Exercise training is a powerful tool for prevention and rehabilitation of cardiovascular and metabolic diseases. A number of biological mechanisms are addressed to varying degrees by differential exercise modalities – frequency, intensity, type, duration. Most of us therefore believe that by fine-tuning exercise modalities we can tailor exercise protocols to each patient´s specific needs - therapy targets, main risk factors, underlying disease, maybe even to genetically conferred risk.
One of the biological mechanisms that has been studied as a potential target of physical exercise is the shortening of telomeres which normally occurs during cell division in terminally differentiated somatic cells – a mechanism conferring cellular dysfunction during aging. Accelerated telomere shortening has been reported for various chronic pathological conditions and is associated with increased cardiovascular risk . A number of studies have provided associations between habitual physical activity and telomere length, with an apparent dose-response relationship between the amount of regular physical activity and telomere length [2, 3]. Although these observational data are suggestive, associations were mainly between baseline telomere length and self-reported physical activity status. Follow-up measurements 10 years later, or interventional studies have not been able to confirm a causal effect of exercise on telomere length so far [4-7].
In their recent interventional study, Werner et al. investigate whether a 6-month exercise programme employing differential exercise modalities - resistance exercise, moderate continuous or high-intensity interval endurance training - differentially affect telomerase activity and telomere length in various types of leukocytes . They report that telomere length was indeed increased in lymphocytes and granulocytes of healthy individuals participating in an endurance exercise programme (either moderate-intensity continuous training or high-intensity interval training) . In contrast, performing resistance training for 6 months did not result in telomere elongation . In addition, the acute effects of endurance and resistance exercise on telomerase activity in the same individuals were compared and the impact of a marathon race on telomerase activity in athletes was assessed .
The study supports application of endurance exercise rather than resistance exercise for the protection of telomere length – at least in healthy individuals. It would be relevant to understand whether the same can be observed in patients with established cardiovascular or metabolic diseases, such as diabetes.
Several potential mechanisms linking physical activity, cardiovascular disease state and telomere length have been discussed in the field in the last 15 years, including inflammation, oxidative stress and stress hormones [3, 9]. Cellular energy sensors, such as AMPK and sirtuins might provide another mechanism linking exercise type and intensity to telomerase activity [10-12]. Werner et al. excluded a role of stress hormones for telomerase activity in their setting and suggested an association with nitric oxide synthase expression . A connexion between NO synthesis and cellular senescence has been discussed for endothelium and leukocytes before, albeit causality is unclear and both effects might rather be downstream of a common signalling process.
Werner et al. have observed that an acute bout of endurance exercise increased telomerase activity, albeit with wide inter-individual variation . This appears to be at variance with earlier studies at first glance . Experimental design may explain most of the differences. In addition, the wide variation of effect in the recent study indicates inter-individual and/or inter-experimental differences. Moreover, telomerase activity might not necessarily translate into measurable telomere lengthening, thus underlining the importance of experimental design.
In conclusion, the study by Werner et al. adds to the notion that endurance exercise rather than resistance exercise may protect telomere erosion in healthy adults, with no difference between moderate or high exercise intensity observed. Future studies need to verify these observations in patients with cardiovascular and metabolic diseases.
Note: The content of this article reflects the personal opinion of the author and is not necessarily the official position of the European Society of Cardiology.