scholarly journals An intricate balance of muscle damage and protein synthesis: the key players in skeletal muscle hypertrophy following resistance training

2016 ◽  
Vol 594 (24) ◽  
pp. 7157-7158 ◽  
Author(s):  
Giselle Keefe ◽  
Craig Wright
Keyword(s):  
Skeletal Muscle ◽  
Protein Synthesis ◽  
Resistance Training ◽  
Muscle Damage ◽  
Muscle Hypertrophy ◽  
Skeletal Muscle Hypertrophy ◽  
Key Players

scholarly journals Exercise-Induced Muscle Damage and Hypertrophy: A Closer Look Reveals the Jury is Still Out

2018 ◽  
Author(s):  
Brad Jon Schoenfeld ◽  
Bret Contreras
Keyword(s):  
Skeletal Muscle ◽  
Protein Synthesis ◽  
Resistance Training ◽  
Muscle Damage ◽  
Muscle Hypertrophy ◽  
Muscle Protein ◽  
Muscle Protein Synthesis ◽  
Skeletal Muscle Hypertrophy ◽  
Exercise Induced

This letter is a response to the paper by Damas et al (2017) titled, “The development of skeletal muscle hypertrophy through resistance training: the role of muscle damage and muscle protein synthesis,” which, in part, endeavored to review the role of exercise-induced muscle damage on muscle hypertrophy. We feel there are a number of issues in interpretation of research and extrapolation that preclude drawing the inference expressed in the paper that muscle damage neither explains nor potentiates increases in muscle hypertrophy. The intent of our letter is not to suggest that a causal role exists between hypertrophy and microinjury. Rather, we hope to provide balance to the evidence presented and offer the opinion that the jury is still very much out as to providing answers on the topic.

scholarly journals Revisiting the roles of protein synthesis during skeletal muscle hypertrophy induced by exercise

2019 ◽  
Vol 317 (5) ◽  
pp. R709-R718 ◽  
Author(s):  
Vandré Casagrande Figueiredo
Keyword(s):  
Skeletal Muscle ◽  
Protein Synthesis ◽  
Resistance Training ◽  
Resistance Exercise ◽  
Muscle Hypertrophy ◽  
Current Model ◽  
Muscle Growth ◽  
Exercise Session ◽  
Skeletal Muscle Hypertrophy ◽  
Resistance Exercise Session

Protein synthesis is deemed the underpinning mechanism enhancing protein balance required for skeletal muscle hypertrophy in response to resistance exercise. The current model of skeletal muscle hypertrophy induced by resistance training states that the acute increase in the rates of protein synthesis after each bout of resistance exercise is the basis for muscle growth. Within this paradigm, each resistance exercise session would add a specific amount of muscle mass; therefore, muscle hypertrophy could be defined as the result of intermittent and short-lived increases in muscle protein synthesis rates following each resistance exercise session. Although a substantial amount of data has accumulated in the last decades regarding the acute changes in protein synthesis (or translational efficiency) following resistance exercise, considerable gaps on the mechanism of muscle growth still exist. Ribosome biogenesis and translational capacity have emerged as important mediators of skeletal muscle hypertrophy. Recent advances in the field have demonstrated that skeletal muscle hypertrophy is associated with markers of translational capacity and long-term changes in protein synthesis under resting conditions. This review will discuss the caveats of the current model of skeletal muscle hypertrophy induced by resistance training while proposing a working model that takes into consideration the novel data generated by independent laboratories utilizing different methodologies. It is argued, herein, that the role of protein synthesis in the current model of muscle hypertrophy warrants revisiting.

scholarly journals Is an Energy Surplus Required to Maximize Skeletal Muscle Hypertrophy Associated With Resistance Training

2019 ◽  
Vol 6 ◽  
Author(s):  
Gary John Slater ◽  
Brad P. Dieter ◽  
Damian James Marsh ◽  
Eric Russell Helms ◽  
Gregory Shaw ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Resistance Training ◽  
Muscle Hypertrophy ◽  
Skeletal Muscle Hypertrophy ◽  
Energy Surplus

scholarly journals Stimuli and sensors that initiate skeletal muscle hypertrophy following resistance exercise

2019 ◽  
Vol 126 (1) ◽  
pp. 30-43 ◽  
Author(s):  
Henning Wackerhage ◽  
Brad J. Schoenfeld ◽  
D. Lee Hamilton ◽  
Maarit Lehti ◽  
Juha J. Hulmi
Keyword(s):  
Skeletal Muscle ◽  
Resistance Exercise ◽  
Muscle Damage ◽  
Muscle Hypertrophy ◽  
Muscle Protein ◽  
Large Body ◽  
Focal Adhesions ◽  
Indirect Evidence ◽  
Skeletal Muscle Hypertrophy ◽  
Exercise Induced

