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Muscle strength is a key indicator of overall health and physical ability. Genetic factors play a significant role in determining muscle strength and mass, with heritability estimates ranging from 30-85% for muscle strength and 50-80% for lean mass. Despite this strong genetic contribution, the specific genes and gene variants influencing muscle traits are not yet fully understood. However, studies have identified certain genetic variants, such as the ACTN3 gene, which is commonly found in elite power athletes, and mutations in the myostatin gene, which can lead to a dramatic increase in muscle mass. Research in this area has important implications for understanding muscle-related diseases and developing personalized treatments.
| Characteristics | Values |
|---|---|
| Muscle strength | Heritability estimates range from 30-85% |
| Muscle lean mass | Heritability estimates range from 50-80% |
| Muscle composition | Two main types of fibres: slow-twitch and fast-twitch |
| Muscle hypertrophy-regulating genes | Involved in transcription and ubiquitination |
| Muscle hypertrophy-inducing genes | Belong to three signalling pathways: Igf1-Akt-mTOR, myostatin-Smad, and angiotensin-bradykinin |
| Muscle diseases | Monogenetic muscle diseases can cause very poor muscle function |
| Muscle strength loss | Genetic factors may play a role in early muscle strength loss |
| Muscle performance | The ACTN3 gene is associated with muscle performance in elite power athletes |
| Muscle metabolism | The ACTN3 gene is associated with muscle metabolism |
| Muscle wasting diseases | Myostatin may have therapeutic applications in treating muscle wasting diseases |
| Muscle mass | Myostatin deficiency results in a dramatic increase in muscle mass |
| Muscle function | KDM5B and GIGYF1 variants are associated with skeletal muscle function |
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What You'll Learn
Muscle strength and its heritability
Muscle strength is a key measure of physical ability and overall health. Reduced muscle strength is associated with adverse health outcomes, including disability and mortality. While training and physical fitness influence athletic performance, scientific evidence suggests that genetics also play a role.
Skeletal muscle is a highly heritable quantitative trait, with heritability estimates ranging from 30-85% for muscle strength and 50-80% for lean mass. Despite this strong genetic contribution, the underlying genetic architecture and mechanisms remain unclear. The genetic underpinnings of skeletal muscle traits are not yet fully understood, and large-scale longitudinal clinical studies are needed to provide further insights into the genes and gene variants that contribute to muscle strength and mass.
Hand grip strength is a reliable proxy measure of general muscle strength, and genome-wide association studies (GWAS) have identified over 180 common-variant-based loci. Rare genetic variants in genes such as KDM5B and GIGYF1 have been associated with hand grip strength, and there is evidence of a tight link between brain and muscle function. For example, variants in these genes have been linked to blood levels of insulin-like growth factor 1 (IGF-1), suggesting that loss of function may impair skeletal muscle function through perturbing IGF-1 signaling.
In addition to the genes mentioned above, several other genes and genetic variants have been implicated in muscle strength and mass. The ACTN3 gene, also known as the "gene for speed", is found in most elite power athletes. The myostatin gene, discovered in 1997, is another example, as mutations in this gene can lead to a dramatic increase in muscle mass. Naturally occurring deficiencies of myostatin have been identified in some humans, resulting in increased muscle mass.
While genetics play a significant role in muscle strength and mass, environmental factors such as resistance training and nutrition also contribute. The interaction between nature and nurture influences muscle mass and function, and the importance of physical activity and resistance training in slowing the loss of muscle mass and strength with age is well-established.
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Muscle composition and the ACTN3 gene
Muscle composition and athletic performance are influenced by genetics. Studies have found that most elite power athletes have a specific genetic variant in a gene related to muscle composition called the ACTN3 gene. This gene is responsible for the production of the alpha-actinin-3 protein, which is found in almost all elite power athletes who have participated in genetic studies. However, it is important to note that this genetic variant only explains about 2-3% of the difference in muscle performance between individuals, and for most athletes, this margin is too small to be noticeable.
The ACTN3 gene is associated with the "gene for speed" and plays a role in muscle metabolism. It has been shown to influence athletic performance, particularly in sprinting and power sports. The presence of this gene can provide a competitive advantage in sports that require short bursts of powerful energy, such as sprinting, throwing, and jumping.
