scholarly journals Resistance exercise stimulates mixed muscle protein synthesis in lean and obese young adults

2018 ◽  
Vol 6 (14) ◽  
pp. e13799 ◽  
Author(s):  
Carl J. Hulston ◽  
Rachel M. Woods ◽  
Rebecca Dewhurst-Trigg ◽  
Sion A. Parry ◽  
Stephanie Gagnon ◽  
...  
Keyword(s):  
Young Adults ◽  
Protein Synthesis ◽  
Resistance Exercise ◽  
Muscle Protein ◽  
Muscle Protein Synthesis

scholarly journals The response of muscle protein synthesis following whole-body resistance exercise is greater following 40 g than 20 g of ingested whey protein

2016 ◽  
Vol 4 (15) ◽  
pp. e12893 ◽  
Author(s):  
Lindsay S. Macnaughton ◽  
Sophie L. Wardle ◽  
Oliver C. Witard ◽  
Chris McGlory ◽  
D. Lee Hamilton ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Resistance Exercise ◽  
Whey Protein ◽  
Muscle Protein ◽  
Muscle Protein Synthesis ◽  
Whole Body ◽  
Body Resistance

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.

scholarly journals Exercise May Promote Skeletal Muscle Hypertrophy via Enhancing Leucine-Sensing: Preliminary Evidence

2021 ◽  
Vol 12 ◽  
Author(s):  
Yan Zhao ◽  
Jason Cholewa ◽  
Huayu Shang ◽  
Yueqin Yang ◽  
Xiaomin Ding ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Resistance Exercise ◽  
Aerobic Exercise ◽  
Protein Concentration ◽  
Muscle Hypertrophy ◽  
Muscle Protein ◽  
Muscle Protein Synthesis ◽  
Muscle Fibers ◽  
Mtor Signaling ◽  
Treadmill Running

Several studies have indicated a positive effect of exercise (especially resistance exercise) on the mTOR signaling that control muscle protein synthesis and muscle remodeling. However, the relationship between exercise, mTOR activation and leucine-sensing requires further clarification. Two month old Sprague-Dawley rats were subjected to aerobic exercise (treadmill running at 20 m/min, 6° incline for 60 min) and resistance exercise (incremental ladder climbing) for 4 weeks. The gastrocnemius muscles were removed for determination of muscle fibers diameter, cross-sectional area (CSA), protein concentration and proteins involved in muscle leucine-sensing and protein synthesis. The results show that 4 weeks of resistance exercise increased the diameter and CSA of gastrocnemius muscle fibers, protein concentration, the phosphorylation of mTOR (Ser2448), 4E-BP1(Thr37/46), p70S6K (Thr389), and the expression of LeuRS, while aerobic exercise just led to a significant increase in protein concentration and the phosphorylation of 4E-BP1(Thr37/46). Moreover, no difference was found for Sestrin2 expression between groups. The current study shows resistance exercise, but not aerobic exercise, may increase muscle protein synthesis and protein deposition, and induces muscle hypertrophy through LeuRS/mTOR signaling pathway. However, further studies are still warranted to clarify the exact effects of vary intensities and durations of aerobic exercise training.

A Clinically Relevant Decrease in Contractile Force Differentially Regulates Control of Glucocorticoid Receptor Translocation in Mouse Skeletal Muscle

2021 ◽  
Author(s):  
Kirsten R. Dunlap ◽  
Jennifer L. Steiner ◽  
Michael L. Rossetti ◽  
Scot R. Kimball ◽  
Bradley S. Gordon
Keyword(s):  
Protein Synthesis ◽  
Glucocorticoid Receptor ◽  
Resistance Exercise ◽  
Muscle Atrophy ◽  
Nuclear Translocation ◽  
Muscle Protein ◽  
Muscle Protein Synthesis ◽  
Contractile Force ◽  
Force Generation ◽  
Protein Balance