One of the most striking adaptations to exercise is the skeletal muscle hypertrophy that occurs in response to resistance exercise. A large body of work shows that a mammalian target of rapamycin complex 1 (mTORC1)-mediated increase of muscle protein synthesis is the key, but not sole, mechanism by which resistance exercise causes muscle hypertrophy. While much of the hypertrophy signaling cascade has been identified, the initiating, resistance exercise-induced and hypertrophy-stimulating stimuli have remained elusive. For the purpose of this review, we define an initiating, resistance exercise-induced and hypertrophy-stimulating signal as “hypertrophy stimulus,” and the sensor of such a signal as “hypertrophy sensor.” In this review we discuss our current knowledge of specific mechanical stimuli, damage/injury-associated and metabolic stress-associated triggers, as potential hypertrophy stimuli. Mechanical signals are the prime hypertrophy stimuli candidates, and a filamin-C-BAG3-dependent regulation of mTORC1, Hippo, and autophagy signaling is a plausible albeit still incompletely characterized hypertrophy sensor. Other candidate mechanosensing mechanisms are nuclear deformation-initiated signaling or several mechanisms related to costameres, which are the functional equivalents of focal adhesions in other cells. While exercise-induced muscle damage is probably not essential for hypertrophy, it is still unclear whether and how such muscle damage could augment a hypertrophic response. Interventions that combine blood flow restriction and especially low load resistance exercise suggest that resistance exercise-regulated metabolites could be hypertrophy stimuli, but this is based on indirect evidence and metabolite candidates are poorly characterized.

scholarly journals Akt1 deficiency diminishes skeletal muscle hypertrophy by reducing satellite cell proliferation

2018 ◽  
Vol 314 (5) ◽  
pp. R741-R751 ◽  
Author(s):  
Nobuki Moriya ◽  
Mitsunori Miyazaki
Keyword(s):  
Skeletal Muscle ◽  
Cell Proliferation ◽  
Protein Synthesis ◽  
Satellite Cell ◽  
Muscle Mass ◽  
Satellite Cells ◽  
Muscle Hypertrophy ◽  
Mtor Signaling ◽  
Skeletal Muscle Hypertrophy ◽  
Satellite Cell Proliferation

Skeletal muscle mass is determined by the net dynamic balance between protein synthesis and degradation. Although the Akt/mechanistic target of rapamycin (mTOR)-dependent pathway plays an important role in promoting protein synthesis and subsequent skeletal muscle hypertrophy, the precise molecular regulation of mTOR activity by the upstream protein kinase Akt is largely unknown. In addition, the activation of satellite cells has been indicated as a key regulator of muscle mass. However, the requirement of satellite cells for load-induced skeletal muscle hypertrophy is still under intense debate. In this study, female germline Akt1 knockout (KO) mice were used to examine whether Akt1 deficiency attenuates load-induced skeletal muscle hypertrophy through suppressing mTOR-dependent signaling and satellite cell proliferation. Akt1 KO mice showed a blunted hypertrophic response of skeletal muscle, with a diminished rate of satellite cell proliferation following mechanical overload. In contrast, Akt1 deficiency did not affect the load-induced activation of mTOR signaling and the subsequent enhanced rate of protein synthesis in skeletal muscle. These observations suggest that the load-induced activation of mTOR signaling occurs independently of Akt1 regulation and that Akt1 plays a critical role in regulating satellite cell proliferation during load-induced muscle hypertrophy.

scholarly journals Molecular markers of skeletal muscle hypertrophy following 10 wk of resistance training in oral contraceptive users and nonusers

2020 ◽  
Vol 129 (6) ◽  
pp. 1355-1364 ◽  
Author(s):  
Mikkel Oxfeldt ◽  
Line Barner Dalgaard ◽  
Emil Brøbech Jørgensen ◽  
Frank Ted Johansen ◽  
Emil Barner Dalgaard ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Oral Contraceptive ◽  
Resistance Training ◽  
Muscle Hypertrophy ◽  
Contraceptive Use ◽  
Cell Number ◽  
Regulatory Factor ◽  
Regulatory Pathways ◽  
Oral Contraceptive Use ◽  
Skeletal Muscle Hypertrophy

The effect of oral contraceptive use on the skeletal muscle regulatory pathways in response to resistance training has not been investigated previously. Here we present novel data, demonstrating that use of second-generation oral contraceptives in young untrained women increased skeletal muscle regulatory factor 4 expression and satellite cell number following 10 wk of resistance training compared with nonusers.

scholarly journals Regulation of Ribosome Biogenesis in Skeletal Muscle Hypertrophy

Physiology ◽  
2019 ◽  
Vol 34 (1) ◽  
pp. 30-42 ◽  
Author(s):  
Vandré Casagrande Figueiredo ◽  
John J. McCarthy
Keyword(s):  
Skeletal Muscle ◽  
Protein Synthesis ◽  
Ribosome Biogenesis ◽  
Muscle Hypertrophy ◽  
Muscle Growth ◽  
Translational Efficiency ◽  
Resistance Exercise Training ◽  
Skeletal Muscle Growth ◽  
Skeletal Muscle Hypertrophy ◽  
Important Regulator

The ribosome is the enzymatic macromolecular machine responsible for protein synthesis. The rates of protein synthesis are primarily dependent on translational efficiency and capacity. Ribosome biogenesis has emerged as an important regulator of skeletal muscle growth and maintenance by altering the translational capacity of the cell. Here, we provide evidence to support a central role for ribosome biogenesis in skeletal muscle growth during postnatal development and in response to resistance exercise training. Furthermore, we discuss the cellular signaling pathways regulating ribosome biogenesis, discuss how myonuclear accretion affects translational capacity, and explore future areas of investigation within the field.

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