2Akita+/−and streptozotocin-induced Type 1 diabetic models

2009 ◽  
Vol 106 (5) ◽  
pp. 1650-1659 ◽  
Author(s):  
Matthew P. Krause ◽  
Michael C. Riddell ◽  
Carly S. Gordon ◽  
S. Abdullah Imam ◽  
Enzo Cafarelli ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Citrate Synthase ◽  
Genetic Model ◽  
Fiber Type ◽  
Type I ◽  
Phenotypic Properties ◽  
Current State ◽  
Type I Fibers

Mechanistic studies examining the effects of Type 1 diabetes mellitus (T1DM) on skeletal muscle have largely relied on streptozotocin-induced diabetic (STZ) rodents. Unfortunately, characterization of diabetic myopathy in this model is confounded by the effects of streptozotocin on skeletal muscle independent of the diabetic phenotype. Here we define adolescent diabetic myopathy in a novel, genetic model of T1DM, Ins2Akita+/−mice, and contrast these findings with STZ mice. Eight weeks of diabetes resulted in significantly reduced gastrocnemius-plantaris-soleus mass (control: 0.16 ± 0.005 g; Ins2Akita+/−: 0.12 ± 0.003 g; STZ: 0.12 ± 0.01g) and IIB/D fiber area in Ins2Akita+/−(1,294 ± 94 μm2) and STZ (1,768 ± 163 μm2) compared with control (2,241 ± 144 μm2). Conversely, STZ type I fibers (1,535 ± 165 μm2) were significantly larger than Ins2Akita+/−(915 ± 76 μm2) but not control (1,152 ± 86 μm2). Intramyocellular lipid increased in STZ (122.9 ± 3.6% of control) but not Ins2Akita+/−likely resultant from depressed citrate synthase (control: 6.2 ± 1.2 μmol·s−1·mg−1; Ins2Akita+/−: 5.2 ± 0.8 μmol·s−1·mg−1; STZ: 2.8 ± 0.5 μmol·s−1·mg−1) and 3-β-hydroxyacyl coenzyme-A dehydrogenase (control: 4.2 ± 0.6 nmol·s−1·mg−1; Ins2Akita+/−: 5.0 ± 0.6 nmol·s−1·mg−1; STZ: 2.7 ± 0.6 nmol·s−1·mg−1) enzyme activity in STZ muscle. In situ muscle stimulation revealed lower absolute peak tetanic force in Ins2Akita+/−(70.2 ± 8.2% of control) while STZ exhibited an insignificant decrease (87.6 ± 7.9% of control). Corrected for muscle mass, no force loss was observed in Ins2Akita+/−, while STZ was significantly elevated vs. control and Ins2Akita+/−. These results demonstrate that atrophy and specific fiber-type loss in Ins2Akita+/−muscle did not affect contractile properties (relative to muscle mass). Furthermore, we demonstrate distinctive contractile, metabolic, and phenotypic properties in STZ vs. Ins2Akita+/−diabetic muscle despite similarity in hyperglycemia/hypoinsulinemia, raising concerns of our current state of knowledge regarding the effects of T1DM on skeletal muscle.

scholarly journals Methionine restriction plus overload improves skeletal muscle and metabolic health in old mice on a high fat diet

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Anandini Swaminathan ◽  
Andrej Fokin ◽  
Tomas Venckūnas ◽  
Hans Degens
Keyword(s):  
Skeletal Muscle ◽  
Glucose Tolerance ◽  
Muscle Mass ◽  
Body Mass ◽  
High Fat Diet ◽  
Control Diet ◽  
Metabolic Health ◽  
High Fat ◽  
Methionine Restriction ◽  
Old Mice

AbstractMethionine restriction (MR) has been shown to reduce the age-induced inflammation. We examined the effect of MR (0.17% methionine, 10% kCal fat) and MR + high fat diet (HFD) (0.17% methionine, 45% kCal fat) on body mass, food intake, glucose tolerance, resting energy expenditure, hind limb muscle mass, denervation-induced atrophy and overload-induced hypertrophy in young and old mice. In old mice, MR and MR + HFD induced a decrease in body mass. Muscle mass per body mass was lower in old compared to young mice. MR restored some of the HFD-induced reduction in muscle oxidative capacity. The denervation-induced atrophy of the m. gastrocnemius was larger in animals on MR than on a control diet, irrespective of age. Old mice on MR had larger hypertrophy of m. plantaris. Irrespective of age, MR and MR + HFD had better glucose tolerance compared to the other groups. Young and old mice on MR + HFD had a higher resting VO2 per body mass than HFD group. Mice on MR and MR + HFD had a resting respiratory quotient closer to 0.70, irrespective of age, indicating an increased utilization of lipids. In conclusion, MR in combination with resistance training may improve skeletal muscle and metabolic health in old age even in the face of obesity.

