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Muscle hyperplasia is the increase of skeletal muscle fibre number. It is a rare phenomenon in humans, but it has been observed in adult animals and possibly human athletes. Muscle hyperplasia occurs when the rate of muscle contractile protein synthesis is greater than decay, leading to greater numbers of actin and myosin filaments in the myofibrils. The myofibrils within each muscle fibre split, resulting in more myofibrils in each muscle fibre.
| Characteristics | Values |
|---|---|
| Muscle hyperplasia in humans | Rare |
| Muscle hyperplasia in adult animals | Common |
| Muscle hyperplasia in human athletes | Possible |
| Cause of muscle hyperplasia | Extreme muscle force generation |
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What You'll Learn
Muscle hyperplasia is rare in humans
Humans have the potential for hyperplasia, but it does not happen on a large scale. There is limited data to prove this in humans, although there is evidence that it occurs in adult animals and possibly human athletes. It is thought that hyperplasia only occurs under very rare conditions of extreme muscle force generation, and even then, the increase in muscle fibres is only by a few percent.
Hyperplasia has been observed in birds and mammals, where an increase in the number of muscle fibres has been shown. In humans, however, the increase in muscle size is primarily due to an increase in the size of individual muscle fibres, rather than an increase in the number of fibres. This is supported by the fact that myofiber hypertrophy, or an increase in muscle weight, is the primary physiological adaptation to strength training.
There is some suggestion that hyperplasia may play a role in the adaptation to increased workload, but this is not yet fully understood. It has been proposed that satellite cells are recruited during skeletal muscle hypertrophy, which could potentially lead to hyperplasia. However, further study is needed to confirm this.
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Muscle hypertrophy
Hypertrophy occurs in response to a higher load on the muscle, which activates inducible agents such as IGF-1. IGF-1 binds to its receptor, the tyrosine kinase IGF1 receptor (IGF1R), which increases the activation of the downstream phosphatidylinositol-3 kinase (PI3K)/Akt pathway, increasing the rate of protein synthesis.
Myofiber hypertrophy is the primary physiological adaptation to strength training and usually results in an increase in muscle weight. Insulin-like growth factor I (IGF-I) is increased with higher levels of muscle activity and has been reported to stimulate hypertrophy. However, further study is necessary to understand the mechanisms.
According to Fleck and Kraemer (2004), humans have the potential for hyperplasia, but it does not happen on a large scale and is far from the dominating cause of hypertrophy. An increase in the number of muscle fibres has been shown in birds and mammals, but there is limited data to prove this in humans.
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Muscle enlargement in adult animals
Scientists have used three models to study the cellular mechanisms of muscle enlargement: compensatory hypertrophy, stretch, and exercise. Each of these models has provided direct and indirect evidence supporting the occurrence of muscle fibre hyperplasia. Direct counts of muscle fibres have shown that both exercise and stretch overload result in significant increases (range = 9-52%) in fibre number.
Muscle hypertrophy occurs in response to a higher load on the muscle, which activates inducible agents such as IGF-1. IGF-1 binds to its receptor, the tyrosine kinase IGF1 receptor (IGF1R), which increases the activation of the downstream phosphatidylinositol-3 kinase (PI3K)/Akt pathway, increasing the rate of protein synthesis. During muscle hypertrophy, the rate of muscle contractile protein synthesis is greater than decay, leading to greater numbers of actin and myosin filaments in the myofibrils. The myofibrils within each muscle fibre split, resulting in more myofibrils in each muscle fibre.
Myofiber hypertrophy is the primary physiological adaptation to strength training and usually results in an increase in muscle weight. Insulin-like growth factor I (IGF-I) is increased with higher levels of muscle activity and has been reported to stimulate hypertrophy. However, further study is needed to understand the mechanisms.
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Muscle fibre number increase
Hyperplasia is caused by an increase in the rate of muscle contractile protein synthesis, which leads to greater numbers of actin and myosin filaments in the myofibrils. The myofibrils within each muscle fibre split, resulting in more myofibrils in each muscle fibre. This can be caused by extreme muscle force generation, exercise, and stretch overload.
Scientists have used three models to study the cellular mechanisms of muscle enlargement: compensatory hypertrophy, stretch, and exercise. Each of these models has provided direct and indirect evidence supporting the occurrence of muscle fibre hyperplasia. Direct counts of muscle fibres have shown that both exercise and stretch overload can result in significant increases in fibre number, ranging from 9-52%.
The possible role of myofiber hyperplasia in adaptation to increased workload is still an unresolved issue. It has been suggested that satellite cells are recruited during skeletal muscle hypertrophy.
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Muscle contractile protein synthesis
During muscle hypertrophy, the myofibrils within each muscle fibre split, resulting in more myofibrils in each muscle fibre. This process is known as "fibre splitting" or "myofiber hyperplasia" and results in an increase in the number of muscle fibres.
While muscle hypertrophy is a well-documented response to strength training, muscle hyperplasia is less common and not fully understood. It refers to the increase in the number of skeletal muscle fibres and has been observed in adult animals and possibly human athletes. Scientists have used three models to study muscle enlargement: compensatory hypertrophy, stretch, and exercise. Direct counts of muscle fibres have shown that both exercise and stretch overload can result in significant increases in fibre number.
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Frequently asked questions
Muscle hyperplasia is the increase in skeletal muscle fibre number.
Muscle hyperplasia occurs when muscles are stretched to a greater-than-normal length. This causes new sarcomeres to be added at the ends of muscle fibres where they attach to the tendons.
Muscle hypertrophy is the enlargement of muscle fibres, while muscle hyperplasia is the increase in the number of muscle fibres.
Hypertrophy occurs in response to a higher load on the muscle, which activates inducible agents such as IGF-1. IGF-1 binds to its receptor, the tyrosine kinase IGF1 receptor (IGF1R), which increases the activation of the downstream phosphatidylinositol-3 kinase (PI3K)/Akt pathway, increasing the rate of protein synthesis.
The possible role of myofiber hyperplasia in adaptation to increased workload is an unresolved issue. However, it has been suggested that satellite cells are recruited during skeletal muscle hypertrophy.
