Aerobic exercise attenuates ageing of the athletic heart

Healthy cardiac pumping is a remarkably synchronous contraction of various layers and orientations of myocardial fibres, resulting in both longitudinal and radial shortening of the ventricles. A decline in cardiac function is observed with normal ageing, due to a decrease in ventricular volumes concomitant with both increased left ventricular (LV) wall thickness and fibrosis. Despite this phenomenon, lifelong endurance training has been shown to counter the effects of ageing by attenuating declines in both pumping efficiency and cardiac output delivery (Fig. 1). In a recent cross-sectional study in The Journal of Physiology by Steding-Ehrenborg et al. (2015), the age- and endurance training-related effects on cardiac function were investigated in older sedentary (66 ± 4 years old), older athletic (63 ± 4 years old) and younger (29 ± 4 years old) sedentary adults. Using cardiac MRI, resting cardiac volumes and contractility indices were determined in an effort to provide novel insights into changes in the contribution of longitudinal and radial pumping to stroke volume (SV) with lifelong endurance training. The use of cardiac MRI provided a distinct advantage as it enabled the three-dimensional assessment of longitudinal systolic function (e.g. in any plane) with superior soft tissue delineation of the epicardial and endocardial borders, thereby overcoming volumetric underestimations in prior echocardiographic-based studies. Atrioventricular plane displacement (AVPD) was measured (i.e. atrioventricular plane movement towards and away from the apex during systole and diastole) to determine the longitudinal contributions to SV. Notably, AVPD differs from the commonly reported clinical, global index of ejection fraction in that it specifically reflects longitudinal axis fibres of the endocardium. In addition, all subjects performed standardized cardiopulmonary exercise testing and older participants underwent invasive exercise measurements to obtain cardiac output (CO) values. Exercise stress testing was particularly important in revealing subclinical changes in cardiac function, not commonly seen at rest. While resting cardiac index was similar between the three groups, an invasive dye dilution technique during maximal exercise stress revealed that older athletes had a higher cardiac index compared with older sedentary adults. A higher LV-AVPD was also observed in both older athletes and young sedentary adults compared with the older sedentary adults, thereby suggesting that longitudinal contractile function may decrease with ageing, but be attenuated by long-standing aerobic exercise. Furthermore, older sedentary individuals achieved their longitudinal pumping from a greater short-axis area of the ventricle, while the older athletes and young sedentary individuals had a greater LV-AVPD. While the current study provides novel insight into the effects of lifelong exercise training on cardiac function, several questions remain unanswered. (1) What are the independent effects of ageing versus the chronic physical activity dose response? (2) What is the relationship between resting blood pressure and LV-AVPD across the lifespan in both sedentary and active adults? And (3) why is there a decline in LV-AVPD in sedentary older adults, without similar changes in right ventricular (RV) AVPD? The interaction of exercise training and ageing on the human myocardium provides a unique physiological model. In the current study, the independent effects of exercise training on LV-AVPD measures and the mechanism by which older athletes achieve longitudinal pumping differed when compared with young sedentary subjects and could not be distinguished as there was no younger athletic cohort. Future cross-sectional studies should include a younger athletic cohort to more conclusively investigate the independent effects of age versus exercise training history on this phenomenon. A prospective, longitudinal study may offer the most insight into the long-standing effects of aerobic physical activity on changes in cardiac function. In fact, the long-standing physical activity dose (including frequency, intensity, time and type of exercise) may also evoke a significant cardiovascular adaptation marked by changes in cardiac structure (e.g. increased wall thickness), haemodynamics (e.g. higher resting and exercise stroke volume), and pumping (e.g. superior contractile function), independent of age. In the current study, sedentary adults (both younger and older) were compared against middle-aged trained road cyclists with a reported physical activity volume of 5 h per week over at least 30 years (e.g. 5 h per week × 52 weeks per year × 30 years = >7800 h of lifetime physical activity). While phenotypic distinction can be seen as advantageous in identifying remarkable physiological differences in cardiac