scholarly journals Recovery of muscle mass and muscle oxidative phenotype following disuse does not require GSK-3 inactivation

2020 ◽  
Vol 1866 (6) ◽  
pp. 165740 ◽  
Author(s):  
Wessel F. Theeuwes ◽  
Nicholas A.M. Pansters ◽  
Harry R. Gosker ◽  
Annemie M.W.J. Schols ◽  
Koen J.P. Verhees ◽  
...  
Keyword(s):  
Muscle Mass ◽  
Oxidative Phenotype

scholarly journals The mechanisms of cachexia underlying muscle dysfunction in COPD

2013 ◽  
Vol 114 (9) ◽  
pp. 1253-1262 ◽  
Author(s):  
A. H. V. Remels ◽  
H. R. Gosker ◽  
R. C. J. Langen ◽  
A. M. W. J. Schols
Keyword(s):  
Oxidative Stress ◽  
Weight Loss ◽  
Muscle Mass ◽  
Muscle Wasting ◽  
Fiber Type ◽  
Oxidative Capacity ◽  
Diaphragm Muscle ◽  
Energy Deficit ◽  
Peripheral Muscle ◽  
Oxidative Phenotype

Pulmonary cachexia is a prevalent, debilitating, and well-recognized feature of COPD associated with increased mortality and loss of peripheral and respiratory muscle function. The exact cause and underlying mechanisms of cachexia in COPD are still poorly understood. Increasing evidence, however, shows that pathological changes in intracellular mechanisms of muscle mass maintenance (i.e., protein turnover and myonuclear turnover) are likely involved. Potential factors triggering alterations in these mechanisms in COPD include oxidative stress, myostatin, and inflammation. In addition to muscle wasting, peripheral muscle in COPD is characterized by a fiber-type shift toward a more type II, glycolytic phenotype and an impaired oxidative capacity (collectively referred to as an impaired oxidative phenotype). Atrophied diaphragm muscle in COPD, however, displays an enhanced oxidative phenotype. Interestingly, intrinsic abnormalities in (lower limb) peripheral muscle seem more pronounced in either cachectic patients or weight loss-susceptible emphysema patients, suggesting that muscle wasting and intrinsic changes in peripheral muscle's oxidative phenotype are somehow intertwined. In this manuscript, we will review alterations in mechanisms of muscle mass maintenance in COPD and discuss the involvement of oxidative stress, inflammation, and myostatin as potential triggers of cachexia. Moreover, we postulate that an impaired muscle oxidative phenotype in COPD can accelerate the process of cachexia, as it renders muscle in COPD less energy efficient, thereby contributing to an energy deficit and weight loss when not dietary compensated. Furthermore, loss of peripheral muscle oxidative phenotype may increase the muscle's susceptibility to inflammation- and oxidative stress-induced muscle damage and wasting.

Supplementation with beta-hydroxy-beta-methylbutyrate impacts glucose homeostasis and increases liver size in trained mice

2020 ◽  
Vol 90 (1-2) ◽  
pp. 113-123
Author(s):  
Ines Schadock ◽  
Barbara G. Freitas ◽  
Irae L. Moreira ◽  
Joao A. Rincon ◽  
Marcio Nunes Correa ◽  
...  
Keyword(s):  
Strength Training ◽  
Muscle Mass ◽  
Glucose Homeostasis ◽  
Fasting Blood Glucose ◽  
Hepatic Metabolism ◽  
Mass Gain ◽  
Trained Group ◽  
Tissue Mass ◽  
Liver Size ◽  
Intensive Training

Abstract. β-hydroxy-β-methyl butyrate (HMB) is a bioactive metabolite derived from the amino acid leucine, usually applied for muscle mass increase during physical training, as well as for muscle mass maintenance in debilitating chronic diseases. The hypothesis of the present study is that HMB is a safe supplement for muscle mass gain by strength training. Based on this, the objective was to measure changes in body composition, glucose homeostasis and hepatic metabolism of HMB supplemented mice during strength training. Two of four groups of male mice (n = 6/group) underwent an 8-week training period session (climbing stairs) with or without HMB supplementation (190 mg/kgBW per day). We observed lower body mass gain (4.9 ± 0.43% versus 1.2 ± 0.43, p < 0.001) and increased liver mass (40.9 ± 0.9 mg/gBW versus 44.8 ± 1.3, p < 0.001) in the supplemented trained group compared with the non-supplemented groups. The supplemented trained group had an increase in relative adipose tissue mass (12.4 ± 0.63 mg/gBW versus 16.1 ± 0.88, P < 0.01) compared to the non-supplemented untrained group, and an increase in fasting blood glucose (111 ± 4.58 mg/dL versus 122 ± 3.70, P < 0.05) and insulin resistance (3.79 ± 0.19 % glucose decay/min versus 2.45 ± 0.28, P < 0.05) comparing with non-supplemented trained group. Adaptive heart hypertrophy was observed only in the non-supplemented trained group (4.82 ± 0.05 mg/gBW versus 5.12 ± 0.13, P < 0.05). There was a higher hepatic insulin-like growth factor-1 expression (P = 0.002) in supplemented untrained comparing with non-supplemented untrained group. Gene expression of gluconeogenesis regulatory factors was increased by training and reduced by HMB supplementation. These results confirm that HMB supplementation associated with intensive training protocol drives changes in glucose homeostasis and liver metabolism in mice.

