The influence of exercise on telomere biology

Telomeres are repetitive nucleotide sequences located at chromosome ends; their length shortens with age and is proposed to reflect the rate of biological ageing. Negative lifestyle factors, including a lack of exercise, obesity, psychological stress, and smoking appear to increase telomere attrition rate and consequentially accelerate ageing. Conversely, positive lifestyle factors, such as exercise participation, meditation, and a healthy diet are reported to largely attenuate telomere shortening rate. The studies described in this thesis investigated the effect of various exercise modalities on telomere length (TL). Potential exercise-induced cellular mechanisms regulating telomere dynamics (e.g., telomerase reverse transcriptase (TERT) expression, inflammation, antioxidant gene expression) were also explored.

Chapter III demonstrated that a 12-week low-load, high-repetition resistance training (RT) intervention does not influence TL in sedentary middle-aged individuals. TERT gene expression also remained unchanged following the 12 -week RT intervention, although it was borderline significant (p = 0.05). A negative inverse association was observed between TL and serum levels of C-reactive protein (CRP) at pre and post timepoints. Furthermore, a 12-month follow-up visit revealed that TL was maintained in participants who continued to exercise using a variety of modalities. In comparison, individuals who returned to a sedentary lifestyle displayed significant telomere attrition.

Chapter IV revealed that experienced female Pilates practitioners (5.7 ± 1.5 years of training) displayed comparable TL to their sedentary aged-matched counterparts at pre (baseline) and post (12 months) timepoints. Additionally, the longitudinal analysis revealed that neither group exhibited any significant telomere shortening over the subsequent 12-month period. There was also no difference in TERT gene expression between groups at any time point. Tumour necrosis factor-α (TNF-α) serum levels were negatively correlated with TL across the whole cohort (all timepoints).

In Chapter V, young endurance athletes were shown to possess longer telomeres than master endurance runners, master sprinters, and middle-aged controls, which appeared to be the result of their reduced BMI and visceral fat rating. However, these differences in TL were not significant when controlled for covariates. It was also discovered that leukocyte and buccal cell TL are highly correlated in this athlete cohort. TERT gene expression was comparable between all groups and positively associated with TL.

The final study of this thesis, Chapter VI, discovered that young elite swimmers have shortened telomeres compared with age-matched recreationally active controls. When split by sex, only elite female swimmers displayed significantly shorter telomeres than their recreationally active counterparts. These results suggest a negative effect of a high-level swimming competition and/or training on TL and subsequent biological ageing in females. The results of this thesis collectively suggest that a variety of exercise modalities can influence telomere dynamics, although their effects appear to be divergent and modality specific. Low-intensity exercise modalities (e.g., low-load, high- epetition RT and Pilates) do not appear to be a sufficient stimulus to regulate telomere dynamics, and exercise modalities demanding a higher intensity (e.g., swimming) may be necessary to influence TL. Nonetheless, extremely high intensities and/or doses of exercise appear detrimental to TL. Additionally, TERT gene expression does not appear to be regulated by the exercise modalities employed in this thesis.