WordNet

make ones way by force; "He muscled his way into the office"
animal tissue consisting predominantly of contractile cells (同)muscular_tissue
one of the contractile organs of the body (同)musculus
authority or power or force (especially when used in a coercive way); "the senators used their muscle to get the party leader to resign"
abnormal enlargement of a body part or organ
undergo hypertrophy; "muscles can hypertrophy when people take steroids"

PrepTutorEJDIC

〈U〉(動物体の組織としての)『筋肉』,筋(きん);〈C〉(体の各部を動かす)筋肉 / 〈U〉力,(特に)筋力,腕力 / 《俗に》(…に)強引に割り込む《+『in on』(『into, through』)+『名』》
(生物体の部分・器官の)異常肥大,異常発達
筋肉の,筋力のある / 力ずくの

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/10/22 07:42:49」(JST)

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Athletes use a combination of strength training, diet, and supplementation to induce muscle hypertrophy.

Muscle hypertrophy involves an increase in size of skeletal muscle through an increase in the size of its component cells. Hypertrophy can be broken down into two types of categories: myofibrillar and sarcoplasmic. Each of these specific types of muscle hypertrophy will result in increasing size of cells, but not of equal effect. Sarcoplasmic hypertrophy is focused on increasing the actual size of the muscle, and less on increasing strength. Myofibril hypertrophy will focus more on strength increase and less on an increase in the size of the skeletal muscle.

Hypertrophy stimuli[edit]

A range of stimuli can increase the volume of muscle cells. Summarizing, these changes occur as an adaptive response that serves to increase the ability to generate force or resist fatigue in anaerobic conditions.

Strength training[edit]

Main article: Strength training

Strength training typically produces a combination of the two different types of hypertrophy: contraction against 80 to 90% of the one-repetition maximum for 2–6 repetitions (reps) causes myofibrillated hypertrophy to dominate (as in powerlifters, Olympic lifters and strength athletes), whereas several repetitions (generally 8–12 for bodybuilding or 12 or more for muscular endurance) against a submaximal load facilitates mainly sarcoplasmic hypertrophy (professional bodybuilders and endurance athletes).^{[citation needed]} The first measurable effect is an increase in the neural drive stimulating muscle contraction. Within just a few days, an untrained individual can achieve measurable strength gains resulting from "learning" to use the muscle.^{[citation needed]} As the muscle continues to receive increased demands, the synthetic machinery is upregulated. Although all the steps are not yet clear, this upregulation appears to begin with the ubiquitous second messenger system (including phospholipases, protein kinase C, tyrosine kinase, and others).^{[citation needed]} These, in turn, activate the family of immediate-early genes, including c-fos, c-jun and myc. These genes appear to dictate the contractile protein gene response.^{[citation needed]}

Progressive overload is considered the most important principle behind hypertrophy, so increasing the weight, repetitions (reps), and sets will all have a positive impact on growth. Some experts create complicated plans that manipulate weight, reps, and sets, increasing one while decreasing the others to keep the schedule varied and less repetitive.

Anaerobic training[edit]

Main article: Anaerobic exercise

Experts and professionals differ widely on the best approaches to specifically achieve muscle growth (as opposed to focusing on gaining strength, power, or endurance); it was generally considered that consistent anaerobic strength training will produce hypertrophy over the long term, in addition to its effects on muscular strength and endurance. Muscular hypertrophy can be increased through strength training and other short-duration, high-intensity anaerobic exercises. Lower-intensity, longer-duration aerobic exercise generally does not result in very effective tissue hypertrophy; instead, endurance athletes enhance storage of fats and carbohydrates within the muscles,^[1] as well as neovascularization.^[2]^[3]

Factors affecting hypertrophy[edit]

Several biological factors such as age and nutrition can affect muscle hypertrophy. During puberty in males, hypertrophy occurs at an increased rate. Natural hypertrophy normally stops at full growth in the late teens. An adequate supply of amino acids is essential to produce muscle hypertrophy. As testosterone is one of the body's major growth hormones, on average, men find hypertrophy much easier to achieve than women. Taking additional testosterone, as in anabolic steroids, will increase results. It is also considered a performance-enhancing drug, the use of which can cause competitors to be suspended or banned from competitions. In addition, testosterone is also a medically regulated substance in most countries, making it illegal to possess without a medical prescription.