Our muscles are made up of two main types of fibres: slow-twitch and fast-twitch. The type of fibre influences how a muscle contracts. Slow-twitch fibres contract slowly but tire less easily, making them ideal for endurance activities like marathon running. On the other hand, fast-twitch fibres contract quickly and provide short bursts of powerful energy but fatigue more quickly. This type of fibre is advantageous for sports that require explosive movements, such as sprinting and jumping.
While the ACTN3 gene is a significant discovery in understanding muscle composition and athletic performance, it is important to acknowledge that muscle strength and performance are influenced by a combination of genetic and environmental factors. Research has shown that muscle strength is highly heritable, with heritability estimates ranging from 30-85% for muscle strength and 50-80% for lean mass. However, the underlying genetic architecture and mechanisms are not yet fully understood. Large-scale longitudinal studies are needed to further elucidate the complex interplay between genetics and muscle performance.
Additionally, environmental factors such as resistance training and nutrition also play a crucial role in muscle strength and performance. For example, physical activity and resistance training have been shown to slow the loss of muscle mass and strength, and can even improve athletic performance, regardless of genetic factors. Overall, while the ACTN3 gene provides insight into the genetic basis of muscle composition and athletic performance, it is just one piece of the puzzle, and both genetic and environmental factors contribute to an individual's muscle strength and athletic abilities.
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Myostatin and muscle mass
Muscle is a highly heritable trait, with heritability estimates ranging from 30-85% for muscle strength and 50-80% for lean mass. Genetic studies of skeletal muscle traits have identified a few genes that contribute to variation in muscle strength and mass phenotypes. One such gene is myostatin, which was discovered in 1997 by geneticists Se-Jin Lee and Alexandra McPherron. Myostatin is a growth and differentiation factor-8 (GDF-8) cytokine primarily expressed and secreted in skeletal muscles. It acts as a negative regulator of muscle mass.
Myostatin-related muscle hypertrophy is a rare condition characterised by reduced body fat and increased muscle size. People with a variant in both copies of the MSTN gene in each cell (homozygotes) have significantly increased muscle mass and strength. People with a variant in only one copy of the gene in each cell (heterozygotes) also have increased muscle bulk, but to a lesser degree. Studies have shown that a deficiency in myostatin results in increased muscle mass. However, this increase is not accompanied by a proportionate increase in force generation, indicating that the increase in muscle mass does not confer a strength advantage.
Myostatin inhibition has been shown to increase muscle mass in mice. Additionally, resistance exercise training (RT) and essential amino acids (EAAs) have been found to further increase muscle mass and improve muscle quality. Myostatin inhibition, RT, and EAAs work synergistically to change muscle protein turnover and stimulate mitochondrial biogenesis. While myostatin inhibition can lead to a significant increase in muscle mass, it may also result in decreased muscle quality, highlighting the importance of combining it with RT and EAAs to enhance muscle strength and quality.
Naturally occurring deficiencies of myostatin have been identified in some breeds of cattle, sheep, whippets, and humans, resulting in a dramatic increase in muscle mass. For example, a Belgian Blue bovine with a mutation that inhibits myostatin production will exhibit a significant increase in muscle mass but will also lead to dystocia due to unusually heavy and bulky offspring. The reduction of myostatin could potentially benefit the livestock industry, but animal breeds developed as homozygous for myostatin deficiency require special care and a more expensive diet to achieve superior yield.
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Muscle hypertrophy-regulating genes
Muscle mass is regulated by both muscle growth factors and muscle mass inhibitors, termed "chalones". Skeletal muscle mass, in particular, is a result of the balance between protein breakdown and protein synthesis. Genes regulating muscle hypertrophy can be studied by observing their expression after resistance exercise. For example, a study accessed transcriptome data to discover that the expression of some hypertrophy-causing genes (IGF1, PPARGC1A, BMPR1A, ASB15, CAST, KLF10, and AGTR1) changes significantly by more than 10% after resistance exercise in human muscle.
