Injury risk during training: what role does genetics play?

Tendons and ligaments are largely made of collagen, and collagen, like all other proteins, is encoded by DNA. This leads to an appealing assumption: genetic differences might help assess how connective tissue responds to load. The logic is so compelling that individual variants in collagen genes have been studied for years as potential injury markers.

However, the findings do not add up to a simple predictive model. Even within a single collagen gene, results depend on the specific variant and the type of injury being studied. A biologically plausible mechanism is not enough to predict an event.

Genetics may be associated with certain characteristics of tendons and ligaments, but knowing a genetic profile is not enough to predict an injury. Current tissue status, previous injuries, movement technique, recovery, and the nature of the training load also matter. A genetic report does not determine which exercises are safe, what weight is acceptable, or when the next injury will occur. It is therefore important to understand what genetic context can actually add to injury-risk assessment and training planning.

Which properties of connective tissue may have a hereditary component

The genetic contribution concerns not the injury event itself, but certain biological properties of connective tissue. A tendon consists primarily of extracellular matrix: collagen fibres, water, proteoglycans, and a small number of cells that renew this matrix. Type I collagen makes up most of the dry mass of ligaments, while types III, V, and XII are present in smaller amounts and contribute to fibre formation and organisation (Bulbul et al., Biology, 2023). These proteins are encoded by the genes COL1A1 (collagen type I alpha 1 chain), COL3A1 (collagen type III alpha 1 chain), COL5A1 (collagen type V alpha 1 chain), and COL12A1 (collagen type XII alpha 1 chain), while common single-base differences in their sequences, single-nucleotide polymorphisms (SNPs), are studied as possible modifiers of tissue properties.

This creates a biologically plausible hypothesis: variants in these genes may be associated with differences in tissue properties (Ding et al., Gene, 2026). However, the mechanism itself does not establish a clinically meaningful association with injury. Tendon properties are a complex phenotype influenced by mechanical loading, age, hormonal context, coexisting conditions, and previous injuries; genetic contribution is one factor within that list, not a substitute for it.

Why tendon adaptation may lag behind gains in muscle strength

Muscle strength and the mechanical properties of tendons can change at different rates. Tendon adaptation depends on the magnitude and nature of the mechanical stimulus and may lag behind gains in strength (Epro et al., J. Exp. Biol., 2023).

At the same time, a tendon is not a fixed structure. A meta-analysis of studies of lower-limb tendons found that mechanical loading increases tendon stiffness, with protocols producing greater local strain showing larger effects (Lazarczuk et al., Sports Med., 2022). The question is not whether the tendon changes, but how quickly and under what conditions.

A mismatch can arise when muscle strength increases faster than the tendon can adapt. A stronger muscle can transmit greater force to the tendon while its adaptation is still in progress (Epro et al., J. Exp. Biol., 2023). 

For more on how the capacity for strength gains develops, see The genetic code of strength: how muscle fibre type shapes your athletic potential.

Differences in adaptation rates explain why progress in muscle strength does not necessarily mean that a tendon is ready for the same increase in load. Genetic factors may be one source of interindividual variability, but they currently cannot be used to calculate an exact adaptation period for a specific person.

Why studies on injury genetics produce inconsistent results

Studies of collagen genes do not present a single consistent picture: some variants show associations with injury, while others do not. This becomes clear when studies with different designs are compared.

A meta-analysis of 19 case-control studies — 3,522 cases and 6,399 controls — found no significant association between anterior cruciate ligament rupture and rs12722 in COL5A1 or rs1800255 in COL3A1. By contrast, associations were statistically significant for rs1107946 in COL1A1 and rs970547 in COL12A1 (Bulbul et al., Biology, 2023).

Even within COL5A1, findings differ by variant. For rs13946, a meta-analysis found a significant association with anterior cruciate ligament injury under recessive and allelic models, although the authors emphasised limitations in the evidence base (Sun et al., Int. J. Mol. Sci., 2025). A study of physically active people from Australia, South Africa, and Japan also reported an association between COL5A1 variants and ligament injuries (Alvarez-Romero et al., Eur. J. Sport Sci., 2023).

At the same time, in a sample of 268 professional football players, rs12722 was not associated with anterior cruciate ligament rupture: genotype distribution among those who had sustained this injury during their careers was almost the same as among those who had not (Manchón-Davó et al., Genes, 2025).

These findings do not rule out a genetic contribution. They show that the statistical association of an individual variant must be interpreted in the context of the population, injury type, study design, and model used. A group-level association still cannot predict an injury in a specific person.

How to combine genetic data with injury history and training-load data

Genetic data cannot be interpreted separately from the type of injury, its history, and the nature of the training load. Anterior cruciate ligament rupture, Achilles tendinopathy, muscle injury, and lower-back pain have different mechanisms, so no single indicator is equally informative for all of these conditions.

At the same time, a history of previous injury remains one of the most important sources of practical information. In a systematic review of overuse injuries in runners, a previous running-related injury was the strongest risk factor for long-distance runners, supported by moderate-quality evidence. For short-distance runners, previous non-running-related injuries were the strongest factor, supported by high-quality evidence (van Poppel et al., J. Sport Health Sci., 2021).

