Background Telomere length has been associated with a healthy lifestyle and longevity. However, the effect of increased physical activity on telomere length is still unknown. Therefore, the aim was to study the relationship between changes in physical activity level and sedentary behaviour and changes in telomere length.
Methods Telomere length was measured in blood cells 6 months apart in 49, 68-year-old, sedentary, overweight individuals taking part in a randomised controlled physical activity intervention trial. The intervention group received individualised physical activity on prescription. Physical activity was measured with a 7-day diary, questionnaires and a pedometer. Sitting time was measured with the short version of The International Physical Activity Questionnaire.
Results Time spent exercising as well as steps per day increased significantly in the intervention group. Reported sitting time decreased in both groups. No significant associations between changes in steps per day and changes in telomere length were noted. In the intervention group, there was a negative correlation between changes in time spent exercising and changes in telomere length (rho=−0.39, p=0.07). On the other hand, in the intervention group, telomere lengthening was significantly associated with reduced sitting time (rho=−0.68, p=0.02).
Conclusions Reduced sitting time was associated with telomere lengthening in blood cells in sedentary, overweight 68-year-old individuals participating in a 6-month physical activity intervention trial.
- Genetic Testing
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Increased telomere length is associated with longevity. Cross-sectional studies demonstrate an association between a healthy life style, that is, lower body mass index (BMI), a healthy diet and physical activity, and longer telomeres.1–3 Physical activity in leisure time was associated with longer telomeres in white blood cells after adjustment for age, BMI, smoking, education and physical activity during work time in a study of 2401 white twins.4 Longer telomeres in blood cells were associated with higher exercise capacity in 944 patients having coronary heart disease and with habitual exercise in 44 healthy postmenopausal women.5 ,6 A strong correlation between telomere length in skeletal muscle and oxygen uptake was noted irrespective of age, in a study of 10 endurance trained athletes.7 Sixty-seven ultramarathon runners had 11% longer telomeres than healthy controls.8 Furthermore, telomere length in postural muscle was similar in young and old people who were physically active.9 In a Finnish study, physical activity level in mid-life was associated with telomere length in white blood cells after a 29-year follow-up.10 Interestingly, those reporting moderate physical activity, in comparison with low-intensity or high-intensity physical activity, had significantly longer telomeres. Smoking, stress and major depression are associated with shorter telomeres.1 ,2 ,10–12 Physical activity seems to counteract the deleterious effects of stress on telomere length.13 However, due to a lack of intervention studies, it is still largely unknown whether introduced lifestyle changes can affect telomere length.
We previously reported a clinical trial where 101 68-year-old individuals (57% women) with a sedentary lifestyle, overweight and abdominal obesity were randomised to individualised physical activity on prescription (intervention) or usual care with minimal intervention (controls).14 After 6 months, the intervention group had significantly increased physical activity level; the number of exercise sessions per week (+159 min) and the number of steps per day (+1663 steps) increased, while sitting time decreased (−2 h/day). Bodyweight, waist circumference, fat mass, serum cholesterol and glycated haemoglobin decreased significantly more in the intervention group compared with the control group.14
Telomere length was measured in blood cells taken 6 months apart from 49 randomly selected individuals from the same study. Individual changes in telomere length were pronounced and we reported that telomere length is a dynamic feature. However, we found no difference in changes in telomere length between the intervention group and the control group.15
As physical activity is a most complex behaviour, we aimed to study the relationships between changes in steps per day, minutes performing exercise of low and moderate intensity as well as reported sitting time and changes in telomere length.
The design of the original study, the physical activity intervention and the methods have been described.14 From the original study, a random set of 49 individuals (14 men and 35 women) was analysed with regard to telomere length and changes over time from baseline to the 6-month follow-up. The methods used to analyse telomere length in blood samples have been described.15 In brief, telomere length was measured with the qPCR assay on DNA extracted from whole blood, using human β-globin as the single copy gene.
Within-group and between-group differences were analysed from normalised data using paired t tests and analysis of covariance (adjusted for baseline values), respectively. All analyses were performed in STATA (STATA/SE V.13.0: Stata Corp, College Station, Texas, USA). The relationships between changes in relative telomere length (change per month) and changes in physical activity levels (steps per day, time of moderate-intensity exercise and low-intensity exercise) as well as reported sitting time were studied using Spearman rank correlation.
Measures of sedentary behaviour and physical activity levels at baseline and after 6 months in the studied subgroup are presented in online supplementary table S1. Time spent exercising (moderate-intensity and low-intensity exercise) as well as steps per day increased significantly in the intervention group. Reported sitting time decreased significantly in both groups.
