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• W2898069614 abstract "Arterial stiffness independently predicts cardiovascular disease-related morbidity and mortality (Sardeli et al. 2018; Shibata et al. 2018). The large central elastic arteries (e.g. the aorta and carotid arteries) stiffen with age due to structural and functional changes in the arterial wall (Sardeli et al. 2018) reducing their ability to attenuate large pulsatile pressure waves exiting the heart. Arterial stiffness leads to the transmission of excessive pulsatile pressure into the microcirculation of more sensitive organs and tissues, such as the heart, kidneys and brain (de Roos et al. 2017). Thus, there is an imperative need to identify strategies to combat these deleterious age-related arterial changes. One strategy is regular endurance exercise training. Previous work has found that competitive masters athletes (i.e. individuals ≥65 years, who exercise 6–7 endurance training sessions per week, and regularly engage in competitions) have more compliant central arteries compared to sedentary individuals (<1 session per week) of the same age (Shibata et al. 2018). It may not be feasible for the general population to maintain habitual exercise levels comparable to competitive masters athletes; thus, it is important to determine whether lower amounts of lifelong exercise are sufficient for preventing age-related increases in arterial stiffness. A recent paper by Shibata et al. (2018) in the Journal of Physiology examined the effect of less frequent doses of lifelong (≥25 years) exercise on arterial stiffness to elucidate the ‘minimal dose’ of aerobic exercise for preventing arterial stiffness. Shibata et al. (2018) performed a cross-sectional analysis to determine the effects of varying frequencies of lifelong endurance training on several indices of arterial stiffness including carotid–femoral pulse wave velocity (PWV; the ‘gold standard’ metric of aortic stiffness) and the carotid artery β-stiffness index. Participants were required to have maintained the same frequency of exercise for at least 25 years, determined by self-report through multiple questionnaires. The authors found that committed lifelong exercisers (4–5 sessions per week) and competitive masters athletes exhibited lower central arterial stiffness, compared to their sedentary (<1 session per week) and casual (2–3 sessions per week) exercising counterparts. Interestingly, committed lifelong exercise was sufficient for preventing age-related stiffening of both the aorta and carotid arteries, while the lower frequency of exercise performed by the casual group was only enough to preserve carotid artery compliance (Shibata et al. 2018). The carotid artery may be more sensitive to lower levels of exercise than the aorta (Sardeli et al. 2018). For example, the reduction in carotid artery compliance has been shown to be twice as large as the reduction in PWV following short-term (1–24 weeks) endurance exercise training (Sardeli et al. 2018). This may explain why Shibata et al. (2018) did not observe reductions in aortic stiffness (assessed by PWV) of casual lifelong exercisers, whereas casual exercise preserved carotid artery distensibility and carotid β-stiffness compared with their sedentary counterparts. One advantage of less stiff arteries is a reduced load on the heart, which may lower risk of cardiovascular disease. When blood is ejected from the heart, it is propelled by a forward-traveling pressure wave that is eventually reflected back toward the heart at points of bifurcation, mismatched impedance and smaller vascular beds, normally reaching the heart during diastole (Hickson et al. 2016). As the central arteries stiffen, these pressure waves return during systole, increasing the pressure that the left ventricle must work against to eject blood and contributing to diminished blood flow and poor diastolic coronary perfusion. In young healthy adults, peripheral arteries are naturally stiffer than the central arteries. This stiffness gradient is reversed by age-related increases in central artery stiffness, resulting in an amplification of wave reflection (Hickson et al. 2016). Although not analysed, data presented by Shibata et al. (2018) suggest that committed and masters athletes may be protected from the age-related reversal of this stiffness gradient. If confirmed in a future study, this potential finding may explain how haemodynamic changes associated with exercise protect the heart and other organs from the detrimental effects of arterial stiffness. Finally, the authors found changes in central arterial stiffness occurred independent of changes to central blood pressure using a measure called ‘biological aortic age’, which determines how ‘old’ an artery is relative to chronological age. A benefit of this measure is that it is less dependent upon mean arterial pressure, which may influence arterial stiffness (Shibata et al. 2018). Shibata et al. found that competitive masters athletes and committed exercisers exhibited a younger biological aortic age, as well as lower central PWV, compared to casual exercisers and sedentary individuals. In addition, committed exercisers and competitive masters athletes were estimated to have aortas that were approximately 10 and 25 years younger than sedentary individuals, respectively (Shibata et al. 2018). A younger, more compliant aorta can more effectively buffer left ventricle pulse pressure, and reduce the exposure of barotrauma-sensitive organs such as the kidneys and brain (de Roos et al. 2017). While larger epidemiological studies are needed to validate biological aortic age as a predictor of cardiovascular disease