Background and Purpose— Low cardiorespiratory fitness is associated with increased risk of cardiovascular disease. The present study aims to assess whether change of fitness over time has any impact on long-term risk of stroke and death. Methods— We recruited healthy men aged 40 to 59 years in 1972 to 1975, and followed them until 2007. Physical fitness was assessed with a bicycle ECG test at baseline and again at 7 years, by dividing the total exercise work by body weight. Participants were categorized as remained fit, became unfit, remained unfit, or became fit, depending on whether fitness remained or crossed the median values from baseline to the 7-year visit. Outcome data were collected up to 35 years, from study visits, hospital records, and the National Cause of Death Registry. Risks of stroke and death were estimated by Cox regression analyses and expressed as hazard ratios (HRs) with 95% CIs. Results— Of 2014 participants, 1403 were assessed both at baseline and again at 7 years, and were followed for a mean of 23.6 years. Compared with the became unfit group, risk of stroke was 0.85 (0.54–1.36) for the remained unfit, 0.43 (0.28–0.67) for the remained fit, and 0.34 (0.17–0.67) for the became fit group. For all-cause death, risks were 0.99 (0.76–1.29), 0.57 (0.45–0.74), and 0.65 (0.46–0.90), respectively. Among those with high fitness at baseline, the became unfit group had a significantly higher risk of stroke (HR, 2.35; CI, 1.49–3.63) and death (HR, 1.74; CI, 1.35–2.23) than those who remained fit. Among those who had low fitness at baseline, the became fit group had a significantly lower risk of stroke (HR, 0.40; CI, 0.21–0.72) and death (HR, 0.66; CI, 0.50–0.85) than participants in the remained unfit group. Conclusions— Cardiorespiratory fitness at baseline and change in fitness was associated with large changes in long-term risk of stroke and death. These findings support the encouragement of regular exercise as a stroke prevention strategy.

There is no consensus on the definition of an exaggerated increase in systolic blood pressure (SBP) during exercise. The aim was to explore a potential threshold for exercise SBP associated with increased risk of coronary heart disease (CHD) in healthy men, using repeated exercise testing. 2,014 healthy Caucasian male employees were recruited into the Oslo Ischemia Study during early 1970s. At follow-up seven years later, 1,392 men were still considered healthy. A bicycle exercise test at 100W workload was performed at both visits. Cox regression analyses were performed with increasing cutoff levels of peak SBP during 100W workload (SBP100W) from 160 mmHg to 200 mmHg, adjusted for cardiovascular risk factors and physical fitness. Participants with SBP100W below cutoff level at both baseline and first follow-up were compared to participants with SBP100W equal to or above cutoff level at both visits. Compared to participants with SBP100W below all cutoff levels between 165-195 mmHg, CHD risk was increased amongst participants with SBP100W equal to or above cutoff at all levels. There was no evidence of a distinct threshold level for CHD risk, and the relation between SBP100W and CHD appears linear. When investigating exercise SBP at moderate workload measured at two exercise tests in healthy middle-aged Caucasian men, there is increasing risk of coronary disease with increasing exercise SBP independent of SBP at rest. The association is linear from the low range of exercise SBP and there is no sign of a distinct threshold level for increased coronary disease risk. Participants were divided into groups defined by SBP100W at Visit 1 and Visit 2 (Figure S1). Group 1 includes participants with SBP100W below cutoff level at both Visit 1 and Visit 2. Group 3 includes participants with SBP100W equal to or above cutoff level at both Visit 1 and 2, and Group 2 includes participants with SBP100W equal to or above cutoff level at only one of the two visits, regardless of which. To investigate the risk of CHD, we performed Cox regression analyses adjusted for age, resting SBP, total serum cholesterol, smoking status and family history of CHD. We also performed additional analyses adjusting for physical fitness. Physical fitness was defined as total workload during the exercise test measured in kilojoules divided by body weight. Due to the increases in cutoff levels, the number of participants in each group successively changed in each analysis, as Group 1 expanded and Group 3 diminished.

Background Physical fitness has been shown to predict cardiovascular death during long-term follow-up. In the present study we aimed to investigate how physical fitness and other cardiovascular risk factors at middle-age influenced the risk of cardiovascular death during the early (0-11 years), intermediate (12-23 years) and late (24-35 years) parts of a 35-year observation period. Methods and results Age-adjusted physical fitness was calculated in 2014 apparently healthy, middle-aged men after maximal bicycle electrocardiogram-tests in 1972-1975 (Survey 1) and 1979-1982 (Survey 2). The men were assessed through 35 years after Survey 1, and 28 years after Survey 2 by Cox proportional hazards models. Low Survey 1 physical fitness was independently associated with increased risks of early and intermediate, but not late, cardiovascular death. Survey 1 to Survey 2 change in physical fitness, age, smoking status, systolic blood pressure and cholesterol impacted cardiovascular death risks in all periods. Family history of coronary heart disease impacted early and intermediate, but not late, cardiovascular death. Conclusions Most classical cardiovascular risk factors were strong predictors of early, intermediate and late cardiovascular death. Physical fitness measured at median age 50 years was independently associated with risk of early cardiovascular death, but the association weakened as time progressed. Change in physical fitness during middle-age impacted cardiovascular death risk in a full lifetime perspective. Thus, our data suggest that physical fitness is a modifiable cardiovascular risk factor with limited duration in contrast to the sustained impact of smoking, blood pressure and cholesterol on cardiovascular mortality.