High‐intensity resistance training attenuates dexamethasone‐induced muscle atrophy

Krug, André Luis O.; Macedo, Anderson G.; Zago, Anderson Saranz; Rush, James W. E.; Santos, Carlos; Amaral, Sandra Lia do

doi:10.1002/mus.24906

Cited by 31 publications

(24 citation statements)

References 39 publications

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“…The mechanism responsible for this response is not completely understood, but it may be somewhat explained by food intake reductions [4,7,8,23] since DEX inhibits the production of ghrelin and increases plasma levels of leptin [24,25], which contribute to an increase in satiety signaling in the central nervous system. However, it seems that food intake reductions contribute to trigger BW reductions and other mechanisms are involved in the maintenance of this response, since we have shown that reduced food intake normalizes after 8 days of treatment [4,26].…”

Section: Discussionmentioning

confidence: 82%

“…Although several authors have already demonstrated muscle atrophy induced by DEX (or other glucocorticoid), the mechanism responsible for this response is not completely understood. It may be mediated by increases in catabolic proteins [1,4,9,26,27]. It is important to note that there is a huge difference between DEX doses and treatment periods in the literature and most of them show a final end point only.…”

Section: Discussionmentioning

confidence: 99%

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Time-course changes of catabolic proteins following muscle atrophy induced by dexamethasone

et al. 2016

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This study was designed to describe the time-course changes of catabolic proteins following muscle atrophy induced by 10 days of dexamethasone (DEX). Rats underwent DEX treatment for 1, 3, 5, 7 and 10 days. Body weight (BW) and lean mass were obtained using a dual energy X-ray absorptiometry (DEXA) scan. Muscle ringer finger1 (MuRF-1), atrogin-1 and myostatin protein levels were analyzed in the tibialis anterior (TA), flexor hallucis longus (FHL) and soleus muscles. DEX treatment reduced lean mass since day-3 and reduced BW since day-5. Specific muscle weight reductions were observed after day-10 in TA (-23%) and after day-5 in FHL (-16%, -17% and -29%, for days 5, 7 and 10, respectively). In TA, myostatin protein level was 36% higher on day-5 and its values were normalized in comparison with controls on day-10. MuRF-1 protein level was increased in TA muscle from day-7 and in FHL muscle only on day-10. This study suggests that DEX-induced muscle atrophy is a dynamic process which involves important signaling factors over time. As demonstrated by DEXA scan, lean mass declines earlier than BW and this response may involve other catabolic proteins than myostatin and MuRF-1. Specifically for TA and FHL, it seems that myostatin may trigger the catabolic process, and MuRF-1 may contribute to maintain muscle atrophy. This information may support any intervention in order to attenuate the muscle atrophy during long period of treatment.

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Section: Discussionmentioning

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Time-course changes of catabolic proteins following muscle atrophy induced by dexamethasone

et al. 2016

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“…Our hypothesis was that a diet consisting solely of whey protein will attenuate the loss of muscle mass and that this effect will be enhanced locally by exercise in a dose-dependent manner, and modulated by the changes in plasma levels of cortisol, testosterone, and amino acids. This hypothesis is based on the fact that exercised muscles are more sensitive to the anabolic effects of circulating amino acids (Apro and Blomstrand, 2010) and testosterone (Bhasin et al, 1996), while being more resistant to the atrophying effects of cortisol (Crowley and Matt, 1996; Krug et al, 2016). …”

Section: Introductionmentioning

confidence: 99%

Exercise Preserves Lean Mass and Performance during Severe Energy Deficit: The Role of Exercise Volume and Dietary Protein Content

