Epidemiological evidence suggests that a high resting heart rate (RHR) is associated with increased cardiovascular morbidity and mortality in the general population, independent of conventional risk factors.^1-3 An elevated RHR also has been associated with poorer prognosis within subgroups of patients with cardiovascular disease.^4-6

Methods In this prospective cohort study, we used a previously published nonexercise test to estimate CRF in healthy men (n = 18,348) and women (n = 18,764) from the first HUNT study (1984–1986) in Norway. We used Cox regression to obtain HR for mortality during a mean follow-up of 24 yr. Assessment of model validity was performed by standard procedures of discrimination and calibration. Results CRF was inversely associated with all-cause and CVD mortality in men and women below 60 yr of age at baseline, after adjustment for confounders. For each MET-higher CRF (MET, approximately 3.5 mL·kg−1·min−1), HR for CVD mortality was 21% lower in both men (95% confidence interval (CI), 17%–26%) and women (95% CI, 12%–29%). HR for all-cause mortality was 15% (95% CI, 12%–17%) lower in men and 8% (95% CI, 3%–3%) lower in women for each MET-higher CRF. The ability of the model to discriminate mortality risk among participants below 60 yr was better for CRF (area under the curve (AUC), 0.70–0.77) compared with that for each variable that constituted the model (AUC, 0.55–0.63) and an aggregated sum of z-scores for each variable (AUC, 0.61–0.65). Comparison of observed and predicted risk indicated good model calibration. Conclusions This method of assessing CRF is feasible and practically useful in primary care for identification of apparently healthy individuals at increased risk of premature CVD disease and all-cause mortality....

Telomeres are potential markers of mitotic cellular age and are associated with physical ageing process. Long-term endurance training and higher aerobic exercise capacity (VO_2max) are associated with improved survival, and dynamic effects of exercise are evident with ageing. However, the association of telomere length with exercise training and VO_2max has so far been inconsistent. Our aim was to assess whether muscle telomere length is associated with endurance exercise training and VO_2max in younger and older people. Twenty men; 10 young (22–27 years) and 10 old (66–77 years), were studied in this cross-sectional study. Five out of 10 young adults and 5 out of 10 older were endurance athletes, while other halves were exercising at a medium level of activity. Mean telomere length was measured as telomere/single copy gene-ratio (T/S-ratio) using quantitative real time polymerase chain reaction. VO_2max was measured directly running on a treadmill. Older endurance trained athletes had longer telomere length compared with older people with medium activity levels (T/S ratio 1.12±0.1 vs. 0.92±0.2, p = 0.04). Telomere length of young endurance trained athletes was not different than young non-athletes (1.47±0.2 vs. 1.33±0.1, p = 0.12). Overall, there was a positive association between T/S ratio and VO_2max (r = 0.70, p = 0.001). Among endurance trained athletes, we found a strong correlation between VO_2max and T/S ratio (r = 0.78, p = 0.02). However, corresponding association among non-athlete participants was relatively weak (r = 0.58, p = 0.09). Our data suggest that VO_2max is positively associated with telomere length, and we found that long-term endurance exercise training may provide a protective effect on muscle telomere length in older people.

Cardiorespiratory fitness is associated with risk of dementia, but whether temporal changes in cardiorespiratory fitness influence the risk of dementia incidence and mortality is still unknown. We aimed to study whether change in estimated cardiorespiratory fitness over time is associated with change in risk of incident dementia, dementia-related mortality, time of onset dementia, and longevity after diagnosis in healthy men and women at baseline. We linked data from the prospective Nord-Trøndelag Health Study (HUNT) done in Nord-Trøndelag, Norway with dementia data from the Health and Memory Study and cause of death registries (n=30 375). Included participants were apparently healthy individuals for whom data were available on estimated cardiorespiratory fitness and important confounding factors. Datasets were matched to each participant through their 11-digit personal identification number. Cardiorespiratory fitness was estimated on two occasions 10 years apart, during HUNT1 (1984-86) and HUNT2 (1995-97). HUNT2 was used as the baseline for follow-up. Participants were classified into two sex-specific estimated cardiorespiratory fitness groups according to their age (10-year categories): unfit (least fit 20% of participants) and fit (most fit 80% of participants). To assess the association between change in estimated cardiorespiratory fitness and dementia, we used four categories of change: unfit at both HUNT1 and HUNT2, unfit at HUNT1 and fit at HUNT2, fit at HUNT1 and unfit at HUNT2, fit at both HUNT1 and HUNT2. Using Cox proportional hazard analyses, we estimated adjusted hazard ratios (AHR) for dementia incidence and mortality related to temporal changes in estimated cardiorespiratory fitness. During a median follow-up of 19·6 years for mortality, and 7·6 years for incidence, there were 814 dementia-related deaths, and 320 incident dementia cases. Compared with participants who were unfit at both assessments, participants who sustained high estimated cardiorespiratory fitness had a reduced risk of incident dementia (AHR 0·60, 95% CI 0·36-0·99) and a reduced risk of dementia mortality (0·56, 0·43-0·75). Participants who had an increased estimated cardiorespiratory fitness over time had a reduced risk of incident dementia (AHR 0·52, 95% CI 0·30-0·90) and dementia mortality (0·72, 0·52-0·99) when compared with those who remained unfit at both assessments. Each metabolic equivalent of task increase in estimated cardiorespiratory fitness was associated with a risk reduction of incident dementia (adjusted HR 0·84, 95% CI 0·75-0·93) and dementia mortality (0·90, 0·84-0·97). Participants who increased their estimated cardiorespiratory fitness over time gained 2·2 (95% CI 1·0-3·5) dementia-free years, and 2·7 (0·4-5·8) years of life when compared with those who remained unfit at both assessments. Change in estimated cardiorespiratory fitness is an independent risk factor for incidence dementia and dementia mortality. Maintaining or improving cardiorespiratory fitness over time may be a target to reduce risk of dementia incidence and mortality, delay onset, and increase longevity after diagnosis. Our data highlight the importance of assessing cardiorespiratory fitness in health risk assessment for people at risk of dementia. The KG Jebsen Foundation, the Norwegian Research Council, the Liaison Committee between the Central Norway Regional Health Authority, and the Norwegian University of Science and Technology.