Initiating life‐long aerobic exercise 4–5 days per week before or near age 50 years: is this the ‘holy‐grail’ of preventing age‐related central artery stiffness?

Stiffening of the large elastic central arteries, including the aorta and carotid arteries, occurs with advancing age in sedentary adults and predicts cardiovascular disease (CVD) events independent of blood pressure and other risk factors (Ben‐Shlomo et al. 2014; van Sloten et al. 2015). In cross‐sectional studies, this age‐related aortic stiffening, measured by carotid‐femoral pulse wave velocity (CFPWV), is attenuated in normotensive middle‐aged/older (MA/O) adults who perform habitual aerobic exercise ≥5 days week⁻¹ for at least 2 years. Similarly, carotid artery stiffness is lower in MA/O endurance‐trained adults who exercise ≥5 days week⁻¹ for at least the previous 2 years, but is not different between recreationally active (3 days week⁻¹) and sedentary (<2 days week⁻¹) MA/O adults. In contrast, short‐term (3–4 months) and longer (1 year) intervention studies typically consisting of 3–4 days week⁻¹ of aerobic exercise initiated in previously sedentary MA/O adults without hypertension demonstrate minimal or no changes in aortic stiffness (Pierce, 2017). Interestingly, only 3 months of aerobic exercise commenced in previously sedentary MA/O men and women 4–6 days week⁻¹ reduces carotid artery stiffness back to or near levels of young adults (Pierce, 2017). Thus, these studies suggest that age‐related stiffening of the aorta and carotid arteries is attenuated in MA/O adults who have been endurance‐training for ≥5 days week⁻¹, >30 min day⁻¹ for at least 2 years or more (6–7 days week⁻¹ and >10 years in many studies), whereas the carotid artery appears to be more amenable than the aorta in response to short‐term aerobic exercise interventions ≥5 days week⁻¹ when started in the early/mid 60s. However, less is known about the minimal frequency of ‘life‐long’ (defined as for at least the past 25 years) aerobic exercise required to attenuate the age‐related rise in stiffness of the aorta and the carotid arteries and if this ‘dose’ of exercise differs between aorta and carotid arteries.

The study by Shibata et al. (2018) in this issue of The Journal of Physiology investigated whether the frequency ‘dose’ of ‘lifelong’ habitual aerobic exercise training of 4–5 days week⁻¹ for >30 min day⁻¹ among MA/O adults, was sufficient to lower central artery stiffness compared with 2–3 days week⁻¹ or <2 days week⁻¹. In a cross‐sectional study from the well characterized Cooper Centre Longitudinal Study, they studied four groups of MA/O adults who consistently reported the same level of regular aerobic exercise in repeated follow‐up exams over 20 or more years. Groups were stratified and named by exercise frequency: <2 days week⁻¹ (‘sedentary’), 2–3 days week⁻¹ (‘casual exercisers’), 4–5 days week⁻¹ (‘committed exercisers’), and 6–7 days week⁻¹ (‘Masters athletes’). These authors previously reported that 4–5 days week⁻¹ among the ‘committed exercisers’ was sufficient to prevent sedentary ageing‐associated decreases in left ventricular (LV) compliance in older adults (mean age ∼68 years) (Bhella et al. 2014). In the current study, the authors found that CFPWV, carotid β‐stiffness and distensibility were not different between committed exercisers and Masters athletes, suggesting that there was no additive benefit of 1–2 more days week⁻¹ of aerobic exercise beyond 4–5 days week⁻¹. However, both CFPWV and biological aortic age, an index calculated from the Modelflow stroke volume, were lower in committed exercisers compared with casual exercisers, indicating that 4–5 days week⁻¹ of aerobic exercise may be the minimal frequency that is sufficient to attenuate age‐related aortic stiffening. Importantly, carotid β‐stiffness was lower among the casual exercisers compared with the sedentary group in the absence of differences in CFPWV, suggesting that the carotid artery may respond to less frequent exercise (2–3 days week⁻¹) than the aorta. Furthermore, biological aortic age was lower in Masters athletes compared with the committed exercisers, indicating an additive benefit of 1–2 more days week⁻¹ of exercise on biological aortic age but not CFPWV. These data suggest a possible dissociation between the biological aortic age index and CFPWV, or indeed that biological aortic age may be more sensitive in detecting changes in aortic stiffness with more frequent exercise. Because the mean age of the participants was 70 years, these individuals had been performing this aerobic exercise frequency at least since their mid‐40s/early 50s. This is important because the stiffening of central elastic arteries accelerates rapidly after age 50–60 years (Mitchell et al. 2010), suggesting that commencing habitual aerobic exercise before and sustaining it beyond this decade may be a critical window in preventing age‐associated central arterial stiffening. Consistent with this idea of the optimal time for exercise‐related cardiovascular plasticity with ageing, the authors recently reported that beginning 4–5 days of aerobic exercise during middle‐age (mean age ∼53 years) for 2 years improved left ventricular compliance in previously sedentary adults (Howden et al. 2018), whereas this dose of exercise at least for 1 year had no effect on left ventricular compliance in seniors (Fujimoto et al. 2010).

A major limitation of this study as discussed by the authors is that it is unclear if there were differences in intensity and duration of each bout of exercise among the groups, because the committed exercisers may have performed exercise bouts at higher intensities and/or for longer durations per session compared with the casual exercisers, thus confounding the use of frequency to stratify participants. Methodical limitations include the use of the biological age index because it is unknown if this variable increases across the lifespan similar to CFPWV or predicts CVD risk beyond blood pressure and other risk factors. Furthermore, using the pulsed Doppler ultrasound to measure CFPWV was not in agreement with CFPWV data from the Sphygmocor® device. The divergent results could have been related to subjective visual identification of diastolic foot of carotid and femoral waveforms from pulsed Doppler rather than intersecting tangents algorithm used by software in the Sphygmocor for objective identification of the diastolic foot of the pressure waveforms.

In summary, the current study supports the idea that 4–5 days week⁻¹ of life‐long habitual aerobic exercise may be the optimal frequency for attenuation of age‐associated aortic stiffness and that 2–3 days week⁻¹ may be ideal for carotid artery stiffness. Importantly, initiating this regimen before or near the age of 50 years and sustaining it into older age might be the ‘holy grail’ to prevent the progression of age‐related central artery stiffening. Future studies should attempt to better characterize intensity, duration and frequency in cohorts currently in early middle‐age so that this critical information on preventing age‐related arterial stiffening can be attained at repeated follow‐ups over the next two to three decades.

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Competing interests

None declared.