et al. 2017

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The loss of fat-free mass (FFM) caused by very-low-calorie diets (VLCD) can be attenuated by exercise. The aim of this study was to determine the role played by exercise and dietary protein content in preserving the lean mass and performance of exercised and non-exercised muscles, during a short period of extreme energy deficit (~23 MJ deficit/day). Fifteen overweight men underwent three consecutive experimental phases: baseline assessment (PRE), followed by 4 days of caloric restriction and exercise (CRE) and then 3 days on a control diet combined with reduced exercise (CD). During CRE, the participants ingested a VLCD and performed 45 min of one-arm cranking followed by 8 h walking each day. The VLCD consisted of 0.8 g/kg body weight/day of either whey protein (PRO, n = 8) or sucrose (SU, n = 7). FFM was reduced after CRE (P < 0.001), with the legs and the exercised arm losing proportionally less FFM than the control arm [57% (P < 0.05) and 29% (P = 0.05), respectively]. Performance during leg pedaling, as reflected by the peak oxygen uptake and power output (Wpeak), was reduced after CRE by 15 and 12%, respectively (P < 0.05), and recovered only partially after CD. The deterioration of cycling performance was more pronounced in the whey protein than sucrose group (P < 0.05). Wpeak during arm cranking was unchanged in the control arm, but improved in the contralateral arm by arm cranking. There was a linear relationship between the reduction in whole-body FFM between PRE and CRE and the changes in the cortisol/free testosterone ratio (C/FT), serum isoleucine, leucine, tryptophan, valine, BCAA, and EAA (r = −0.54 to −0.71, respectively, P < 0.05). C/FT tended to be higher in the PRO than the SU group following CRE (P = 0.06). In conclusion, concomitant low-intensity exercise such as walking or arm cranking even during an extreme energy deficit results in remarkable preservation of lean mass. The intake of proteins alone may be associated with greater cortisol/free testosterone ratio and is not better than the ingestion of only carbohydrates for preserving FFM and muscle performance in interventions of short duration.

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“…However, C2C12s cultured in OM demonstrated a decrease in desmin presence with an increase in nondesmin-associated nuclei and punctate staining. The low-glucose aspect of the OM potentially caused a reduction in metabolic activity, accompanied by the presence of dexamethasone, a known inducer of atrophy [76][77][78] and other osteogenic factors may have caused a reversion to a more progenitor-like state, alluded to in skeletal muscle calcification conditions. [69] A lack of RUNX2/Cbfa1 upregulation supports a reversion theory to a less committed cell type, rather than a direct lineage change as in the case of BMP-2 stimulated culture.…”

Section: Discussionmentioning

confidence: 99%

Development of a 3D Tissue‐Engineered Skeletal Muscle and Bone Co‐culture System

Wragg

Mosqueira

Blokpeol‐Ferreras

et al. 2019

Biotechnology Journal

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In vitro 3D tissue-engineered (TE) structures have been shown to better represent in vivo tissue morphology and biochemical pathways than monolayer culture, and are less ethically questionable than animal models. However, to create systems with even greater relevance, multiple integrated tissue systems should be recreated in vitro. In the present study, the effects and conditions most suitable for the co-culture of TE skeletal muscle and bone are investigated. High-glucose Dulbecco's modified Eagle medium (HG-DMEM) supplemented with 20% fetal bovine serum followed by HG-DMEM with 2% horse serum is found to enable proliferation of both C2C12 muscle precursor cells and TE85 human osteosarcoma cells, fusion of C2C12s into myotubes, as well as an upregulation of RUNX2/CBFa1 in TE85s. Myotube formation is also evident within indirect contact monolayer cultures. Finally, in 3D co-cultures, TE85 collagen/hydroxyapatite constructs have significantly greater expression of RUNX2/CBFa1 and osteocalcin/BGLAP in the presence of collagen-based C2C12 skeletal muscle constructs; however, fusion within these constructs appears reduced. This work demonstrates the first report of the simultaneous co-culture and differentiation of 3D TE skeletal muscle and bone, and represents a significant step toward a full in vitro 3D musculoskeletal junction model.

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High‐intensity resistance training attenuates dexamethasone‐induced muscle atrophy

Abstract: RT attenuated DEX-induced muscle atrophy through a combination of increases in mTOR and p70S6K protein levels and a low increase in MuRF-1 protein level.

Cited by 31 publications

References 39 publications

Time-course changes of catabolic proteins following muscle atrophy induced by dexamethasone

Time-course changes of catabolic proteins following muscle atrophy induced by dexamethasone

Exercise Preserves Lean Mass and Performance during Severe Energy Deficit: The Role of Exercise Volume and Dietary Protein Content

Development of a 3D Tissue‐Engineered Skeletal Muscle and Bone Co‐culture System

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