function, there are two inherent weaknesses that arise. First, non-elite athletes who perform high volumes of physical activity (>4500 h of lifetime aerobic exercise) are at a fivefold increased risk of atrial fibrillation (Wilhelm et al., 2011), which has been associated with a decline in AVPD (Emilsson & Wandt, 2000). While the current cohort had not been diagnosed with overt cardiovascular disease, an assessment for subclinical and clinical presentation of cardiac rhythm disorders was not performed. It is possible that any presence of cardiac rhythm abnormalities among this small, highly active group may confound study findings. Second, current physical activity recommendations (ranging from 75 min of vigorous physical activity to 150 min of moderate-to-vigorous physical activity per week) were greatly exceeded by the athletic cohort in the current study. From a clinical perspective, it remains unclear if AVPD is preserved in recreationally active middle-aged adults who adhere to more modest physical activity guidelines. Current study findings, therefore, have limited generalizability to the larger population of recreationally active adults. Thus, a prospective, longitudinal study examining highly trained athletes relative to both recreationally active and sedentary adults may further our understanding of the effects of aerobic exercise on changes in cardiac function with healthy ageing. Hypertension is associated cardiac remodelling from increased myocardial fibrosis and collagen synthesis, and elicits a progressive decline in cardiac function. In the current study, high systolic blood pressure (SBP) was observed in the older sedentary group (SBP: 145 ± 6 mmHg) and borderline hypertension was also observed in the older athletic cohort (SBP: 139 ± 13 mmHg), while the younger sedentary cohort was normotensive (126 ± 6 mmHg). Ballo et al. (2010) investigated LV longitudinal systolic performance in an older hypertensive group, and found that AVPD was reduced compared with age- and sex-matched healthy controls. The main independent determinant of LV longitudinal systolic function in the hypertensive group was LV mass, suggesting that the resulting LV hypertrophy from pressure overload is likely to be associated with cardiac systolic dysfunction. Thus, it may have been more appropriate to recruit individuals with similar resting blood pressure status, as the reduced AVPD may be in part attributable to their high resting SBP and not due to physical inactivity alone. The age-related reduction in LV-AVPD would probably be attenuated in normotensive older adults (sedentary or physically active). A comparison of left and right ventricular function has both physiological and clinical relevance. RV dysfunction has prognostic significance independent of LV function in many clinical conditions (including heart failure and pulmonary hypertension). Interestingly, the current study by Steding-Ehrenborg et al. (2015) observed a higher LV-AVPD in both older athletes and young sedentary compared with the older sedentary participants, without similar changes in right ventricular AVPD. The underlying mechanisms contributing to a 'mismatch' in ventricular function were not discussed in the current study. It remains unclear as to why no changes were observed in RV AVPD, given that the cardiovascular system is a closed-loop system and healthy ageing has been associated with changes in RV longitudinal contractile function and increases in pulmonary vascular resistance (Chia et al., 2014). Future studies are warranted to understand the biventricular response to long-standing aerobic exercise. In conclusion, Steding-Ehrenborg et al. (2015) provide some novel insights into the effects of lifelong exercise training on cardiac function using a strong cardiac MRI-based methodological approach. In the absence of regular physical activity, it appears that older sedentary subjects may have a lower LV-AVPD than older athletes, compensated for by a larger short-axis area of the ventricle. This alternative mechanism for cardiac pumping is less efficient, expending more energy during the cardiac cycle in order to expel adequate blood into the circulation. While results from this study emphasize the importance for lifelong endurance exercise in preserving the function of the atrioventricular plane and maintaining cardiac output at levels similar to young sedentary individuals, future work needs to explore the effects of exercise training volume on LV and RV function in both younger and older normotensive cohorts to more conclusively substantiate these intriguing study findings. None declared. All authors have approved the final version of the manuscript and agree to be accountable for all aspects of the work. All persons designated as authors qualify for authorship, and all those who qualify for authorship are listed.

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