What you carry at this position in your DNA and what research says about it.
Muscle Type and Endurance: 7/10 evidence, 23 publications.
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Sample genotype (not yours): C/C
Natural Power and Sprint Advantage
Two copies of the functional gene ensure normal levels of the alpha-actinin-3 protein. This supports explosive muscle power and typical sleep patterns.
What this genotype means: Optimal fast-twitch muscle power; Typical sleep patterns; Standard cold tolerance.
Sample genotype (not yours): C/T
Balanced Power and Endurance Profile
A single copy of the functional gene provides a versatile mix of muscle performance traits. Sleep and cold tolerance remain at typical baseline levels.
What this genotype means: Versatile muscle fiber mix; Typical sleep patterns; Standard cold tolerance.
Sample genotype (not yours): T/T
Endurance and Cold Tolerance with Higher Insomnia Risk
A complete lack of alpha-actinin-3 shifts muscles toward endurance and superior cold tolerance, but carries a higher risk of insomnia.
What this genotype means: Superior muscle endurance; Enhanced cold tolerance; Higher risk of insomnia.
Gene function and biological role
Gene Function: The ACTN3 gene provides instructions for producing alpha-actinin-3, a structural protein found exclusively in fast-twitch muscle fibers [1]. These specialized fibers are responsible for generating rapid, explosive force during high-intensity activities like sprinting and weightlifting [2]. In contrast, slow-twitch fibers rely on aerobic metabolism and excel at sustained, endurance-based activities [3]. While alpha-actinin-3 is crucial for peak power performance, its complete absence does not cause muscle disease due to compensation by a sister protein, alpha-actinin-2 [4].
Variant Impact: This variant, known as R577X, is a common single-nucleotide change that introduces a premature stop codon in the ACTN3 gene sequence [1]. The presence of the T allele halts the production of the alpha-actinin-3 protein entirely, leading to a functional deficiency in fast-twitch muscle fibers [2]. Approximately one in five people worldwide completely lack this protein due to carrying two copies of the T allele [5]. This genetic variation directly influences the ratio of fast-twitch to slow-twitch muscle characteristics, shaping natural athletic predispositions [6].
Read on the Muscle Composition page
Key Insight: Completely lacking the alpha-actinin-3 protein does not cause muscle disease, but instead shifts muscle fibers to a highly efficient endurance profile that also doubles your ability to tolerate extreme cold.
Location: ACTN3. Chromosome 11 · 11q13.2 · 66.6 Mb
Origin Story: As early humans migrated out of Africa into colder northern climates, the T allele became significantly more common. Evolutionary biologists discovered that the loss of alpha-actinin-3 shifts muscle metabolism toward a highly efficient, slow-twitch profile that generates heat more effectively without shivering. This metabolic shift provided a critical survival advantage in freezing environments, explaining why the T allele is highly prevalent in populations of European and Asian descent but rare in those of African descent.
Estimated prevalence by population
Global 40.9%; European 31.1%; African 68.8%; East Asian 28.6%; South Asian 17.4%; Americas 20.6%; Ashkenazi 29.7%; Finnish 47.6%; Middle Eastern 33.8%; Amish 18.8%.
Estimated CC genotype frequency.
Global 43.1%; European 49.3%; African 28.3%; East Asian 49.8%; South Asian 48.6%; Americas 49.6%; Ashkenazi 49.6%; Finnish 42.8%; Middle Eastern 48.7%; Amish 49.1%.
Estimated CT genotype frequency.
Global 16.0%; European 19.6%; African 2.9%; East Asian 21.7%; South Asian 34.0%; Americas 29.8%; Ashkenazi 20.7%; Finnish 9.6%; Middle Eastern 17.5%; Amish 32.1%.
Estimated TT genotype frequency.
Showing effects for C/C genotype
Lifestyle, Fitness & Aging
Muscle Strength & Power
Muscle Performance. Evidence: 5/10. Source: PMID 12879365. Sprint and Power.
Stress Response & Resilience
Cold Tolerance. Evidence: 3/10. Source: PMID 12879365. Typical Tolerance.
Neurology & Mental Health
Sleep & Circadian Rhythm
Insomnia. Evidence: 7/10. Source: PMID 35835914. Typical Risk.
Showing effects for C/T genotype
Muscle Performance. Evidence: 5/10. Source: PMID 12879365. Balanced Profile.
Showing effects for T/T genotype
Muscle Performance. Evidence: 5/10. Source: PMID 12879365. Endurance and Stamina.
Cold Tolerance. Evidence: 3/10. Source: PMID 12879365. Enhanced Tolerance.
Insomnia. Evidence: 7/10. Source: PMID 35835914. Higher Risk.
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
Muscles are naturally optimized for rapid, high-force contractions due to the presence of alpha-actinin-3 in fast-twitch fibers [1]. This genetic profile is highly over-represented among elite sprinters, powerlifters, and explosive athletes [2]. Beyond athletic performance, typical sleep patterns are expected as there is no elevated genetic risk for insomnia associated with this genotype [3]. However, the metabolic profile of these fast-twitch fibers is less efficient at conserving energy in cold environments compared to those lacking the protein [4]. Physical training should focus on developing speed, power, and strength to maximize this genetic baseline.
Optimal fast-twitch muscle power; Typical sleep patterns; Standard cold tolerance.
Sample genotype: CT (Heterozygous)
Skeletal muscles produce a partial amount of the alpha-actinin-3 protein, resulting in a balanced blend of fast-twitch and slow-twitch muscle characteristics [1]. This versatile profile allows for success in both sprint-oriented and endurance-oriented sports [2]. Sleep quality and insomnia risk remain at typical population levels, as a single copy of the T allele does not strongly elevate sleep disturbances [3]. Cold tolerance is also typical, as the body still relies primarily on standard shivering mechanisms to maintain core temperature [4]. Training programs can be highly customized, as the body adapts well to a wide variety of physical demands.
Versatile muscle fiber mix; Typical sleep patterns; Standard cold tolerance.
Sample genotype: TT (Homozygous)
Muscles completely lack the alpha-actinin-3 protein, which shifts the muscle fiber profile toward highly efficient, fatigue-resistant slow-twitch fibers [1]. This genetic makeup is common among elite endurance athletes, such as marathon runners and long-distance cyclists [2]. The metabolic shift also provides a unique physiological advantage in cold environments, allowing the body to maintain its core temperature efficiently without shivering [3]. However, this genotype is also associated with a higher genetic susceptibility to insomnia [4]. Training should leverage natural stamina and aerobic capacity while prioritizing sleep hygiene to mitigate sleep risks.
Superior muscle endurance; Enhanced cold tolerance; Higher risk of insomnia.
Variants with shared genetic architecture
rs4994 · ADRB3 Gene · Chr 8 · Heart Risk and Endurance
rs1799752 · ACE Gene · Chr 17 · Blood Pressure and Fitness
rs12722 · COL5A1 Gene · Chr 9 · Tendon Injury Risk
ACTN3 genotype is associated with human elite athletic performance.
A common nonsense mutation results in alpha-actinin-3 deficiency in the general population.
Nonsense mutation of the alpha-actinin-3 gene is not associated with dystrophinopathy.
Mitochondrial DNA and ACTN3 genotypes in Finnish elite endurance and sprint athletes.
ACTN3 R577X genotype and athletic performance in a large cohort of Japanese athletes.
Association between the ACTN3 R577X polymorphism and female endurance athletes in China.
Content updated August 2026.
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