Genetic studies have shown that muscle composition and performance are influenced by genetics. For instance, almost all elite power athletes produce the alpha-actinin-3 protein, which is encoded by the ACTN3 gene. This genetic variant explains about 2-3% of the difference in muscle performance between different people. Similarly, the gene encoding myostatin was discovered in 1997, and when geneticists produced a knockout strain of mice that lack the gene, they found that these mice had approximately twice as much muscle as normal mice. These mice were subsequently named "mighty mice". Naturally occurring deficiencies of myostatin have been identified in some breeds of cattle, sheep, whippets, and humans, and in each case, there is a significant increase in muscle mass.
Despite these findings, the genetic underpinnings of muscle traits remain largely unknown. For example, it is not known whether various models of muscle hypertrophy are similarly regulated by a common transcriptional program. However, studies have shown that muscle atrophy occurring in different catabolic conditions shows similar transcriptional adaptations. Furthermore, muscle growth is characterized more by translational regulation than transcriptional regulation, with all conditions showing a marked increase in mTORC1 signaling and increased ribosome biogenesis.
Additionally, the IGF-1-Akt-mTORC1 pathway is a major pathway that regulates adult muscle mass, acting mainly through increases in protein synthesis by modulating translation initiation. mTORC1 also controls the translation of terminal oligopyrimidine (TOP) mRNAs, which code for ribosomal proteins and several initiation and elongation factors. The upstream activators of mTOR include growth factors such as IGF1 and insulin acting through the PI3K-Akt cascade, different amino acids, and mechanical signals such as phosphatidic acid generated by DGKζ.
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Muscle strength and cognitive function
Muscle strength is a powerful predictor of mortality and cognitive function, especially in older people. A study of 1,424 adults over 60 years old found that muscle strength and physical activity independently predicted performance in the digit symbol substitution test, with muscle strength explaining 5% of the variance in cognitive function. Another study of 338 men and women with an average age of 66 years found that greater muscle strength was associated with better cognitive function, but handgrip strength was not associated with cognitive function. Instead, an association between muscle strength and cognitive function was observed when sum scores depicting upper or lower body muscle strength were included in the model.
The link between muscle strength and cognitive function may be due to several reasons. Firstly, resistance exercises and training have been shown to lead to cognitive improvements through functional and structural brain changes. For example, resistance training decreases the level of plasma and serum homocysteine, which is linked to a higher extent of white matter lesions and a higher brain atrophy rate. By reducing homocysteine levels, resistance training may positively affect brain structure and cognitive functions. Secondly, muscle strength and cognitive function may be linked through their shared association with physical activity and resistance training. Physical activity and resistance training have been shown to protect against the loss of skeletal muscle and may reduce the risk of cognitive decline.
Genetics also plays a role in muscle strength and cognitive function. Skeletal muscle strength and mass are highly heritable traits, with heritability estimates ranging from 30-85% for muscle strength and 50-80% for lean mass. Genetic variation explains a significant fraction of the inter-individual variability in skeletal muscle phenotypes, and studies have found that most elite power athletes have a specific genetic variant in a gene related to muscle composition called the ACTN3 gene. Additionally, the myostatin gene, discovered in 1997, has been found to regulate muscle mass. Mutations in the myostatin gene can lead to a dramatic increase in muscle mass in various species, including humans.
While the association between muscle strength and cognitive function is well-established, further research is needed to understand the underlying mechanisms fully. Future studies should investigate the influence of different resistance exercise variables, such as load, number of sets, training frequency, and training duration, on brain changes and cognitive functions. Additionally, the optimal exercise prescription for resistance exercises and training to promote brain health is yet to be determined.
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Frequently asked questions
The muscle gene is a term that can refer to several genes that influence muscle composition, strength, and mass. Genes such as ACTN3, TTN, KDM5B, GIGYF1, and myostatin have been identified as having an impact on muscle performance, strength, and mass.
The ACTN3 gene is also known as the "gene for speed" as it is often found in elite power athletes and influences muscle composition.
The ACTN3 gene influences muscle performance by producing the alpha-actinin-3 protein, which is associated with muscle metabolism and powerful bursts of energy.
The myostatin gene was discovered in 1997 and is involved in muscle hypertrophy and muscle mass regulation. Mutations in the myostatin gene can lead to a dramatic increase in muscle mass.
