scholarly journals Vibration mechanosignals superimposed to resistive exercise result in baseline skeletal muscle transcriptome profiles following chronic disuse in bed rest

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Michele Salanova ◽  
Guido Gambara ◽  
Manuela Moriggi ◽  
Michele Vasso ◽  
Ute Ungethuem ◽  
...  
2019 ◽  
Vol 51 (Supplement) ◽  
pp. 146
Author(s):  
Rodrigo Fernandez-Gonzalo ◽  
Per A. Tesch ◽  
Tommy R. Lundberg ◽  
Eric Rullman ◽  
Thomas Gustafsson

1998 ◽  
Vol 85 (2) ◽  
pp. 593-600 ◽  
Author(s):  
Mark S. F. Clarke ◽  
Marcas M. Bamman ◽  
Daniel L. Feeback

Using a terrestrial model of spaceflight (i.e., bed rest), we investigated the amount of myofiber wounding and fibroblast growth factor (FGF) release that occurs during unloading. Myofiber wounding was determined by serum levels of the creatine kinase MM (CKMM) isoform before and after bed rest. Serum levels of both acidic FGF (aFGF) and basic FGF were also determined. A second group of subjects was treated in an identical fashion except that they underwent a resistive exercise program during bed rest. Bed rest alone caused significant ( P < 0.05; n = 7) reductions in post-bed-rest serum levels of both CKMM and aFGF, which were paralleled by a significant ( P < 0.05; n = 7) decrease in myofiber size. In contrast, bed rest plus resistive exercise resulted in significant ( P < 0.05; n = 7) increases in post-bed-rest serum levels of both CKMM and aFGF, which were paralleled by inhibition of the atrophic response. These results suggest that mechanically induced, myofiber wound-mediated FGF release may play an important role in the etiology of unloading-induced skeletal muscle atrophy.


1997 ◽  
Vol 82 (3) ◽  
pp. 807-810 ◽  
Author(s):  
Arny A. Ferrando ◽  
Kevin D. Tipton ◽  
Marcas M. Bamman ◽  
Robert R. Wolfe

Ferrando, Arny A., Kevin D. Tipton, Marcas M. Bamman, and Robert R. Wolfe. Resistance exercise maintains skeletal muscle protein synthesis during bed rest. J. Appl. Physiol. 82(3): 807–810, 1997.—Spaceflight results in a loss of lean body mass and muscular strength. A ground-based model for microgravity, bed rest, results in a loss of lean body mass due to a decrease in muscle protein synthesis (MPS). Resistance training is suggested as a proposed countermeasure for spaceflight-induced atrophy because it is known to increase both MPS and skeletal muscle strength. We therefore hypothesized that scheduled resistance training throughout bed rest would ameliorate the decrease in MPS. Two groups of healthy volunteers were studied during 14 days of simulated microgravity. One group adhered to strict bed rest (BR; n = 5), whereas a second group engaged in leg resistance exercise every other day throughout bed rest (BREx; n = 6). MPS was determined directly by the incorporation of infusedl-[ ring-13C6]phenylalanine into vastus lateralis protein. After 14 days of bed rest, MPS in the BREx group did not change and was significantly greater than in the BR group. Thus moderate-resistance exercise can counteract the decrease in MPS during bed rest.


Author(s):  
Emily J. Arentson-Lantz ◽  
Jasmine Mikovic ◽  
Nisha Bhattarai ◽  
Christopher S. Fry ◽  
Séverine Lamon ◽  
...  

Leucine supplementation attenuates the loss of skeletal muscle mass and function in older adults during bed rest. We sought to determine if leucine could also preserve and/or restore mitochondrial function and muscle oxidative capacity during periods of disuse and rehabilitation. Healthy older adults (69.1 ± 1.1 years) consumed a structured diet with supplemental leucine (LEU: 0.06 g/ kg body weight/ meal; n=8) or alanine (CON: 0.06 g/ kg body weight/meal; n=8) during 7 days of bed rest and 5 days of inpatient rehabilitation. A 75 g oral glucose tolerance test was performed at baseline (PreBR), after bed rest (PostBR) and rehabilitation (PostRehab) and used to calculate an indicator of insulin sensitivity, metabolic clearance rate. (MCR). Tissue samples from the m. vastus lateralis were collected PreBR, PostBR, and PostRehab to assess mitochondrial respiratory capacity and protein markers of the oxidative phosphorylation and a marker of the antioxidant defense systems. During bed rest, leucine tended to preserve insulin sensitivity (Change in MCR, CON vs. LEU: -3.5 ± 0.82 vs LEU: -0.98 ± 0.88, p=0.054), but had no effect on mitochondrial respiratory capacity (Change in State 3+succinate CON vs. LEU -8.7 ± 6.1 vs. 7.3 ± 4.1 pmol O2/sec/mg tissue, p=0.10) Following rehabilitation, leucine increased ATP-linked respiration (CON vs. LEU: -8.9 ± 6.2 vs. 15.5± 4.4 pmol O2/sec/mg tissue, p=0.0042). While the expression of mitochondrial respiratory and antioxidant proteins was not impacted, leucine supplementation preserved specific pathways of mitochondrial respiration, insulin sensitivity and a marker of oxidative stress during bed rest and rehabilitation.


2015 ◽  
Vol 29 (S1) ◽  
Author(s):  
Ruth Tanner ◽  
Lucille Brunker ◽  
Jakob Agergaard ◽  
Oh‐Sung Kwon ◽  
Katherine Barrows ◽  
...  

2020 ◽  
Vol 31 (9-12) ◽  
pp. 309-324
Author(s):  
Md Mahmodul Hasan Sohel ◽  
Bilal Akyuz ◽  
Yusuf Konca ◽  
Korhan Arslan ◽  
Kutlay Gurbulak ◽  
...  

JAMA ◽  
2007 ◽  
Vol 297 (16) ◽  
pp. 1769 ◽  
Author(s):  
Patrick Kortebein ◽  
Arny Ferrando ◽  
Juan Lombeida ◽  
Robert Wolfe ◽  
William J. Evans

2015 ◽  
Vol 593 (18) ◽  
pp. 4259-4273 ◽  
Author(s):  
Ruth E. Tanner ◽  
Lucille B. Brunker ◽  
Jakob Agergaard ◽  
Katherine M. Barrows ◽  
Robert A. Briggs ◽  
...  

Author(s):  
Zudin Puthucheary ◽  
Hugh Montgomery ◽  
Nicholas Hart ◽  
Stephen Harridge

Muscle is a dynamic, plastic, and malleable tissue that is highly sensitive to mechanical and metabolic signals. Muscle mass is regulated by protein homeostasis, with protein being continually turned over, reflecting a balance between synthesis and breakdown. This chapter discusses the effect of critical illness on skeletal muscle mass, protein homeostasis, and the intracellular signalling driving anabolism and catabolism. The focus will be on the unique challenges to which the skeletal muscle are exposed, such as inflammation, sepsis, sedation, and inadequate nutrition, which, in combination with the disuse signals of immobilization and bed rest, engender dramatic changes in muscle structure and function. The mechanisms regulating muscle loss during critical illness are being unravelled, but many questions remain unanswered. Detailed understanding of these mechanisms will help drive strategies to minimize or prevent intensive care-acquired muscle weakness and the long-term consequences experienced by ICU survivors.


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