Changes in protein synthesis and muscle cell biology associated with stimuli[edit]

Protein synthesis[edit]

Main article: Protein biosynthesis

Ultimately the message filters down to alter the pattern of protein expression. The additional contractile proteins appear to be incorporated into existing myofibrils (the chains of sarcomeres within a muscle cell). There appears to be some limit to how large a myofibril can become: at some point, they split. These events appear to occur within each muscle fiber. That is, hypertrophy results primarily from the growth of each muscle cell, rather than an increase in the number of cells. Skeletal muscle cells are however unique in the body in that they can contain multiple nuclei, and the number of nuclei can increase.^[4]

Cortisol decreases amino acid uptake by muscle tissue, and inhibits protein synthesis.^[5] The short-term increase in protein synthesis that occurs subsequent to resistance training returns to normal after approximately 28 hours in adequately fed male youths. ^[6] Another study determined that muscle protein synthesis was elevated even 72 hours following training.^[7]

A small study performed on young and elderly found that ingestion of 340 grams of lean beef (90 g protein) did not increase muscle protein synthesis any more than ingestion of 113 grams of lean beef (30 g protein). In both groups, muscle protein synthesis increased by 50%. The study concluded that more than 30 g protein in a single meal did not further enhance the stimulation of muscle protein synthesis in young and elderly.^[8] However, this study didn't check protein synthesis in relation to training; therefore conclusions from this research are controversial.

It is not uncommon for bodybuilders to advise a protein intake as high as 2–4 g per kilogram of bodyweight per day.^[9] However, scientific literature has suggested this is higher than necessary, as protein intakes greater than 1.8 g per kilogram of body weight showed to have no greater effect on muscle hypertrophy.^[10] A study carried out by American College of Sports Medicine (2002) put the recommended daily protein intake for athletes at 1.2–1.8 g per kilogram of body weight.^[11]^[12]^[10] Conversely, Di Pasquale (2008), citing recent studies, recommends a minimum protein intake of 2.2 g/kg "for anyone involved in competitive or intense recreational sports who wants to maximize lean body mass but does not wish to gain weight. However athletes involved in strength events (..) may need even more to maximize body composition and athletic performance. In those attempting to minimize body fat and thus maximize body composition, for example in sports with weight classes and in bodybuilding, it’s possible that protein may well make up over 50% of their daily caloric intake."^[13]

Microtrauma[edit]

Main article: Microtrauma

Microtrauma, which is tiny damage to the fibers, may play a significant role in muscle growth. ^[14] When microtrauma occurs (from weight training or other strenuous activities), the body responds by overcompensating, replacing the damaged tissue and adding more, so that the risk of repeat damage is reduced. Damage to these fibers have been theorized as the possible cause for the symptoms of delayed onset muscle soreness (DOMS), and is why progressive overload is essential to continued improvement, as the body adapts and becomes more resistant to stress.

Myofibrillar vs. sarcoplasmic hypertrophy[edit]

In the bodybuilding and fitness community and even in some academic books skeletal muscle hypertrophy is described as being in one of two types: Sarcoplasmic or myofibrillar. According to this hypothesis, during sarcoplasmic hypertrophy, the volume of sarcoplasmic fluid in the muscle cell increases with no accompanying increase in muscular strength, whereas during myofibrillar hypertrophy, actin and myosin contractile proteins increase in number and add to muscular strength as well as a small increase in the size of the muscle. Sarcoplasmic hypertrophy is greater in the muscles of bodybuilders while myofibrillar hypertrophy is more dominant in Olympic weightlifters.^[15] These two forms of adaptations rarely occur completely independently of one another; one can experience a large increase in fluid with a slight increase in proteins, a large increase in proteins with a small increase in fluid, or a relatively balanced combination of the two.

In sports[edit]

Examples of increased muscle hypertrophy are seen in various professional sports, mainly strength related sports such as boxing, bodybuilding, mixed martial arts, rugby, professional wrestling and various forms of gymnastics. These athletes train extensively in strength as well as cardiovascular and muscular endurance training.

References[edit]

