This preliminary study investigates the impact of a 16-week online supervised physical activity (PA) intervention on biological age in postsurgery female breast cancer (BC) patients
Introduction
Biological age is produced as consequence of the gradual accumulation of damage in the body over the lifespan, leading to an increased risk of age-related diseases, disability, and mortality.
Cancer and its treatments prominently contribute to accelerated biological aging.
Accelerated aging, where biological age overtakes chronological age, has been implicated in heightened risks of cardiovascular disease, diabetes, dementia, and cancer.
There are a number of reasons why breast cancer (BC) recovery is a significant context for understanding these effects.
Telomeres, genomic complexes at the end of chromosomes, protect DNA during replication and are associated with age-related diseases, lifespan, and cancer.
When telomere length (TL) is critically short, it can lead to apoptosis, senescence, and increased cancer risk.
Evidence has shown that physical activity decreases chronic inflammation and oxidative stress, especially in older, obese individuals, and may thus reduce telomere shortening observed with aging.
Several epigenetic clocks have been used in cancer research to understand the relationship between DNA methylation (DNAm) patterns and biological age.
These clocks could contribute to a comprehensive understanding of the biological age landscape in cancer and potentially lead to targeted therapeutic interventions.
Methods
The participants were randomly divided into a Control Group (CG, n = 9) and an Exercise Group (EG, n = 14)
All patients (CG and EG) received standard anticancer medical treatment as administered by the hospital, but EG performed an additional exercise training intervention (Physical Activity, PA).
Functional capacity parameters and patient-reported outcomes were assessed at the beginning and at the end of a 16-week experimental period.
In addition, a non-cancerous group (NG), a sample of 40–60-year-old non-cancerous females (n = 16), who had already been analyzed for biological age using the ELOVL2-based epigenetic clock, was included to serve as a as referent biological age of age-matched healthy females measured by the ELOVL2-based epigenetic clock.
Conclusion
During the 16 weeks TL remained unchanged.
After the 16 weeks of the study the ELOVL2 epigenetic clock indicated a significant decrease in biological age in the PA group, suggesting the potential of PA interventions to reverse accelerated aging processes in BC survivors.
The PA group showed improved cardiovascular fitness, highlighting PA’s health impact.
Epigenetic clocks can potentially assess health status and recovery progress in BC patients, identifying at-risk individuals in clinical practice.
