leonidas1977
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A jurnal i read online. so i downloaded the doc, and thought i would copy and paste it here. its a good read. enjoy.
The Mechanisms of Muscle Hypertrophy and Their Application to Resistance Training
Schoenfeld, Brad J.
Global Fitness Services, Scarsdale, New York
(from Journal of Strength and Conditioning Research, 24 (10)/2857-2873)
HIGHLIGHTS…
Contractile hypertrophy can occur either by adding sarcomeres in series or in parallel.
The majority of exercise-induced hypertrophy subsequent to traditional resistance training programs results from an increase of sarcomeres and myofibrils added in parallel. When skeletal muscle is subjected to an overload stimulus, it causes perturbations in myofibers and the related extracellular matrix. This sets off a chain of myogenic events that ultimately leads to an increase in the size and amounts of the myofibrillar contractile proteins actin and myosin, and the total number of sarcomeres in parallel. This, in turn, augments the diameter of individual fibers and thereby results in an increase in muscle cross-sectional area.
Muscle is a postmitotic tissue, meaning that it does not undergo significant cell replacement throughout life.
Satellite cells are thought to facilitate muscle hypertrophy in several ways. For one, they donate extra nuclei to muscle fibers, increasing the capacity to synthesize new contractile proteins. Because a muscle's nuclear-content-to-fiber-mass ratio remains constant during hypertrophy, changes require an external source of mitotically active cells. Satellite cells retain mitotic capability and thus serve as the pool of a myonuclei to support muscle growth. This is consistent with the concept of myonuclear domain, which proposes that the myonucleus regulates mRNA production for a finite sarcoplasmic volume and any increases in fiber size must be accompanied by a proportional increase in myonuclei. Given that muscles are comprised of multiple myonuclear domains, hypertrophy could conceivably occur as a result of either an increase in the number of domains (via an increase in myonuclear number) or an increase in the size of existing domains. Both are thought to occur in hypertrophy, with a significant contribution from satellite cells.
Structurally, IGF-1 is a peptide hormone, so named because of its structural similarities to insulin. Insulin-like growth factor receptors are found in activated satellite cells, adult myofibers, and Schwann cells.
Although the exact mechanisms of IGF-1's mode of action have not been fully elucidated, it is believed that mechano-stimulation causes the IGF-1 gene to be spliced toward MGF, which in turn “kick starts” muscle hypertrophy.
Testosterone is a cholesterol-derived hormone that has a considerable anabolic effect on muscle tissue. In addition to its effects on muscle, testosterone also can interact with receptors on neurons and thereby increase the amount of neurotransmitters released, regenerate nerves, and increase cell body size.
Although the effects of testosterone on muscle are seen in the absence of exercise, its actions are magnified by mechanical loading, promoting anabolism both by increasing the protein synthetic rate and inhibiting protein breakdown.
The Mechanisms of Muscle Hypertrophy and Their Application to Resistance Training
Schoenfeld, Brad J.
Global Fitness Services, Scarsdale, New York
(from Journal of Strength and Conditioning Research, 24 (10)/2857-2873)
HIGHLIGHTS…
Contractile hypertrophy can occur either by adding sarcomeres in series or in parallel.
The majority of exercise-induced hypertrophy subsequent to traditional resistance training programs results from an increase of sarcomeres and myofibrils added in parallel. When skeletal muscle is subjected to an overload stimulus, it causes perturbations in myofibers and the related extracellular matrix. This sets off a chain of myogenic events that ultimately leads to an increase in the size and amounts of the myofibrillar contractile proteins actin and myosin, and the total number of sarcomeres in parallel. This, in turn, augments the diameter of individual fibers and thereby results in an increase in muscle cross-sectional area.
Muscle is a postmitotic tissue, meaning that it does not undergo significant cell replacement throughout life.
Satellite cells are thought to facilitate muscle hypertrophy in several ways. For one, they donate extra nuclei to muscle fibers, increasing the capacity to synthesize new contractile proteins. Because a muscle's nuclear-content-to-fiber-mass ratio remains constant during hypertrophy, changes require an external source of mitotically active cells. Satellite cells retain mitotic capability and thus serve as the pool of a myonuclei to support muscle growth. This is consistent with the concept of myonuclear domain, which proposes that the myonucleus regulates mRNA production for a finite sarcoplasmic volume and any increases in fiber size must be accompanied by a proportional increase in myonuclei. Given that muscles are comprised of multiple myonuclear domains, hypertrophy could conceivably occur as a result of either an increase in the number of domains (via an increase in myonuclear number) or an increase in the size of existing domains. Both are thought to occur in hypertrophy, with a significant contribution from satellite cells.
Structurally, IGF-1 is a peptide hormone, so named because of its structural similarities to insulin. Insulin-like growth factor receptors are found in activated satellite cells, adult myofibers, and Schwann cells.
Although the exact mechanisms of IGF-1's mode of action have not been fully elucidated, it is believed that mechano-stimulation causes the IGF-1 gene to be spliced toward MGF, which in turn “kick starts” muscle hypertrophy.
Testosterone is a cholesterol-derived hormone that has a considerable anabolic effect on muscle tissue. In addition to its effects on muscle, testosterone also can interact with receptors on neurons and thereby increase the amount of neurotransmitters released, regenerate nerves, and increase cell body size.
Although the effects of testosterone on muscle are seen in the absence of exercise, its actions are magnified by mechanical loading, promoting anabolism both by increasing the protein synthetic rate and inhibiting protein breakdown.