risk, these findings suggest that the benefits of exercise for preventing age-related central arterial stiffening may occur independent of central blood pressure (Shibata et al. 2018). These findings provide insight into the optimal dose of aerobic exercise for preventing arterial ageing, but factors such as intensity, duration and type of exercise warrant future consideration (Sardeli et al. 2018). Long duration (>10 weeks), high frequency and continuous exercise bouts (vs. intervals), have been shown to cause the largest reductions in carotid artery compliance (Sardeli et al. 2018). Therefore, it is plausible that not only the frequency of exercise training, but also the intensity, time and type of exercise may be affecting the differences in arterial stiffness. In addition to cardiovascular diseases, the findings by Shibata et al. (2018) may have relevance for preventing other age-related diseases. Arterial stiffness has increasingly been associated with age-related cognitive impairment and risk for dementia, whereas higher cardiorespiratory fitness is associated with lower arterial stiffness and enhanced cognitive function (Tarumi et al. 2013). The brain, with its high metabolic demand and limited capacity for energy storage, consumes a large amount of the total cardiac output and is perfused by a dense network of low resistance arterioles and capillaries (Tarumi et al. 2013). The large elastic arteries normally act to protect these sensitive vascular beds by buffering pressure waves exiting the heart. Stiffening of the large elastic arteries results in transmission of excessive flow pulsatility into the brain, causing damage to the cerebral microvasculature (de Roos et al. 2017). As a consequence, cerebral blood flow is decreased (Tarumi et al. 2013), resulting in cerebral hypoxia, hypoperfusion (Tarumi et al. 2013) and the development of vascular lesions, which have been linked to age-related cognitive impairment (de Roos et al. 2017). Although a greater frequency of exercise training is needed to prevent aortic stiffening, Shibata et al. (2018) found that casual exercise is sufficient for preventing the decline in carotid artery compliance with ageing. This may be particularly important for preserving cognitive function as the carotid arteries are the final defence against excessive pulsatile pressure entering the brain. Thus, even moderate intensity exercise may be enough to limit the entry of damaging pressure waves into the brain and preserve cognitive function. One of the primary mechanisms by which arterial stiffness occurs with ageing is through structural remodelling of the arterial wall, contributing to the development of midlife vascular disease and hypertension, both of which have been implicated in age-related dementia risk (Tarumi et al. 2013). The data by Shibata et al. (2018) suggests that the benefits of chronic exercise training on carotid artery compliance can be achieved when casual or committed exercise is implemented starting in midlife (∼50 years) and may help explain why exercise training is associated with a decreased risk of age-related dementia (Tarumi et al. 2013). In summary, endurance training is an easily accessible lifestyle intervention for sedentary adults, which maintains the youth and compliance of the large elastic arteries. Shibata et al. (2018) have shown that chronic high frequency exercise training at the masters level may not be necessary to maintain carotid compliance, as even casual exercise, 2–3 days per week, improved the compliance of the carotid arteries; however, increased exercise frequency might be associated with greater benefits such as decreased aortic stiffness. Maintaining carotid artery compliance may reduce the risk for age-related dementia by buffering the excessive pulsatile pressure ejected from the left ventricle during systole that would normally be transmitted into the cerebrovasculature. Furthermore, implementing casual or committed exercise in midlife may be sufficient to reduce the risk of age-related dementia by improving arterial compliance and reducing the risk of developing midlife hypertension. Given the impact of arterial stiffness and midlife hypertension on later risk of dementia, it will be important for future studies to determine whether the optimal dose of exercise reported by Shibata et al. (2018) is also sufficient for preserving cerebrovascular and cognitive function with ageing. Future analyses should also consider the effects of other parameters such as the intensity, duration and type of exercise on arterial stiffness as the effect of these other exercise variables on arterial stiffness and biological aortic age remain to be elucidated. Finally, longitudinal exercise interventions are needed to directly test whether this level of exercise can ameliorate/prevent the effects of arterial stiffness on other age-related diseases such as cognitive impairment and dementia. The authors have no conflicts of interests to disclose. All authors have read and approved the final version of this manuscript and agree to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All persons designated as authors qualify for authorship, and all those who qualify for authorship are listed. None. The authors apologize for not citing all relevant articles due to reference limitations. We would like to thank Dr Christopher Martens for his critical evaluation and feedback during the preparation of the manuscript." @default.
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• W2898069614 title "‘Compliance’ to exercise: how much is<i>really</i>needed for a healthy heart (and mind)?" @default.
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