^ van Loon LJ, Goodpaster BH (2006). "Increased intramuscular lipid storage in the insulin-resistant and endurance-trained state". Pflugers Arch. 451 (5): 606–16. doi:10.1007/s00424-005-1509-0. PMID 16155759.
^ Soares JM (1992). "Effects of training on muscle capillary pattern: intermittent vs continuous exercise". The Journal of sports medicine and physical fitness 32 (2): 123–7. PMID 1279273.
^ Prior BM, Yang HT, Terjung RL (2004). "What makes vessels grow with exercise training?". J. Appl. Physiol. 97 (3): 1119–28. doi:10.1152/japplphysiol.00035.2004. PMID 15333630.
^ Bruusgaard JC, Johansen IB, Egner IM, Rana ZA & Gundersen K. (2010). Myonuclei acquired by overload exercise precede hypertrophy and are not lost on detraining. Proc Natl Acad Sci U S A 107, 15111-15116.
^ Manchester, K.L., “Sites of Hormonal Regulation of Protein Metabolism. p. 229”, Mammalian Protein [Munro, H.N., Ed.]. Academic Press, New York. p. 273.
^ Am J Physiol Regul Integr Comp Physiol. 2008 Jan;294(1):R172-8. Epub 2007 Nov 21. "Resistance training alters the response of fed state mixed muscle protein synthesis in young men." Exercise Metabolism Research Group, McMaster University, Hamilton, Ontario, Canada.
^ Miller B.F., Olesen J.L., Hansen M. et al. (2005) Coordinated collagen and muscle protein synthesis in human patella tendon and quadriceps muscle after exercise. J Physiol, 567, 1021-1033.
^ Symons, T. B.; Sheffield-Moore, M.; Wolfe, R. R.; Paddon-Jones, D. (2009). "A Moderate Serving of High-Quality Protein Maximally Stimulates Skeletal Muscle Protein Synthesis in Young and Elderly Subjects". Journal of the American Dietetic Association 109 (9): 1582–1586. doi:10.1016/j.jada.2009.06.369. PMID 19699838. edit
^ Bodybuilders and Protein – Part 2. Leehayward.com. Retrieved on 2011-06-19.
^ ^a ^b Tarnopolsky, MA; Atkinson, SA; MacDougall, JD; Chesley, A; Phillips, S; Schwarcz, HP (1992). "Evaluation of protein requirements for trained strength athletes". Journal of applied physiology (Bethesda, Md. : 1985) 73 (5): 1986–95. PMID 1474076.
^ Rankin, JW (2002). "Weight loss and gain in athletes". Current sports medicine reports 1 (4): 208–13. PMID 12831697.
^ . doi:10.1080/02640419108729866. Missing or empty |title= (help)
^ Di Pasquale, Mauro G. (2008). "Utilization of Proteins in Energy Metabolism". In Ira Wolinsky, Judy A. Driskell. Sports Nutrition: Energy metabolism and exercise. CRC Press. p. 79. ISBN 978-0-8493-7950-5.
^ http://www.unm.edu/~lkravitz/Article%20folder/musclesgrowLK.html
^ Kraemer, William J.; Zatsiorsky, Vladimir M. (2006). Science and practice of strength training. Champaign, IL: Human Kinetics. p. 50. ISBN 0-7360-5628-9.

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English Journal

Direct role for smooth muscle cell mineralocorticoid receptors in vascular remodeling: novel mechanisms and clinical implications.

Koenig JB1, Jaffe IZ.Author information 1Sackler School of Graduate Biomedical Sciences at Tufts University School of Medicine, Boston, MA, USA, jennybkoenig@gmail.com.AbstractThe mineralocorticoid receptor (MR) is a key regulator of blood pressure. MR antagonist drugs are used to treat hypertension and heart failure, resulting in decreased mortality by mechanisms that are not completely understood. In addition to the kidney, MR is also expressed in the smooth muscle cells (SMCs) of the vasculature, where it is activated by the hormone aldosterone and affects the expression of genes involved in vascular function at the cellular and systemic levels. Following vascular injury due to mechanical or physiological stresses, vessels undergo remodeling resulting in SMC hypertrophy, migration, and proliferation, as well as vessel fibrosis. Exuberant vascular remodeling is associated with poor outcomes in cardiovascular patients. This review compiles recent findings on the specific role of SMC-MR in the vascular remodeling process. The development and characterization of a SMC-specific MR-knockout mouse has demonstrated a direct role for SMC-MR in vascular remodeling. Additionally, several novel mechanisms contributing to SMC-MR-mediated vascular remodeling have been identified and are reviewed here, including Rho-kinase signaling, placental growth factor signaling through vascular endothelial growth factor type 1 receptor, and galectin signaling.
Current hypertension reports.Curr Hypertens Rep.2014 May;16(5):427. doi: 10.1007/s11906-014-0427-y.
The mineralocorticoid receptor (MR) is a key regulator of blood pressure. MR antagonist drugs are used to treat hypertension and heart failure, resulting in decreased mortality by mechanisms that are not completely understood. In addition to the kidney, MR is also expressed in the smooth muscle cell
PMID 24633842

The A55T and K153R polymorphisms of MSTN gene are associated with the strength training-induced muscle hypertrophy among Han Chinese men.

