Protein Intake and Exercise-Induced Skeletal Muscle Hypertrophy: An Update

Skeletal muscle mass is critical for sport performance and in many pathological conditions. The combination of protein intake and resistance exercise is the most efficient strategy to promote skeletal muscle hypertrophy and remodeling. However, to be really efficient, certain conditions need to be considered. The amount, type and source of proteins do all matter as well as the timing of ingestion and spreading over the whole day. Optimizing those conditions favor a positive net protein balance, which in the long term, may result in muscle mass accretion. Last but not least, it is also essential to take the nutritional status and the exercise training load into consideration when looking for maintenance or gain of skeletal muscle mass.

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Recent advances in understanding resistance exercise training-induced skeletal muscle hypertrophy in humans

F1000Research ◽

10.12688/f1000research.21588.1 ◽

2020 ◽

Vol 9 ◽

pp. 141 ◽

Cited By ~ 3

Author(s):

Sophie Joanisse ◽

Changhyun Lim ◽

James McKendry ◽

Jonathan C. Mcleod ◽

Tanner Stokes ◽

...

Keyword(s):

Skeletal Muscle ◽

Resistance Exercise ◽

Muscle Mass ◽

Skeletal Muscle Mass ◽

Muscle Hypertrophy ◽

Resistance Exercise Training ◽

Skeletal Muscle Hypertrophy ◽

Recent Advances ◽

Development And Utilization ◽

Exercise Induced

Skeletal muscle plays a pivotal role in the maintenance of physical and metabolic health and, critically, mobility. Accordingly, strategies focused on increasing the quality and quantity of skeletal muscle are relevant, and resistance exercise is foundational to the process of functional hypertrophy. Much of our current understanding of skeletal muscle hypertrophy can be attributed to the development and utilization of stable isotopically labeled tracers. We know that resistance exercise and sufficient protein intake act synergistically and provide the most effective stimuli to enhance skeletal muscle mass; however, the molecular intricacies that underpin the tremendous response variability to resistance exercise-induced hypertrophy are complex. The purpose of this review is to discuss recent studies with the aim of shedding light on key regulatory mechanisms that dictate hypertrophic gains in skeletal muscle mass. We also aim to provide a brief up-to-date summary of the recent advances in our understanding of skeletal muscle hypertrophy in response to resistance training in humans.

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Protein Intake for Skeletal Muscle Hypertrophy with Resistance Training in Seniors

International Journal of Sport Nutrition and Exercise Metabolism ◽

10.1123/ijsnem.16.4.362 ◽

2006 ◽

Vol 16 (4) ◽

pp. 362-372 ◽

Cited By ~ 22

Author(s):

Ryan D. Andrews ◽

David A. MacLean ◽

Steven E. Riechman

Keyword(s):

Skeletal Muscle ◽

Muscle Mass ◽

Lean Mass ◽

Protein Intake ◽

Muscle Hypertrophy ◽

Protein Supplementation ◽

Protein Supplement ◽

Resistance Exercise Training ◽

Post Exercise ◽

Skeletal Muscle Hypertrophy

Variability in protein consumption may influence muscle mass changes induced by resistance exercise training (RET). We sought to administer a post-exercise protein supplement and determine if daily protein intake variability affected variability in muscle mass gains. Men (N = 22) and women (N = 30) ranging in age from 60 to 69 y participated in a 12-wk RET program. At each RET session, participants consumed a post-exercise drink (0.4 g/kg lean mass protein). RET resulted in significant increases in lean mass (1.1 ±1.5 kg), similar between sexes (P > 0.05). Variability in mean daily protein intake was not associated with change in lean mass (r < 0.10, P > 0.05). The group with the highest protein intake (1.35 g · kg−1 · d−1, n = 8) had similar (P > 0.05) changes in lean mass as the group with the lowest daily protein intake (0.72 g · kg−1 · d−1, n = 9). These data suggest that variability in total daily protein intake does not affect variability in lean mass gains with RET in the context of post-exercise protein supplementation.

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p21-Activated Kinase 1 Is Permissive for the Skeletal Muscle Hypertrophy Induced by Myostatin Inhibition

Frontiers in Physiology ◽

10.3389/fphys.2021.677746 ◽

2021 ◽

Vol 12 ◽

Author(s):

Caroline Barbé ◽

Audrey Loumaye ◽

Pascale Lause ◽

Olli Ritvos ◽

Jean-Paul Thissen

Keyword(s):

Skeletal Muscle ◽

Muscle Mass ◽

Skeletal Muscle Mass ◽

Muscle Hypertrophy ◽

Molecular Mechanisms ◽

Muscle Development ◽

The Body ◽

Negative Regulator ◽

Skeletal Muscle Hypertrophy ◽

Myostatin Inhibition

Skeletal muscle, the most abundant tissue in the body, plays vital roles in locomotion and metabolism. Understanding the cellular processes that govern regulation of muscle mass and function represents an essential step in the development of therapeutic strategies for muscular disorders. Myostatin, a member of the TGF-β family, has been identified as a negative regulator of muscle development. Indeed, its inhibition induces an extensive skeletal muscle hypertrophy requiring the activation of Smad 1/5/8 and the Insulin/IGF-I signaling pathway, but whether other molecular mechanisms are involved in this process remains to be determined. Using transcriptomic data from various Myostatin inhibition models, we identified Pak1 as a potential mediator of Myostatin action on skeletal muscle mass. Our results show that muscle PAK1 levels are systematically increased in response to Myostatin inhibition, parallel to skeletal muscle mass, regardless of the Myostatin inhibition model. Using Pak1 knockout mice, we investigated the role of Pak1 in the skeletal muscle hypertrophy induced by different approaches of Myostatin inhibition. Our findings show that Pak1 deletion does not impede the skeletal muscle hypertrophy magnitude in response to Myostatin inhibition. Therefore, Pak1 is permissive for the skeletal muscle mass increase caused by Myostatin inhibition.

