People who carry one copy of a rare myostatin gene variant that reduces its function have 3–7% more total muscle volume and at least 10% more muscle in specific areas like the gluteus maximus, with the amount of increase directly related to how much the gene's function is disrupted, as measured by automated MRI analysis in 77,572 people.
See the scientific wording
Heterozygous carriers of rare, function-disrupting myostatin gene variants exhibit a 3–7% increase in overall muscle volume and a 10% or greater increase in specific muscle groups such as the gluteus maximus, with the magnitude of increase proportional to the degree of functional disruption as quantified by automated MRI segmentation in a cohort of 77,572 individuals.
Correlational — new studies may shift this
ObservationalOne moderate-quality study links this claim to the outcome, but causation is not established.
What the research says
1 study reviewedSupporting (1)
Cohort StudyHuman2026
People born with one broken copy of the myostatin gene naturally have more muscle — up to 10% more in their butt and thighs — and the more the gene is broken, the more muscle they have. This was confirmed by scanning 77,572 people with MRI.
Contradicting (0)
No contradicting studies found yet
That doesn't mean it's settled — it just means no study has tested the opposite.
Quality-weighted scoring: we follow the GRADE framework — each study is rated High, Moderate, Low, or Very Low based on study design, methodology rigor, and risk of bias. A single high-quality RCT can outweigh several weaker observational studies.
Scores reflect study quality, not just count.
A broken copy of the myostatin gene produces a faulty protein that cannot properly turn off muscle growth. This allows muscle cells to grow larger and multiply more, increasing muscle volume, especially in large muscles like the glutes. At the same time, the body shifts energy use toward building muscle instead of storing fat, reducing overall body fat.
Score breakdown, mechanism chain, raw evidence, ideal studies needed & 1 supporting study
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People who carry one copy of a rare myostatin gene variant that reduces its function have 3–7% more total muscle volume and at least 10% more muscle in specific areas like the gluteus maximus, with the amount of increase directly related to how much the gene's function is disrupted, as measured by automated MRI analysis in 77,572 people.
Mechanism
1 studyWhen the myostatin gene is broken, it can't stop muscles from growing. Muscles get bigger, especially in the buttocks and thighs, and the body stores less fat because it uses more energy to build muscle. The more broken the gene, the bigger the muscles and the less fat.
A broken copy of the myostatin gene produces a faulty protein that cannot properly turn off muscle growth. This allows muscle cells to grow larger and multiply more, increasing muscle volume, especially in large muscles like the glutes. At the same time, the body shifts energy use toward building muscle instead of storing fat, reducing overall body fat.
Function-disrupting variants in the myostatin gene alter the structure of the myostatin precursor protein, impairing its proper folding, stability, or cleavage into the mature active form
Reduced levels of bioactive myostatin ligand decrease binding to ActRIIA/B and ALK4/5 receptors on skeletal muscle cells
De-repression of the SMAD2/3 signaling pathway increases satellite cell activation, myoblast proliferation, and protein synthesis in muscle fibers
Muscle fibers undergo hypertrophy, increasing total muscle volume proportionally to the severity of myostatin disruption
Increased muscle mass elevates metabolic demand, shifting systemic energy partitioning away from adipose tissue storage and reducing fat accumulation
Evidence from Studies
Supporting (1)
Community contributions welcome
People born with one broken copy of the myostatin gene naturally have more muscle — up to 10% more in their butt and thighs — and the more the gene is broken, the more muscle they have. This was confirmed by scanning 77,572 people with MRI.
Contradicting (0)
Community contributions welcome
Score Breakdown
No multi-axis breakdown available yet. The overall Pro / Against score above is the best signal.
- No clinical evidence is available; the score reflects mechanistic plausibility only.
What Would Prove This
Per GRADE and EBM methodology, here is what ideal scientific evidence would look like to definitively prove or disprove this claim, ordered from strongest to weakest.
Systematic Review of Myostatin Gene Variant Carriers and Muscle Volume Across Population Cohorts with Automated MRI Quantification
Systematic review and meta-analysis of all published cross-sectional and cohort studies measuring muscle volume via automated MRI in heterozygous carriers of rare, function-disrupting myostatin variants compared to non-carriers, with stratification by variant severity and adjustment for age, sex, and body composition.
Randomized Trial of Myostatin Inhibition via Gene Therapy in Heterozygous Carriers vs Non-Carriers for Muscle Volume Change
Double-blind, placebo-controlled trial in 500 heterozygous carriers of rare, function-disrupting myostatin variants, comparing a myostatin-targeting therapeutic agent to placebo, with primary outcome of change in total and regional muscle volume via automated MRI over 12 months.
Prospective Cohort Study of Myostatin Variant Carriers and Muscle Volume Trajectory Over 5 Years Using Automated MRI
Prospective cohort of 10,000 individuals genotyped for rare myostatin variants, with annual automated MRI scans of muscle volume over 5 years, comparing trajectory of change between carriers and non-carriers.
Cross-Sectional Analysis of Muscle Volume in 77,572 Individuals by Myostatin Variant Status Using Automated MRI
Cross-sectional analysis of muscle volume via automated MRI in 77,572 individuals stratified by presence of rare, function-disrupting myostatin variants, with adjustment for age, sex, BMI, and physical activity.
In Vitro Assessment of Myostatin Variant Effects on Human Myoblast Proliferation and Differentiation
In vitro comparison of myoblast proliferation, fusion, and myotube formation in cell lines engineered to express wild-type vs. rare heterozygous myostatin variants under standardized differentiation conditions.