related to muscle hypertrophy. Determining if hypertrophy occurs after rehabilitation and if it may be responsible for increases in measured force will allow for more informed decisions regarding the prescription of therapeutic exercise for the treatment of LAS and CAI. Analyzing muscle morphological
Mark A. Feger, Luke Donovan, C. Collin Herb, Geoffrey G. Handsfield, Silvia S. Blemker, Joseph M. Hart, Susan A. Saliba, Mark F. Abel, Joseph S. Park and Jay Hertel
Christopher Kevin Wong, Lizbeth Conway, Grant Fleming, Caitlin Gopie, Dara Liebeskind and Stephen Xue
attributed to neural adaptations that facilitate muscle activation, 1 while muscle hypertrophy and strength gains occur later, after 6 to 13 weeks. 2 Recent research has shown that, despite muscle hypertrophy, weakness can persist, particularly in the early stages of joint pathology. 3 , 4 Joint and
Samuel R. Heaselgrave, Joe Blacker, Benoit Smeuninx, James McKendry and Leigh Breen
Skeletal muscle is pivotal in the maintenance of a healthy lifestyle, 1 favoring preservation and/or accretion of muscle mass, strength, and power. The most potent nonpharmacological stimulus inducing skeletal muscle hypertrophy and strength is resistance training (RT). Mechanical tension and
Manoel E. Lixandrão, Hamilton Roschel, Carlos Ugrinowitsch, Maira Miquelini, Ieda F. Alvarez and Cleiton Augusto Libardi
partial blood-flow restriction (BFR-RE) results in comparable muscle hypertrophy to that observed in HI-RE, even in the absence of muscular failure. 5 – 7 In spite of a similar muscle hypertrophy, little is known about the psychophysiological stress imposed by these different exercise protocols. A simple
Gary J. Slater, Jennifer Sygo and Majke Jorgensen
interested in promoting muscle hypertrophy. Although athletes may periodically attempt to promote skeletal muscle hypertrophy, key nutritional issues are broader than those pertinent to hypertrophy alone. These include the strategic timing of nutrient intake to maximize fuelling and recovery objectives, plus
Lauren Anne Lipker, Caitlyn Rae Persinger, Bradley Steven Michalko and Christopher J. Durall
Clinical Scenario Quadriceps atrophy and weakness are common after anterior cruciate ligament reconstruction (ACLR). 1 , 2 Blood flow restriction (BFR) therapy, alone or in combination with exercise, has shown some promise in promoting muscular hypertrophy. 1 – 3 This review was conducted to
Gustavo Monnerat, Alex S. Maior, Marcio Tannure, Lia K.F.C. Back and Caleb G.M. Santos
Classical twin studies that presented heritability rates associated with performance in various sports disciplines support the value of genetics in determining the response. In addition, numerous trials involving physiological responses such as hypertrophy, energy expenditure, vasodilation, cardiac output
Iván Chulvi-Medrano, Moisés Picón-Martínez, Juan Manuel Cortell-Tormo, Juan Tortosa-Martínez, Diego Alexandre Alonso-Aubin and Yasser Alakhdar
contribute to understanding the physiopathology of tendinopathy. 19 Additionally, LI-BFR has been suggested as an alternative RT method to improve hypertrophy and strength in a clinical population and individuals who have contraindicated the high mechanical stress associated with conventional vigorous RT in
John C. Lawrence Jr.
Muscle mass is influenced by many factors including genetically programmed changes, hormonal state, level of activity, and disease processes. Ultimately, whether or not a muscle hypertrophies or atrophies is determined by a simple relationship between the rates of protein synthesis and degradation. When synthesis exceeds degradation, the muscle hypertrophies, and vice versa. In contrast to this simple relationship, the processes that control muscle protein synthesis and degradation are complex. Recently, significant progress has been made in understanding the biochemical mechanisms that control the rate of translation initiation, which is generally the limiting phase in protein synthesis.
Resistance exercise can effectively result in an increase in muscle mass, or hypertrophy, which generally becomes apparent after several weeks of training. Muscle hypertrophy requires muscle protein synthesis to exceed protein breakdown during an extended time period. It has been firmly established that the interaction between exercise and nutrition (i.e., protein intake) is necessary to attain net protein accretion in skeletal muscle. The stimulation of protein synthesis is caused in part by stimulation of mRNA translation initiation. There is relatively little information on the response of intracellular signaling controlling mRNA translation to exercise and nutrition, especially in humans, but the available data in humans seem to suggest that a single bout of resistance exercise does not substantially enhance PI-3 kinase/mTOR signaling during the first 2 h after exercise. Moreover, it is demonstrated that the ingestion of protein or amino acids after exercise is crucial to further stimulate molecular signaling that controls translation initiation. The aim of this review is to provide an overview of the intracellular signaling related to translational control and to provide a summary of the current knowledge about the response of the signaling pathways controlling the anabolic response to exercise and nutrient intake in vivo in humans.