Li X1, Wang SJ, Tan SC, Chew PL, Liu L, Wang L, Wen L, Ma L.Author information 1a Department of Physical Education , Jiaozuo Teachers' College , Jiaozuo , China.AbstractAbstract Myostatin, encoded by the MSTN gene, is a strong regulator of skeletal muscle growth. The present study aimed to investigate whether the A55T and K153R polymorphisms of MSTN were associated with the strength training-induced muscle hypertrophy among Han Chinese men. A total of 94 healthy, untrained men were recruited for an 8-week strength training programme. The thicknesses of biceps and quadriceps, along with anthropometric measurements of the participants, were assessed before and after the programme. The MSTN polymorphisms were subsequently genotyped employing polymerase chain reaction-restriction fragment length polymorphism technique and confirmed by DNA sequencing. One-way analysis of variance was used to compare the pre- and post-training measurements between carriers of different polymorphic genotypes. Our results indicated that individuals with AT + TT genotype of the A55T polymorphism showed a significant increase in the thickness of biceps (0.292 ± 0.210 cm, P = 0.03), but not quadriceps (0.254 ± 0.198 cm, P = 0.07), compared to carriers of AA genotype. For the K153R polymorphism, the increases in the thicknesses of both biceps (0.300 ± 0.131 cm) and quadriceps (0.421 ± 0.281 cm) were significantly higher among individuals with KR than those with KK genotypes (P < 0.01 for both muscles). The results obtained therefore suggested a possible association between the two polymorphisms and the strength training-induced muscle hypertrophy among men of Han Chinese ethnicity.
Journal of sports sciences.J Sports Sci.2014 May;32(9):883-91. doi: 10.1080/02640414.2013.865252. Epub 2014 Jan 30.
Abstract Myostatin, encoded by the MSTN gene, is a strong regulator of skeletal muscle growth. The present study aimed to investigate whether the A55T and K153R polymorphisms of MSTN were associated with the strength training-induced muscle hypertrophy among Han Chinese men. A total of 94 healthy, u
PMID 24479661

Skeletal muscle reactive oxygen species: A target of good cop/bad cop for exercise and disease.

Mason S, Wadley GD.AbstractMetabolic stresses associated with disease, ageing, and exercise increase the levels of reactive oxygen species (ROS) in skeletal muscle. These ROS have been linked mechanistically to adaptations in skeletal muscle that can be favourable (i.e. in response to exercise) or detrimental (i.e. in response to disease). The magnitude, duration (acute versus chronic), and cellular origin of the ROS are important underlying factors in determining the metabolic perturbations associated with the ROS produced in skeletal muscle. In particular, insulin resistance has been linked to excess ROS production in skeletal muscle mitochondria. A chronic excess of mitochondrial ROS can impair normal insulin signalling pathways and glucose disposal in skeletal muscle. In contrast, ROS produced in skeletal muscle in response to exercise has been linked to beneficial metabolic adaptations including mitochondrial biogenesis and muscle hypertrophy. Moreover, unlike insulin resistance, exercise-induced ROS appears to be primarily of non-mitochondrial origin. The present review summarizes the diverse ROS-targeted metabolic outcomes associated with insulin resistance versus exercise in skeletal muscle, thus, presenting two contrasting perspectives of pathologically harmful versus physiologically beneficial ROS. Here, we discuss the key sites of ROS production during exercise and the effect of ROS in skeletal muscle of people with type 2 diabetes.
Redox report : communications in free radical research.Redox Rep.2014 May;19(3):97-106. doi: 10.1179/1351000213Y.0000000077. Epub 2014 Jan 3.
Metabolic stresses associated with disease, ageing, and exercise increase the levels of reactive oxygen species (ROS) in skeletal muscle. These ROS have been linked mechanistically to adaptations in skeletal muscle that can be favourable (i.e. in response to exercise) or detrimental (i.e. in respons
PMID 24620937

Japanese Journal

筋肥大のメカニズムとレジスタンストレーニングへの応用

Schoenfeld Brad J.
Strength & conditioning journal : 日本ストレングス&コンディショニング協会機関誌 19(10), 59-71, 2012-12
NAID 40019499758

Effect of multiple set on intramuscular metabolic stress during low-intensity resistance exercise with blood flow restriction

Suga Tadashi,Okita Koichi,Takada Shingo,Omokawa Masashi,Kadoguchi Tomoyasu,Yokota Takashi,Hirabayashi Kagami,Takahashi Masashige,Morita Noriteru,Horiuchi Masahiro,Kinugawa Shintaro,Tsutsui Hiroyuki
European Journal of Applied Physiology 112(11), 3915-3920, 2012-11
… Intramuscular metabolic stress, defined as intramuscular metabolites and pH, and muscle fiber recruitment were evaluated by 31P-magnetic resonance spectroscopy. …
NAID 120004979511