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Growth factor-dependent and independent regulation of skeletal muscle mass - Is IGF-1 necessary for skeletal muscle hypertrophy? -

The Journal of Physical Fitness and Sports Medicine ◽

10.7600/jpfsm.2.101 ◽

2013 ◽

Vol 2 (1) ◽

pp. 101-106 ◽

Cited By ~ 2

Author(s):

Mitsunori Miyazaki

Keyword(s):

Skeletal Muscle ◽

Growth Factor ◽

Muscle Mass ◽

Skeletal Muscle Mass ◽

Muscle Hypertrophy ◽

Skeletal Muscle Hypertrophy

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Role of IGF-I in follistatin-induced skeletal muscle hypertrophy

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00098.2015 ◽

2015 ◽

Vol 309 (6) ◽

pp. E557-E567 ◽

Cited By ~ 16

Author(s):

Caroline Barbé ◽

Stéphanie Kalista ◽

Audrey Loumaye ◽

Olli Ritvos ◽

Pascale Lause ◽

...

Keyword(s):

Skeletal Muscle ◽

Muscle Mass ◽

Skeletal Muscle Mass ◽

Muscle Hypertrophy ◽

Muscle Growth ◽

Skeletal Muscle Hypertrophy ◽

Low Concentrations ◽

Igf I

Follistatin, a physiological inhibitor of myostatin, induces a dramatic increase in skeletal muscle mass, requiring the type 1 IGF-I receptor/Akt/mTOR pathway. The aim of the present study was to investigate the role of IGF-I and insulin, two ligands of the IGF-I receptor, in the follistatin hypertrophic action on skeletal muscle. In a first step, we showed that follistatin increases muscle mass while being associated with a downregulation of muscle IGF-I expression. In addition, follistatin retained its full hypertrophic effect toward muscle in hypophysectomized animals despite very low concentrations of circulating and muscle IGF-I. Furthermore, follistatin did not increase muscle sensitivity to IGF-I in stimulating phosphorylation of Akt but, surprisingly, decreased it once hypertrophy was present. Taken together, these observations indicate that increased muscle IGF-I production or sensitivity does not contribute to the muscle hypertrophy caused by follistatin. Unlike low IGF-I, low insulin, as obtained by streptozotocin injection, attenuated the hypertrophic action of follistatin on skeletal muscle. Moreover, the full anabolic response to follistatin was restored in this condition by insulin but also by IGF-I infusion. Therefore, follistatin-induced muscle hypertrophy requires the activation of the insulin/IGF-I pathway by either insulin or IGF-I. When insulin or IGF-I alone is missing, follistatin retains its full anabolic effect, but when both are deficient, as in streptozotocin-treated animals, follistatin fails to stimulate muscle growth.

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Effect of a High Fat and High Protein Diet on Exercise-Induced Skeletal Muscle Hypertrophy in Rats

International Journal Of Nutrition ◽

10.14302/issn.2379-7835.ijn-19-3011 ◽

2019 ◽

Vol 4 (3) ◽

pp. 29-40

Author(s):

Takako Fujii ◽

Tomohiro Sonou ◽

Naoya Nakai ◽

Koji Okamura

Keyword(s):

Skeletal Muscle ◽

Body Weight ◽

Amino Acid ◽

Muscle Mass ◽

Acid Concentration ◽

Skeletal Muscle Mass ◽

Muscle Hypertrophy ◽

High Protein Diet ◽

High Fat ◽

Exercise Induced

The skeletal muscle mass varies by race. Dietary habits over generations are a factor that influences the skeletal muscle mass, as well as genetic factors. Therefore, we investigated the effects of diets with different macronutrient contents on exercise-induced muscle hypertrophy in rats. Male 4-week-old Sprague–Dawley rats were randomly divided into three groups: a normal-diet (N), high-protein diet (HP) and high-fat diet (HF) group. The food intake was manipulated to gain comparable body weight across the three groups. All rats were performed a climbing training exercise for 8 weeks. The final body weight and weight of the liver, kidneys and adipose tissues did not significantly differ among the groups. The flexor hullucis lingus was significantly higher in the HF group than in the HP group. The total lipid content in the muscle was significantly higher in the HF group than in the N group, while it did not differ significant between the HF and HP groups. There were no marked differences in the water or protein content in the muscle among the groups. The plasma amino acid concentration was significantly or tended to be lower in the HP group than in the HF or N group, except for the branched-chain amino acid concentration, which tended to be higher after ingesting the HP diet than other diets. These findings suggest that consuming an HP diet is not likely to facilitate exercise-induced muscle hypertrophy, partly due to the plasma amino acid imbalance induced by habitual HP diet consumption.

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