Exercise for Cardiovascular Disease Prevention and Treatment From Molecular to Clinical, Part 1

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A meta-analysis of 23 studies demonstrated a slight reduction of ejection fraction

(−2%), of uncertain clinical significance that is, in part, explainable with a different


load condition [ 21 ]. Some echocardiographic studies found wall regional abnor-


malities and reduced pulsed DTI e’ velocity of both septal and lateral mitral annulus


in runners after a marathon [ 2 ]. After long exercise, a decrease of longitudinal, cir-


cumferential and radial strain and a reduction and delay of peak twisting were also


documented in thriathletes. Of interest, while the LV systolic function return to the


normality in 2 days, the diastolic dysfunction persists until 1 months after a mara-


thon. In some studies, the late gadolinium enhancement distribution on CMR is used


to verify the presence of myocardial fibrosis in athletes as a sign of permanent


injury. It was observed LGE in 12% of marathon runners and its prevalence was


correlated with the number of marathons previously performed, suggesting that an


intense training determine the development of small myocardial scars [ 60 ].


5 Aortic Root


Adaptations of athlete’s heart involve also the aortic root (AoR). Endurance and


strength exercise have different effects on the aortic root. During endurance exercise


the increase of stroke volume repeated and protracted over time determines a major


distension of the aortic wall and, so, a great systolic pressure during the exercise.


The strength exercise is characterized by short exercise of high intensity that deter-


mine rapid and brief increase of cardiac output. At the same time, the enhanced


sympathetic nervous system activity and external compression of blood vessels


makes a rapid increase of heart rate and of the systemic peripheral resistance. Thus,


during heavy-resistance static exercise, the arterial rapidly increase with values


which arrive to 480/350 mmHg [ 61 ]. Starting from the pathologic model of aortic


dilatation in arterial hypertension, it has been hypotized that the hemodynamic load


during prolonged exercise and, particularly, the pressure overload during strength


exercise may lead to AoR dilatation. A recent study [ 62 ] has explored the aortic root


dimension on 615 elite athletes (370 endurance-trained athletes, 245 strength-


trained athletes, with a mean age of 28.4  ±  10.2  years) using transthoracic-


echocardiography (Table 2.4). The aortic root diameters were significantly greater


in all segments in the strength-trained athletes with greater diameters in men than in


women, even if this difference abolished when the data were indexed for BSA. Only


Table 2.4 Bi-dimensional echocardiographic root diameters in athletes (p value < 0.05) [ 62 ]


Variable (cm) Overall (n = 615) Endurance (n = 370) Strenght (n = 245)
Aortic annulus 2.3 (1.8–2.8) 2.1 (1.8–2.4) 2.5 (2.2–2.8)
Sinuses of Valsalva 3.3 (2.8–4.2) 3.1 (2.8–3.6) 3.6 (3.2–4.2)
Supra-aortic ridge 3.1 (2.6–3.7) 2.9 (2.6–3.2) 3.3 (2.9–3.7)
Proximal ascending aorta 3.3 (2.8–3.9) 3.1 (2.8–3.4) 3.5 (3.1–3.9)

Data are presented as mean (range)


2 Acute and Chronic Response to Exercise in Athletes: The “Supernormal Heart”

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