Muscle atrophy decreases physical function and overall health. Increased glucocorticoid production and/or use of prescription glucocorticoids can significantly induce muscle atrophy by activating the glucocorticoid receptor thereby transcribing genes that shift protein balance in favor of net protein degradation. While mechanical overload can blunt glucocorticoid-induced atrophy in young muscle, those affected by glucocorticoids generally have impaired force generation. It is unknown whether contractile force alters the ability of resistance exercise to mitigate glucocorticoid receptor translocation and induce a desirable shift in protein balance when glucocorticoids are elevated. In the present study, mice were subjected to a single bout of unilateral, electrically induced muscle contractions by stimulating the sciatic nerve at 100 Hz or 50 Hz frequencies to elicit high force or moderate force contractions of the tibialis anterior, respectively. Dexamethasone was used to activate the glucocorticoid receptor. Dexamethasone increased glucocorticoid signaling, including nuclear translocation of the receptor, but this was mitigated only by high force contractions. The ability of high force contractions to mitigate glucocorticoid receptor translocation coincided with a contraction-mediated increase in muscle protein synthesis, which did not occur in the dexamethasone treated mice subjected to moderate force contractions. Though moderate force contractions failed to increase protein synthesis following dexamethasone treatment, both high and moderate force contractions blunted the glucocorticoid-mediated increase in LC3 II:I marker of autophagy. Thus, these data show that force generation is important for the ability of resistance exercise to mitigate glucocorticoid receptor translocation and promote a desirable shift in protein balance when glucocorticoids are elevated.

scholarly journals Anabolic sensitivity of postprandial muscle protein synthesis to the ingestion of a protein-dense food is reduced in overweight and obese young adults

2016 ◽  
Vol 104 (4) ◽  
pp. 1014-1022 ◽  
Author(s):  
Joseph W Beals ◽  
Richard A Sukiennik ◽  
Julian Nallabelli ◽  
Russell S Emmons ◽  
Stephan van Vliet ◽  
...  
Keyword(s):  
Young Adults ◽  
Protein Synthesis ◽  
Muscle Protein ◽  
Muscle Protein Synthesis

scholarly journals Severe diabetes prohibits elevations in muscle protein synthesis after acute resistance exercise in rats

2000 ◽  
Vol 88 (1) ◽  
pp. 102-108 ◽  
Author(s):  
Mark J. Fedele ◽  
Jazmir M. Hernandez ◽  
Charles H. Lang ◽  
Thomas C. Vary ◽  
Scot R. Kimball ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Growth Factor ◽  
Resistance Exercise ◽  
Muscle Protein ◽  
Muscle Protein Synthesis ◽  
Critical Concentration ◽  
Diabetic Rats ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Growth Factor I

This study determined whether rates of protein synthesis increase after acute resistance exercise in skeletal muscle from severely diabetic rats. Previous studies consistently show that postexercise rates of protein synthesis are elevated in nondiabetic and moderately diabetic rats. Severely diabetic rats performed acute resistance exercise ( n= 8) or remained sedentary ( n = 8). A group of nondiabetic age-matched rats served as controls ( n = 9). Rates of protein synthesis were measured 16 h after exercise. Plasma glucose concentrations were >500 mg/dl in the diabetic rats. Rates of protein synthesis (nmol phenylalanine incorporated ⋅ g muscle−1 ⋅ h−1, means ± SE) were not different between exercised (117 ± 7) and sedentary (106 ± 9) diabetic rats but were significantly ( P < 0.05) lower than in sedentary nondiabetic rats (162 ± 9) and in exercised nondiabetic rats (197 ± 7). Circulating insulin concentrations were 442 ± 65 pM in nondiabetic rats and 53 ± 11 and 72 ± 19 pM in sedentary and exercised diabetic rats, respectively. Plasma insulin-like growth factor I concentrations were reduced by 33% in diabetic rats compared with nondiabetic rats, and there was no difference between exercised and sedentary diabetic rats. Muscle insulin-like growth factor I was not affected by resistance exercise in diabetic rats. The results show that there is a critical concentration of insulin below which rates of protein synthesis begin to decline in vivo. In contrast to previous studies using less diabetic rats, severely diabetic rats cannot increase rates of protein synthesis after acute resistance exercise.

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