scholarly journals Post‐exercise ingestion of a high protein diet does not enhance exercise‐induced skeletal muscle hypertrophy in rats

2011 ◽  
Vol 25 (S1) ◽  
Author(s):  
Tomotsugu Matsui ◽  
Yukari Yokota ◽  
Emi Kondo ◽  
Koji Okamura
Keyword(s):  
Skeletal Muscle ◽  
Muscle Hypertrophy ◽  
High Protein Diet ◽  
High Protein ◽  
Protein Diet ◽  
Post Exercise ◽  
Skeletal Muscle Hypertrophy ◽  
Exercise Induced

scholarly journals Post‐exercise meal timing alleviates decreased protein efficiency for skeletal muscle growth in rats fed high‐protein diet

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Emi Kondo ◽  
Nagisa Inoue ◽  
Sachiko Okada ◽  
Keiko Yaji ◽  
Ayumi Hirota ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Growth ◽  
High Protein Diet ◽  
High Protein ◽  
Protein Diet ◽  
Post Exercise ◽  
Skeletal Muscle Growth ◽  
Meal Timing

scholarly journals Pericytes Contribute to Exercise‐Induced Skeletal Muscle Hypertrophy

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Kai Zou ◽  
Heather D. Huntsman ◽  
Carmen Valero ◽  
John T. Skelton ◽  
Joseph T. Adams ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Hypertrophy ◽  
Skeletal Muscle Hypertrophy ◽  
Exercise Induced

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.

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 A high protein diet maintains glucose production and enhances gluconeogenesis during exercise induced energy deficit

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Tracey J Smith ◽  
Matthew A Pikosky ◽  
Jean‐Marc Schwartz ◽  
Jennifer Rood ◽  
Carmen Castaneda‐Sceppa ◽  
...  
Keyword(s):  
High Protein Diet ◽  
Glucose Production ◽  
High Protein ◽  
Protein Diet ◽  
Energy Deficit ◽  
Exercise Induced

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.

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