Exercise Protects Your DNA: The Genetic Benefits of Physical Exercise

In recent years, the link between physical activity and genetic health has garnered increasing attention. Since the early 2000’s, more research has been published to support the fundamental role physical activity & exercise plays in DNA synthesis and the prevention of genetic mutations.

Having a physically active lifestyle can can contribute to healthier ageing, reduce the risks of dis-ease (including cancer) and neuro-degeneration.

DNA Synthesis: A Cellular Foundation

Cell Division is the fundamental biological process through which a single cell divides into two daughter cells. This process is essential for growth, repair, reproduction, and the general maintenance of all living organisms.

When it comes to DNA, it must be understood that 24% is in a transient state. This is where the cell division process takes place via a cell cycle:

• G1 Phase (Gap 1) - The cell grows.

• S Phase (DNA Synthesis) - The cell copies all of its DNA to be passed on to new cells.

• G2 Phase (2nd Gap) - The cell checks the copied DNA for mistakes and gets ready to divide.

• M Phase (Mitosis/Meiosis) - The cell divides into two new cells, each with the same DNA.

The condition of the cell replication at the 'DNA Synthesis' phase will be determined by the condition of the environment it exists in (i.e. your molecular and physical being as well as the environment you exist within).

The benefits of Physical Activity on DNA Synthesis

A study published in the Journal of Applied Physiology demonstrated that moderate endurance training up-regulates Nucleotide Excision Repair pathways (Radak et al., 2008). During exercise, there is an increased demand for tissue repair and regeneration, which in turn stimulates rapid reproduction of cells.

Nucleotide Excision Repair (NER) is a repair mechanism that removes and replaces abnormal DNA to ensure accurate DNA synthesis and genome stability. This is vital for removing cell mutations and the prevention of various stem cell diseases & cancers.

Physical Activity Preventing Mitochondria DNA (mtDNA) Mutation

The mitochondria are tiny structures inside almost all of your cells; often referred to as the "powerhouses" of the cell. Their main job is to produce energy in the form of ATP (Adenosine Tri-Phosphate) through a process called cellular respiration. This takes place via the electron transport chain (ETC).

Mitochondria also contain their own DNA; mtDNA. It is separate from the DNA in the cell nucleus and helps produce essential proteins needed for energy production within the mitochondria. It’s location is very close to the ETC, therefore making it vulnerable to damage from reactive molecules.

As electrons (hydrogen ions) move across the ETC, a small percentage leaks out and reacts with oxygen creating a ‘superoxide’ called Reactive Oxygen Species (ROS). These are highly unstable molecules that can damage DNA. When ROS starts to react and damage mtDNA, this is a form of oxidative stress. As DNA continues to damage, cells begin to mutate.

Physical activity and exercise can improve and manage mitochondrial oxidative stress, alongside many other positive lifestyle adjustments. By improving mitochondrial DNA integrity, physical activity lowers the systemic burden of mutated cells and oxidative stress.

Exercise and Telomere Maintenance

Telomeres are the protective caps at the ends of chromosomes that prevents DNA damage during cell division. Chromosome are where DNA is stored. Each time a cell divides, the telomeres get shorter. When the telomeres become too short the cell can no longer divide efficiently, causing the cell to become incompetent and eventually die.

Physical activity and exercise has been associated with longer telomere length and increased activity of telomerase; the enzyme that replenishes telomere ends. Telomere integrity is vital not only for maintaining the efficiency of DNA synthesis, but also preventing chromosome instability and the development of tumours.

A landmark study published in the well-recognised scientific journal Circulation, found that adults with higher levels of physical activity had significantly longer leukocyte telomere lengths, suggesting a slower biological ageing process and lower mutation burden in somatic cells (Cherkas et al., 2008).

Implications for Cancer Prevention

Most cancers start because of mutations in genes. Some of these mutations can encourage tumours to grow (oncogenes) and others can stop cells from growing out of control (tumour suppressor genes). Exercise helps protect your DNA from these harmful changes, which makes it an important way to help prevent cancer.

A study by C.M Friedenreich and colleagues 2016, showed that people who exercise regularly have a lower chance of getting cancers like colon, breast, and prostate cancer due to healthier maintenance of DNA.

Conclusion

The benefits of physical activity go far beyond muscle tone and cardiovascular health. At the molecular level, regular exercise safeguards DNA integrity by enhancing synthesis fidelity, promoting mitochondrial health, upregulating repair mechanisms, and maintaining telomere length. These protective effects reduce the risk of mutation-driven diseases, particularly cancers and age-related disorders.

By integrating physical activity into daily routines, you can empower your body to resist the genetic damage that accumulates with time. As the research continues to evolve, one message remains clear: exercise is not just a lifestyle choice — it’s a genetic investment.

Further Reading

Cherkas, L. F., Hunkin, J. L., Kato, B. S., Richards, J. B., Gardner, J. P., Surdulescu, G. L., ... & Spector, T. D. (2008). The association between physical activity in leisure time and leukocyte telomere length. Archives of Internal Medicine, 168(2), 154–158. https://doi.org/10.1001/archinternmed.2007.39

Radak, Z., Chung, H. Y., & Goto, S. (2008). Systemic adaptation to oxidative challenge induced by regular exercise. Free Radical Biology and Medicine, 44(2), 153–159. https://doi.org/10.1016/j.freeradbiomed.2007.01.029

Lenaz, G., & Genova, M. L. (2009). Role of mitochondria in oxidative stress and aging. Biochimica et Biophysica Acta (BBA) - Bioenergetics, 1787(5), 502–511. https://doi.org/10.1016/j.bbabio.2009.01.005

Powers, S. K., Duarte, J., Kavazis, A. N., & Talbert, E. E. (2011). Reactive oxygen species are signalling molecules for skeletal muscle adaptation. Experimental Physiology, 96(6), 620–630. https://doi.org/10.1113/expphysiol.2010.056853

Calabrese, E. J., & Mattson, M. P. (2011).
Hormesis provides a generalized quantitative estimate of biological plasticity.
Journal of Cell Communication and Signaling, 5(1), 25–38. https://doi.org/10.1007/s12079-011-0127-x

Nieman, D. C. (2011). Exercise Testing and Prescription: A Health-Related Approach.
McGraw-Hill Education.

Booth, F. W., Roberts, C. K., & Laye, M. J. (2012). Lack of exercise is a major cause of chronic diseases.
In Comprehensive Physiology, 2(2), 1143–1211. https://doi.org/10.1002/cphy.c110025

López-Otín, C., Blasco, M. A., Partridge, L., Serrano, M., & Kroemer, G. (2013).
The hallmarks of aging Cell, 153(6), 1194–1217. https://doi.org/10.1016/j.cell.2013.05.039

Friedenreich, C. M., Neilson, H. K., & Lynch, B. M. (2016). State of the epidemiological evidence on physical activity and cancer prevention. European Journal of Cancer, 68, S40–S50. https://doi.org/10.1016/j.ejca.2016.07.016

Sinclair, D. A., & LaPlante, M. D. (2019).
Lifespan: Why We Age—and Why We Don't Have To. New York: Atria Books