In parallel and in accordance with the original study, positive changes in several cardiovascular risk factors were noted in both groups, especially in the intervention group (data not shown).14 Weight reduction was significantly greater in the intervention group compared with the control group (data not shown).14
We found no significant associations between changes in steps per day and changes in telomere length. In both groups, increases in exercise time (moderate intensity) were negatively associated with changes in telomere length although not significantly (figure 1A, B). Corresponding relationships were seen for increases in exercise time of low intensity (data not shown). However, as demonstrated in figure 2A, B, in the intervention group, telomere lengthening was significantly associated with reduced sitting time (rho=−0.68, p=0.02). This was equivalent to an effect size of 0.28 (η2).
In this 6-month randomised controlled physical activity trial in 68-year-old, sedentary and overweight men and women, reduced sitting time was significantly associated with telomere lengthening in blood cells. An increase in time spent exercising, on the other hand, was associated with telomere shortening. We found no association between changes in telomere length and changes in steps per day.
In many countries formal exercise may be increasing, but at the same time people spend more time sitting.16 ,17 There is growing concern that not only low physical activity level in populations, but probably also sitting and sedentary behaviour, is an important and new health hazard of our time.18 Epidemiological studies, of cross-sectional and prospective design, demonstrate that there is a substantially increased risk for obesity, metabolic syndrome, type 2 diabetes, cardiovascular disease, as well as total mortality in sedentary individuals, independent of the number of total exercise sessions per week or total physical activity.19 ,20 On the other hand, observational as well as intervention studies demonstrate positive effects on waist circumference, lipids, glucose homoeostasis and inflammatory markers because of short breaks during prolonged sitting.21–24
In the Finnish Diabetes Prevention Study, the incidence of type 2 diabetes was substantially reduced (58%) after 5 years in individuals with impaired glucose tolerance receiving a combined intervention with a healthy diet and increased physical activity.25 Telomere length in white blood cells increased in two-thirds of the participants in the intervention group and the control group.26 Telomere length was not associated with lifestyle changes or the development of type 2 diabetes.
To the best of our knowledge, the effect from different aspects of physical activity like steps per day, intensity during exercise or sedentary time has not been studied before in relation to telomere dynamics, and therefore our results might add to the current knowledge. However, there are several weaknesses to be taken into account. For example, the study sample is small and we cannot rule out that the findings are a chance phenomenon. The methods used to capture sedentary time (questionnaires) are not objective but have a long history in the field. Still, we find the results from this pilot study interesting and they fit well into the findings from Dunstan et al,22 showing a pronounced effect on, for example, glucose and insulin metabolism after short breaks during prolonged sitting. Acute effects on gene expression of health-related genes in skeletal muscle were also demonstrated after 2 min activity during prolonged sitting for 5 h.27 We hypothesise that a reduction in sitting hours is of greater importance than an increase in exercise time for elderly risk individuals.
Our novel finding of an association between telomere lengthening in blood cells and reduced sitting hours in elderly risk individuals adds to the current knowledge regarding the importance of avoidance of prolonged sitting.
The results from this pilot study need to be repeated in other populations. Furthermore, studying the effects of reduced sedentary hours on telomere length and telomere dynamics in other tissues such as skeletal muscle and adipose tissue is of utmost importance.
Contributors PS, RF and M-LH were involved in study concept and design. LK, US, GR and M-LH were involved in acquisition of the data. PS, RF and M-LH were involved in analysis and interpretation of the data. PS and M-LH were involved in drafting of the manuscript. All authors were involved in critical revision of the manuscript for important intellectual content.
Funding This study was supported by grants from the Swedish Cancer Society (GR), the Lion's Cancer Research Foundation, Umeå (GR), the Swedish Research Council (GR), the County Council of Västerbotten (GR), the Novo Nordisk Foundation (RF), the Swedish Diabetes Association (RF), the Swedish National Institute of Public Health (M-LH), The Swedish Heart and Lung Foundation (M-LH), The Swedish Order of Freemasons Grand Swedish Lodge (M-LH), Tornspiran Foundation (M-LH) and The Albert and Gerda Svensson Foundation (M-LH). The research leading to these results has received funding from the European Community's Seventh Framework Program FP7/2007–2011 under grant agreement no. 200950 (GR).
Competing interests None.
Patient consent Obtained.
Ethics approval Ethical Board of Karolinska Institutet.
Provenance and peer review Not commissioned; externally peer reviewed.
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