REF-434 · Sommers et al., 2024 (ACE I/D meta-analysis) · International Journal of Environmental Research and Public Health · Paper
ACE Insertion/Deletion polymorphism and the elite endurance phenotype
Updated systematic review and meta-analysis
Background
ACE gene Insertion/Deletion (I/D) polymorphism:
I allele (insertion): associated in the literature with the endurance phenotype
D allele (deletion): associated in the literature with the power phenotype
Not from this paper: the serum-ACE / bradykinin / angiotensin II pathway is textbook background, not reported in this abstract
Key Findings (meta-analysis)
Studies on the ACE I/D polymorphism and elite endurance and power collected until 15 June 2024; 137 studies identified and screened; studies on running, swimming and cycling systematically reviewed; meta-analysis under different genetic models
Elite endurance athletes vs healthy inactive controls: II genotype more frequent, OR 1.54 (95% CI 1.24-1.91)
Elite endurance vs elite power athletes: OR 1.56 (95% CI 1.07-2.28)
Runners vs controls: OR 1.76 (95% CI 1.26-2.47, p = 0.001); triathletes vs controls: OR 2.69 (95% CI 1.15-6.32, p = 0.023)
Endurance swimmers vs short-distance/power swimmers: OR 2.27 (95% CI 1.49-3.45, p < 0.001)
Cycling was among the reviewed sports, but the abstract reports no cycling-specific estimate
Conclusion: the association between elite endurance and the ACE I/D polymorphism is confirmed and strengthened across sporting modalities
Mechanism Hypotheses
Not from this paper: the usual explanation — lower serum ACE with the I allele, preserved bradykinin, altered angiotensin II signalling, possible fibre-type effects — is not tested or stated in this abstract
Practical Application
Across 137 screened studies, elite endurance athletes were more likely to carry the ACE II genotype than inactive controls (OR 1.54, 95% CI 1.24-1.91) and than elite power athletes (OR 1.56); the association held in runners (OR 1.76), triathletes (OR 2.69) and endurance vs sprint swimmers (OR 2.27).An odds ratio of 1.54 is a population-level enrichment, not an individual test: most elite endurance athletes do not carry II, and carrying it predicts nothing about a given athlete's response to training.
The abstract reports no cycling-specific estimate — do not tell a cyclist the marker is "null in cycling" or "confirmed in cycling"; it is simply not broken out.
Limitations
Genetic association meta-analysis: case-control comparisons of elite athletes vs controls; effect sizes modest (OR 1.54-2.69); heterogeneity across sports and cohorts
No cycling-specific estimate in the abstract
Does not predict individual trainability or performance
Not from this paper: ancestry-specific allele frequencies complicate cross-population comparison
How this entry was checked and changed
Content correction 2026-09-27
"NOT significant in cyclists (interesting null)" and the cycling-specific mechanism/limitation bullets -> deleted; the abstract reports no cycling-specific result.
"DD genotype enriched in power/sprint, OR ~1.3-1.5" -> deleted; not in the abstract.
"Significant in rowers" -> deleted (rowing not mentioned); added the actual estimates with 95% CIs, 137 screened studies, search cut-off 15 June 2024.
Bradykinin/angiotensin mechanism relabelled "Not from this paper". Tier and Sport lines added.
2026-10-01: cross-reference to SYNTH-13 no longer names an archetype — that model was retired as an unvalidated composite.