However, the label “previous injury” does not explain why a problem recurs. It may reflect incomplete recovery, changes in biomechanics, a return to the same training load, or individual differences in tissue adaptation. An injury history shows that tissue damage has already occurred under real-world loading conditions. Genetic context may add information about one possible biological contributor to this vulnerability.

The nature of the training load also matters. A systematic review of basketball studies found that the relationship between training load and injury is actively being investigated, but reliable universal thresholds for a safe increase in volume have not yet been established (Chan et al., Healthcare, 2024). This means that decisions cannot be based on a formula alone or on genotype alone.

The practical value of genetic data is that they complement information about injury history, symptoms, and training load. A genetic report does not establish the cause of a specific injury, but it can help account for hereditary characteristics related to connective tissue, muscle function, and recovery. Together, these data provide a more complete basis for planning training load with a coach, rehabilitation specialist, or doctor.

For more on what determines recovery speed between training sessions, see Recovery speed after training: the role of genetics.

How to use this information in practice

An increase in muscle strength should not automatically be treated as proof that a tendon is ready for greater load. Working weight, pace, or volume should be increased with the tissue response in mind, not solely on the basis of strength gains.

Genetic data may add information about hereditary characteristics worth considering when planning progression. However, genotype alone is not a reason to automatically exclude jumping, heavy squats, sprinting, or other loads. Whether they are appropriate should be assessed in the context of technique, injury history, current symptoms, and tissue status.

If symptoms recur, the entire loading system needs review: total volume and the rate at which it increases, movement quality, recovery, and the body’s response between sessions. A genetic report can complement this assessment, but it cannot independently determine a return-to-training date.

What genetics changes in the approach to training

The results of the DNA test Sport and Movement add information about hereditary characteristics of connective tissue, muscle function, and recovery to the assessment of training adaptation. They help frame injury risk not as the result of a single “injury gene”, but as an interaction between tissue properties, previous injuries, recovery, and actual training load.

A genetic report does not predict a specific injury, but it can provide additional data for better-informed training decisions.

A broader overview of genetic testing for sport is available in a separate article — Athletic potential and recovery: what a DNA test can show.

Genetic test results are not a diagnosis and do not replace a medical consultation. The Apixmed Prism report provides genetic context that complements examination results and helps you make decisions together with your doctor.

References

1. Bulbul, A., Ari, E., Apaydin, N., Ipekoglu, G. (2023). The impact of genetic polymorphisms on anterior cruciate ligament injuries in athletes: a meta-analytical approach. Biology, 12(12), 1526. https://doi.org/10.3390/biology12121526

2. Sun, Z., Cięszczyk, P., Bojarczuk, A. (2025). COL5A1 rs13946 polymorphism and anterior cruciate ligament injury: systematic review and meta-analysis. International Journal of Molecular Sciences, 26(13), 6340. https://doi.org/10.3390/ijms26136340 

3. Manchón-Davó, M., Del Coso, J., Vera-Garcia, F. J., González-Rodenas, J., Miralles-Iborra, A., Rodas, G., López-Del Campo, R., Moreno-Pérez, V. (2025). Association between the COL5A1 rs12722 genotype and the prevalence of anterior cruciate ligament rupture in professional football players. Genes, 16(6), 649. https://doi.org/10.3390/genes16060649

4. Alvarez-Romero, J., Laguette, M. J. N., Seale, K., Jacques, M., Voisin, S., Hiam, D., Feller, J. A., Eynon, N. (2023). Genetic variants within the COL5A1 gene are associated with ligament injuries in physically active populations from Australia, South Africa, and Japan. European Journal of Sport Science, 23(2), 284–293. https://doi.org/10.1080/17461391.2021.2011426

5. Epro, G., Suhr, F., Karamanidis, K. (2023). Human muscle–tendon unit mechanobiological responses to consecutive high strain cyclic loading. Journal of Experimental Biology, 226(20), jeb246507. https://doi.org/10.1242/jeb.246507

6. Lazarczuk, S. L., Maniar, N., Opar, D. A., Duhig, S. J., Shield, A., Barrett, R. S., Bourne, M. N. (2022). Mechanical, material and morphological adaptations of healthy lower limb tendons to mechanical loading: a systematic review and meta-analysis. Sports Medicine, 52(10), 2405–2429. https://doi.org/10.1007/s40279-022-01695-y

7. van Poppel, D., van der Worp, M., Slabbekoorn, A., van den Heuvel, S. S. P., van Middelkoop, M., Koes, B. W., Verhagen, A. P., Scholten-Peeters, G. G. M. (2021). Risk factors for overuse injuries in short- and long-distance running: a systematic review. Journal of Sport and Health Science, 10(1), 14–28. https://doi.org/10.1016/j.jshs.2020.06.006

8. Chan, C.-C., Yung, P. S.-H., Mok, K.-M. (2024). The relationship between training load and injury risk in basketball: a systematic review. Healthcare, 12(18), 1829. https://doi.org/10.3390/healthcare12181829 

9. Ding, H., Deng, Q., Guo, Z. (2026). Genetic and epigenetic determinants of injury risk and recovery in elite athletes: toward precision sports medicine. Gene, 980, 149957. https://doi.org/10.1016/j.gene.2025.149957