Clinical and Experimental Analysis of 201Thallium Uptake of the Heart

1978 ◽  
Vol 17 (04) ◽  
pp. 142-148
Author(s):  
U. Büll ◽  
S. Bürger ◽  
B. E. Strauer
Keyword(s):  
Oxygen Consumption ◽  
Left Ventricle ◽  
Muscle Mass ◽  
Myocardial Oxygen Consumption ◽  
Animal Experiments ◽  
Left Ventricular ◽  
Left Ventricular Wall ◽  
Ventricular Wall ◽  
Flow Measurements ◽  
Myocardial Flow

Studies were carried out in order to determine the factors influencing myocardial 201T1 uptake. A total of 158 patients was examined with regard to both 201T1 uptake and the assessment of left ventricular and coronary function (e. g. quantitative ventriculography, coronary arteriography, coronary blood flow measurements). Moreover, 42 animal experiments (closed chest cat) were performed. The results demonstrate that:1) 201T1 uptake in the normal and hypertrophied human heart is linearly correlated with the muscle mass of the left ventricle (LVMM);2) 201T1 uptake is enhanced in the inner (subendocardial) layer and is decreased in the outer (subepicardial) layer of the left ventricular wall. The 201T1 uptake of the right ventricle is 40% lower in comparison to the left ventricle;3) the basic correlation between 201T1 uptake and LVMM is influenced by alterations of both myocardial flow and myocardial oxygen consumption; and4) inotropic interventions (isoproterenol, calcium, norepinephrine) as well as coronary dilatation (dipyridamole) may considerably augment 201T1 uptake in accordance with changes in myocardial oxygen consumption and/or myocardial flow.It is concluded that myocardial 201T1 uptake is determined by multiple factors. The major determinants have been shown to include (i) muscle mass, (ii) myocardial flow and (iii) myocardial oxygen consumption. The clinical data obtained from patient groups with normal ventricular function, with coronary artery disease, with left ventricular wall motion abnormalities and with different degree of left ventricular hypertrophy are correlated with quantitated myocardial 201T1 uptake.

Low birthweight is associated with poorer limb muscle mass and grip strength in middle age: findings from the UK Biobank Imaging Enhancement

2019 ◽  
Author(s):  
Elizabeth Curtis ◽  
Justin Liu ◽  
Kate Ward ◽  
Karen Jameson ◽  
Zahra Raisi-Estabragh ◽  
...  
Keyword(s):  
Grip Strength ◽  
Muscle Mass ◽  
Low Birthweight ◽  
Middle Age ◽  
Limb Muscle ◽  
Uk Biobank ◽  
The Uk

Androgenic and estrogenic regulation of skeletal muscle mass and atrophy signaling in male mice

2013 ◽  
Author(s):  
Naeyer Helene De ◽  
Inge Everaert ◽  
Spaey Annelies De ◽  
Jean-Marc Kaufman ◽  
Youri Taes ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Male Mice ◽  
Estrogenic Regulation

Improvement of muscle mass and force by certain hormones and endogen factors, contributing in muscle development

2007 ◽  
Vol 148 (10) ◽  
pp. 451-456
Author(s):  
Péter Apor ◽  
József Tihanyi ◽  
Andreas Costa
Keyword(s):  
Muscle Mass ◽  
Muscle Development

Az áttekintés az izomtömeg és az izomerő növelése célzatával alkalmazott hormonok (növekedési hormon, IGF-1, anabolikus-androgén szteroidok) és az izom fejlődésében szereplő, humán használatra kerülhető egyes faktorok fizikai aktivitással kapcsolatos élettanát és klinikai alkalmazásának lehetőségeit érinti. A hatásokat illetően mítoszok, a mellékhatásokat illetően alul- és túlértesültség egyaránt jellemzi e területet. A kórállapotok sorában, s nem csak a hiányállapotok szubsztitúciójában történnek terápiás próbálkozások, amelyekben figyelembe vehetők a sportolók, testépítők tapasztalatai is.

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