scholarly journals PlanHab* : hypoxia does not worsen the impairment of skeletal muscle oxidative function induced by bed rest alone

2018 ◽  
Vol 596 (15) ◽  
pp. 3341-3355 ◽  
Author(s):  
Desy Salvadego ◽  
Michail E. Keramidas ◽  
Roger Kölegård ◽  
Lorenza Brocca ◽  
Stefano Lazzer ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Bed Rest ◽  
Oxidative Function

Heterogeneity of human adaptations to bed rest and hypoxia: a retrospective analysis within the skeletal muscle oxidative function

2021 ◽  
Author(s):  
Desy Salvadego ◽  
Bruno Grassi ◽  
Michail E. Keramidas ◽  
Ola Eiken ◽  
Adam C. McDonnell ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Mitochondrial Respiration ◽  
Bed Rest ◽  
Knee Extension ◽  
Large Variability ◽  
The Individual ◽  
Oxidative Function ◽  
Knee Extension Exercise ◽  
Permeabilized Muscle

This retrospective study was designed to analyse the interindividual variability in the responses of different variables characterizing the skeletal muscle oxidative function to normoxic (N-BR) and hypoxic (H-BR) bed rests, and to a hypoxic ambulatory confinement (H-AMB) of 10 and 21 days. We also assessed whether and how the addition of hypoxia to bed rest might influence the heterogeneity of the responses. In vivo measurements of O2 uptake and muscle fractional O2 extraction were carried out during an incremental one-leg knee-extension exercise. Mitochondrial respiration was assessed in permeabilized muscle fibers. A total of 17 subjects were included in this analysis. This analysis revealed a similar variability among subjects in the alterations induced by N-BR and H-BR both in peak O2 uptake (SD: 4.1 and 3.3% after 10 days; 4.5 and 8.1% after 21 days, respectively) and peak muscle fractional O2 extraction (SD: 5.9 and 7.3% after 10 days; 6.5 and 7.3% after 21 days), independently from the duration of the exposure. The individual changes measured in these variables were significantly related (r=0.66, P=0.004 after N-BR; r=0.61, P=0.009 after H-BR). Mitochondrial respiration showed a large variability of response after both N-BR (SD: 25.0 and 15.7% after 10 and 21 days) and H-BR (SD: 13.0 and 19.8% after 10 and 21 days), no correlation was found between N-BR and H-BR changes. When added to bed rest, hypoxia altered the individual adaptations within the mitochondria but not those intrinsic to the muscle oxidative function in vivo, both after short and medium-term exposures.

scholarly journals Resistance exercise maintains skeletal muscle protein synthesis during bed rest

1997 ◽  
Vol 82 (3) ◽  
pp. 807-810 ◽  
Author(s):  
Arny A. Ferrando ◽  
Kevin D. Tipton ◽  
Marcas M. Bamman ◽  
Robert R. Wolfe
Keyword(s):  
Skeletal Muscle ◽  
Protein Synthesis ◽  
Resistance Training ◽  
Resistance Exercise ◽  
Lean Body Mass ◽  
Muscle Protein ◽  
Muscle Protein Synthesis ◽  
Bed Rest ◽  
Skeletal Muscle Protein ◽  
Skeletal Muscle Protein Synthesis

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.

Leucine augments specific skeletal muscle mitochondrial respiratory pathways during recovery following 7 days of physical inactivity in older adults

2021 ◽  
Author(s):  
Emily J. Arentson-Lantz ◽  
Jasmine Mikovic ◽  
Nisha Bhattarai ◽  
Christopher S. Fry ◽  
Séverine Lamon ◽  
...  
Keyword(s):  
Older Adults ◽  
Skeletal Muscle ◽  
Body Weight ◽  
Insulin Sensitivity ◽  
Bed Rest ◽  
Metabolic Clearance ◽  
Leucine Supplementation ◽  
Respiratory Capacity ◽  
Antioxidant Defense Systems ◽  
Mitochondrial Respiratory

