Protein Intake for Skeletal Muscle Hypertrophy with Resistance Training in Seniors

2006 ◽  
Vol 16 (4) ◽  
pp. 362-372 ◽  
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.

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

F1000Research ◽  
2020 ◽  
Vol 9 ◽  
pp. 141 ◽  
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.

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

Nutrients ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 2023
Author(s):  
Louise Deldicque
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Protein Intake ◽  
Skeletal Muscle Mass ◽  
Muscle Hypertrophy ◽  
Sport Performance ◽  
Skeletal Muscle Hypertrophy ◽  
Exercise Induced ◽  
Net Protein

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.

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 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.

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

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.

Sarcopenia—definitions and epidemiology

2017 ◽  
pp. 409-414
Author(s):  
José A. Morais
Keyword(s):  
Older Adults ◽  
Skeletal Muscle ◽  
Muscle Mass ◽  
Protein Intake ◽  
Skeletal Muscle Mass ◽  
Handgrip Strength ◽  
Resistance Exercise Training ◽  
Adverse Health Outcomes ◽  
Age Related ◽  
Underlying Mechanisms

Sarcopenia is a progressive and inevitable loss of skeletal muscle mass and strength associated with ageing that places older adults at high risk for adverse health outcomes. Up to of 15% of older adults suffer negative healthcare consequences because of sarcopenia. Furthermore, it is responsible for two to four times greater risk of disability. Expert groups have proposed clinical oriented criteria based on gait speed <0.8 m/s and low handgrip strength before performing muscle mass assessment. Multiple aetiologies are implicated in the development of sarcopenia including age-related, lifestyle, neurodegeneration, hormonal, and inflammation factors. Resistance exercise training and higher than recommended protein intake are two accessible means to counteract sarcopenia. Hormonal interventions, despite amelioration in muscle and fat masses, have not led to significant gains in function. Sarcopenia shares many features with frailty and can be considered as one of its underlying mechanisms.

scholarly journals Short-Term Protein Supplementation Does Not Alter Energy Intake, Macronutrient Intake and Appetite in 50–75 Year Old Adults

Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1711
Author(s):  
Esme R. Tuttiett ◽  
Dan J. Green ◽  
Emma J. Stevenson ◽  
Thomas R. Hill ◽  
Bernard M. Corfe ◽  
...  
Keyword(s):  
Muscle Mass ◽  
Protein Intake ◽  
Nutrient Intake ◽  
Phase 1 ◽  
Protein Supplementation ◽  
Older Age ◽  
Protein Supplement ◽  
Dietary Intakes ◽  
Short Term ◽  
Energy And Nutrient Intake

Ageing is associated with a reduction in muscle mass and strength, termed sarcopenia. Dietary protein is important for the maintenance of muscle mass through the promotion of muscle protein synthesis. However, protein is also reported to be a highly satiating nutrient. This raises concerns that protein intake for musculoskeletal health reasons in older adults may exacerbate age-related decreased appetite and may result in reduced energy and nutrient intake. This study aimed to investigate the effect of short-term protein supplementation and its timing (morning vs. evening), on energy and nutrient intake and appetite measures in middle-older age adults. Twenty-four 50–75 year olds were recruited to a randomised cross-over trial. In phase 1 (pre-supplementation) participants completed a food diary and reported hunger and appetite on three alternate days. During the second and third phases, participants consumed a 20 g whey protein gel (78 mL/368 kJ), for four days, either in the morning (after breakfast) or the evening (before bed), whilst completing the same assessments as phase 1. No differences in dietary intakes of energy, macronutrients and micronutrients were recorded when comparing the pre-supplementation phase to the protein supplementation phases, irrespective of timing (excluding the contribution of the protein supplement itself). Similarly, no differences were observed in self-reported feelings of hunger and appetite. In conclusion, a 20 g/day whey protein supplement given outside of meal-times did not alter habitual dietary intakes, hunger or appetite in this middle-older age adult population in the short-term. This approach may be a useful strategy to increasing habitual protein intake in the middle-older age population.

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