Efficacy of a gravity-independent resistance exercise device as a countermeasure to muscle atrophy during 29-day bed rest

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.

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Aerobic exercise and resistance exercise alleviate skeletal muscle atrophy through IGF-1/IGF-1R-PI3K/Akt pathway in mice with myocardial infarction

AJP Cell Physiology ◽

10.1152/ajpcell.00344.2021 ◽

2021 ◽

Author(s):

Feng Li-Li ◽

Li Bo-Wen ◽

Xi Yue ◽

Tian Zhen-Jun ◽

Cai Meng-Xin

Keyword(s):

Myocardial Infarction ◽

Skeletal Muscle ◽

Protein Synthesis ◽

Resistance Exercise ◽

Aerobic Exercise ◽

Muscle Atrophy ◽

Cell Apoptosis ◽

Exercise Group ◽

Skeletal Muscle Atrophy ◽

Akt Pathway

Objectives: Myocardial infarction (MI)-induced heart failure (HF) is commonly accompanied with profound effects on skeletal muscle. With the process of MI-induced HF, perturbations in skeletal muscle contribute to muscle atrophy. Exercise is viewed as a feasible strategy to prevent muscle atrophy. The aims of this study were to investigate whether exercise could alleviate MI-induced skeletal muscle atrophy via insulin-like growth factor 1 (IGF-1) pathway in mice. Materials and Methods: Male C57/BL6 mice were used to establish the MI model and divided into three groups: sedentary MI group, MI with aerobic exercise group and MI with resistance exercise group, sham-operated group was used as control. Exercise-trained animals were subjected to four-weeks of aerobic exercise (AE) or resistance exercise (RE). Cardiac function, muscle weight, myofiber size, levels of IGF-1 signaling and proteins related to myogenesis, protein synthesis and degradation and cell apoptosis in gastrocnemius muscle were detected. And H2O2-treated C2C12 cells were intervened with recombinant human IGF-1, IGF-1R inhibitor NVP-AEW541 and PI3K inhibitor LY294002 to explore the mechanism. Results：Exercises up-regulated the IGF-1/IGF-1R-phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling, increased the expressions of Pax7, myogenic regulatory factors (MRFs) and protein synthesis, reduced protein degradation and cell apoptosis in MI-mice. In vitro, IGF-1 up-regulated the levels of Pax7 and MRFs, mTOR and P70S6K, reduced MuRF1, MAFbx and inhibited cell apoptosis via IGF-1R-PI3K/Akt pathway. Conclusion: AE and RE, safely and effectively, alleviate skeletal muscle atrophy by regulating the levels of myogenesis, protein degradation and cells apoptosis in mice with MI via activating IGF-1/IGF-1R-PI3K/Akt pathway.

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Resistance exercise and growth hormone as countermeasures for skeletal muscle atrophy in hindlimb-suspended rats

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1994.267.2.r365 ◽

1994 ◽

Vol 267 (2) ◽

pp. R365-R371 ◽

Cited By ~ 10

Author(s):

J. K. Linderman ◽

K. L. Gosselink ◽

F. W. Booth ◽

V. R. Mukku ◽

R. E. Grindeland

Keyword(s):

Skeletal Muscle ◽

Growth Hormone ◽

Resistance Exercise ◽

Protein Content ◽

Muscle Atrophy ◽

Myofibrillar Protein ◽

Hindlimb Suspension ◽

Skeletal Muscle Atrophy ◽

Plantar Flexor ◽

Fast Twitch

Unweighting of rat hindlimb muscles results in skeletal muscle atrophy, decreased protein synthesis, and reduced growth hormone (GH) secretion. Resistance exercise (ladder climbing) and GH treatment partially attenuate skeletal muscle atrophy in hypophysectomized hindlimb-suspended rats. It was hypothesized that a combination of multiple bouts of daily resistance exercise and GH (1 mg.kg-1.day-1) would prevent skeletal muscle atrophy in growing nonhypophysectomized hindlimb-suspended rats. Hindlimb suspension decreased the absolute (mg/pair) and relative (mg/100 g body wt) weights of the soleus, a slow-twitch plantar flexor, by 30 and 21%, respectively, and the absolute and relative weights of the gastrocnemius, a predominantly fast-twitch plantar flexor, by 20 and 11%, respectively (P < 0.05). Exercise did not increase soleus mass but attenuated loss of relative wet weight in the gastrocnemius muscles of hindlimb-suspended rats (P < 0.05). Hindlimb suspension decreased gastrocnemius myofibrillar protein content and synthesis (mg/day) by 26 and 64%, respectively (P < 0.05). The combination of exercise and GH attenuated loss of gastrocnemius myofibrillar protein content and synthesis by 70 and 23%, respectively (P < 0.05). Results of the present investigation indicate that a combination of GH and resistance exercise attenuates atrophy of unweighted fast-twitch skeletal muscles.

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Randomized, four-arm, dose-response clinical trial to optimize resistance exercise training for older adults with age-related muscle atrophy

Experimental Gerontology ◽

10.1016/j.exger.2017.09.018 ◽

2017 ◽

Vol 99 ◽

pp. 98-109 ◽

Cited By ~ 27

Author(s):

Michael J. Stec ◽

Anna Thalacker-Mercer ◽

David L. Mayhew ◽

Neil A. Kelly ◽

S. Craig Tuggle ◽

...

Keyword(s):

Older Adults ◽

Clinical Trial ◽

Exercise Training ◽

Resistance Exercise ◽

Muscle Atrophy ◽

Dose Response ◽

Resistance Exercise Training ◽

Age Related

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RESISTANCE EXERCISE PREVENTS THE DECREASE OF MUSCLE PROTEIN SYNTHESIS DURING PROLONGED BED REST 776

Medicine & Science in Sports & Exercise ◽

10.1097/00005768-199605001-00774 ◽

1996 ◽

Vol 28 (Supplement) ◽

pp. 130

Author(s):

A. A. Ferrando ◽

K. D. Tipton ◽

M. M. Bamman ◽

R. R. Wolfe

Keyword(s):

Protein Synthesis ◽

Resistance Exercise ◽

Muscle Protein ◽

Muscle Protein Synthesis ◽

Bed Rest

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Functional and morphological effects of resistance exercise on disuse-induced skeletal muscle atrophy

Brazilian Journal of Medical and Biological Research ◽

10.1590/s0100-879x2011007500125 ◽

2011 ◽

Vol 44 (11) ◽

pp. 1070-1079 ◽

Cited By ~ 7

Author(s):

H. Nicastro ◽

N.E. Zanchi ◽

C.R. da Luz ◽

A.H. Lancha Jr.

Keyword(s):

Skeletal Muscle ◽

Resistance Exercise ◽

Muscle Atrophy ◽

Skeletal Muscle Atrophy

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

Journal of Applied Physiology ◽

10.1152/japplphysiol.01064.2020 ◽

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.

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