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.

scholarly journals mTORC1 Nutrient Signaling and Autophagy in Young and Older Skeletal Muscle after Bed Rest and Rehabilitation

2015 ◽  
Vol 29 (S1) ◽  
Author(s):  
Ruth Tanner ◽  
Lucille Brunker ◽  
Jakob Agergaard ◽  
Oh‐Sung Kwon ◽  
Katherine Barrows ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Bed Rest ◽  
Nutrient Signaling

Effect of 10 Days of Bed Rest on Skeletal Muscle in Healthy Older Adults

JAMA ◽  
2007 ◽  
Vol 297 (16) ◽  
pp. 1769 ◽  
Author(s):  
Patrick Kortebein ◽  
Arny Ferrando ◽  
Juan Lombeida ◽  
Robert Wolfe ◽  
William J. Evans
Keyword(s):  
Older Adults ◽  
Skeletal Muscle ◽  
Bed Rest ◽  
Healthy Older Adults

scholarly journals Age-related differences in lean mass, protein synthesis and skeletal muscle markers of proteolysis after bed rest and exercise rehabilitation

2015 ◽  
Vol 593 (18) ◽  
pp. 4259-4273 ◽  
Author(s):  
Ruth E. Tanner ◽  
Lucille B. Brunker ◽  
Jakob Agergaard ◽  
Katherine M. Barrows ◽  
Robert A. Briggs ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Synthesis ◽  
Lean Mass ◽  
Bed Rest ◽  
Exercise Rehabilitation ◽  
Age Related ◽  
Rest And Exercise

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 ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Bed Rest ◽  
Resistive Exercise ◽  
Skeletal Muscle Transcriptome

Skeletal Muscle Mass Regulation in Critical Illness

2014 ◽  
Author(s):  
Zudin Puthucheary ◽  
Hugh Montgomery ◽  
Nicholas Hart ◽  
Stephen Harridge
Keyword(s):  
Skeletal Muscle ◽  
Critical Illness ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Bed Rest ◽  
Protein Homeostasis ◽  
Highly Sensitive ◽  
And Function ◽  
Inadequate Nutrition

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.

Protein Metabolism and Age: Influence of Insulin and Resistance Exercise

2001 ◽  
Vol 11 (s1) ◽  
pp. S150-S163 ◽  
Author(s):  
Peter A. Farrell
Keyword(s):  
Skeletal Muscle ◽  
Protein Synthesis ◽  
Resistance Exercise ◽  
Muscle Protein ◽  
Muscle Protein Synthesis ◽  
Mrna Translation ◽  
Bed Rest ◽  
Skeletal Muscle Protein ◽  
Amino Acid Availability ◽  
Effects Of Aging

Skeletal muscle proteins are constantly being synthesized and degraded, and the net balance between synthesis and degradation determines the resultant muscle mass. Biochemical pathways that control protein synthesis are complex, and the following must be considered: gene transcription, mRNA splicing, and transport to the cytoplasm; specific amino acyl-tRNA, messenger (mRNA), ribosomal (rRNA) availability; amino acid availability within the cell; the hormonal milieu; rates of mRNA translation; packaging in vesicles for some types of proteins; and post-translational processing such as glycation and phosphorylation/dephosphorylation. Each of these processes is responsive to the need for greater or lesser production of new proteins, and many states such as sepsis, uncontrolled diabetes, prolonged bed-rest, aging, chronic alcohol treatment, and starvation cause marked reductions in rates of skeletal muscle protein synthesis. In contrast, acute and chronic resistance exercise cause elevations in rates of muscle protein synthesis above rates found in nondiseased rested organisms, which are normally fed. Resistance exercise may be unique in this capacity. This chapter focuses on studies that have used exercise to elucidate mechanisms that explain elevations in rates of protein synthesis. Very few studies have investigated the effects of aging on these mechanisms; however, the literature that is available is reviewed.

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