scholarly journals Serum levels of bone formation and resorption markers in relation to vitamin D status in professional gymnastics and physically active men during upper and lower body high-intensity exercise

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Jan Mieszkowski ◽  
Andrzej Kochanowicz ◽  
Elżbieta Piskorska ◽  
Bartłomiej Niespodziński ◽  
Joanna Siódmiak ◽  
...  
Keyword(s):  
Vitamin D ◽  
Bone Formation ◽  
Bone Turnover ◽  
Bone Turnover Markers ◽  
Type I Collagen ◽  
Serum Levels ◽  
Type I ◽  
Vitamin D Metabolites ◽  
Physically Active ◽  
Turnover Markers

Abstract Purpose/introduction To compare serum levels of bone turnover markers in athletes and non-athletes, and to evaluate the relationship between serum levels of vitamin D metabolites and exercise-induced changes in biomarker levels. Methods Sixteen elite male artistic gymnasts (EG; 21.4 ± 0.8 years-old) and 16 physically active men (the control group, PAM; 20.9 ± 1.2 years-old) performed lower and upper body 30-s Wingate anaerobic tests (LBWT and UBWT, respectively). For biomarker analysis, blood samples were collected before, and 5 and 30 min after exercise. Samples for vitamin D levels were collected before exercise. N-terminal propeptide of type I collagen (PINP) was analysed as a marker of bone formation. C-terminal telopeptide of type I collagen (CTX) was analysed as a marker of bone resorption. Results UBWT fitness readings were better in the EG group than in the PAM group, with no difference in LBWT readings between the groups. UBWT mean power was 8.8% higher in subjects with 25(OH)D3 levels over 22.50 ng/ml and in those with 24,25(OH)2D3 levels over 1.27 ng/ml. Serum CTX levels increased after both tests in the PAM group, with no change in the EG group. PINP levels did not change in either group; however, in PAM subjects with 25(OH)D3 levels above the median, they were higher than those in EG subjects. Conclusion Vitamin D metabolites affect the anaerobic performance and bone turnover markers at rest and after exercise. Further, adaptation to physical activity modulates the effect of anaerobic exercise on bone metabolism markers.

scholarly journals Prediagnostic Plasma Vitamin D Metabolites and Mortality among Patients with Prostate Cancer

PLoS ONE ◽  
2011 ◽  
Vol 6 (4) ◽  
pp. e18625 ◽  
Author(s):  
Fang Fang ◽  
Julie L. Kasperzyk ◽  
Irene Shui ◽  
Whitney Hendrickson ◽  
Bruce W. Hollis ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Vitamin D ◽  
Plasma Vitamin ◽  
Vitamin D Metabolites

scholarly journals Combining Amino Acid and Vitamin D Supplementation with Exercise Training Increases Skeletal Muscle Mass and Prevent Bone Mineral Density Loss in Participants with Low Muscle Mass

2017 ◽  
Vol 10 (2) ◽  
pp. 28
Author(s):  
Ha Cao Thi Thu ◽  
Satoshi Kurose ◽  
Yaeko Fukushima ◽  
Nana Takao ◽  
Natsuko Nakamura ◽  
...  
Keyword(s):  
Bone Mineral Density ◽  
Skeletal Muscle ◽  
Vitamin D ◽  
Body Composition ◽  
Amino Acid ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Vitamin D Supplementation ◽  
Mineral Density ◽  
Supplement Group

This study evaluated the impact of exercise training with amino acid and vitamin D supplementation on muscle and bone mass in participants with low muscle volume. Twenty-nine Japanese participants (56-84 years old) were enrolled and assigned into the supplement (n=15) and non-supplement (n=14) groups. All participants underwent a 6-month exercise program. Supplements and nutrition support were provided to the participants in the supplement group for 12 weeks. Body composition and whole bone mineral density (BMD) were measured using dual energy x-ray absorptiometry. The outcomes, including body composition, whole BMD, and skeletal muscle mass index (SMI), were evaluated twice: pre- and post-intervention. The SMI was 6.51(6.28; 7.14) and 5.58 (5.24; 6.05) (kg/m2) in men and women, respectively. The average SMI change was 0.13% (-0.05%; 0.31%) and 2.33% (-0.88%; 5.48%); [mean (lower; upper quartile)]. The average BMD loss in the non-supplement group was -2.78%, and the BMD increased in the supplement group by 4.34%; there was an absolute difference between the two groups (p<0.05). After the intervention, serum myostatin was changed (p=0.001, non-supplement>supplement), serum vitamin D was increased (p=0.03; supplement>non-supplement), and BMD was maintained (p=0.03, supplement>non-supplement). There was a significant difference in the serum myostatin level at baseline and at 6-month in the non-supplement group, with a mean difference of 483.78 ng/ml (p=0.01). There was no significant improvement in the total lean mass, and handgrip strength. Resistance exercise combined with an amino acid supplement affects muscle and bone mass in the short-term intervention.

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