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LA function is an important part of cardiac cycle to determine an adequate LVfilling. In a study conducted by D’Andrea and collegues [ 43 ], it has been demon-
strated that the atrial function, expressed by LA strain is normal in elite athletes
compared with sedentary healthy controls and hypertensive patients, all age- matched
(Table 2.3). Atrial longitudinal strain was performed from the apical four and two
chamber views for the basal segment of LA septum, lateral wall and roof. LA diam-
eter and maximum volume were increased but similar in both groups. The peak
systolic myocardial atrial strain was significantly reduced in patients with patho-
logic LV hypertrophy compared with controls and athletes in all studied segments.
In a multivariate analysis, LV end-diastolic volume and LV mass were the majorpredictive factors of LA lateral wall peak systolic strain. Instead, it was found a
negative correlation of LA lateral wall peak systolic strain with LV mass and cir-
cumferential end-systolic stress in subject with hypertension [ 43 ]. Therefore, LA
myocardial deformation is normal in elite athlete’s compared with aged-matched
sedentary controls and hypertensive patients. Thus, the atrial enlargement oh ath-
lete’s heart does not mean loss of atrial function, but, conversely, it indicates an
increase of functional capacity during exercise.
The LA enlargement is considered a risk factor for atrial fibrillation (AF) in gen-eral population. Several studies have analyzed the relationship between long-term
endurance sport and AF. Firstly, Karjalainen and collegues [ 44 ] published in 1998 a
prospective longitudinal study in which after 10 years of follow up, AF incidence
was 5.3% among athletes compared with 0.9% among the control subjects. After,
Molina and collegues [ 45 ] analyzed the incidence of AF in a group of 183 amateur
marathon runners and in a group of 290 sedentary controls. The annual incidence
was 0.43% in the former and 0.11% in the latter group. Moreover the risk of AF
correlates with hours and intensity of exercise [ 46 ]. On the other hand, Mozaffarian
and collegues [ 47 ] demonstrated that a daily and costant exercise, such as walking,
is associated with significant lower AF incidence in older adult, while a more intense
physical exercise is associated with a moderate increase of risk of AF. Some studies
have defined an exercise risk threshold for developing AF. They reported that a life-
time exercise practice of more than 5000 h and formore than 5 h per week at the age
of 30 years or over increases the risk of AF [ 48 ]. The mechanisms of lone AF in the
athlete’s heart are various: LA remodeling, increased vagal tone and atrial ectopic
beats. Fibrosis is a common feature of atrial remodeling in some pathologic condi-
tions, such as hypertension. There are little data on the atrial wall fibrosis in humans.
In rat models of marathon running, it has been demonstrated a profibrotic process in
rats subjected to endurance exercise. Endurance exercise is associated with acute
post-exercise release of inflammation and oxidative factors, which favour the devel-
opment of wall fibrosis [ 49 – 51 ]. The most studied factor is the tumor necrosis
factor-α (TNF-α) [ 51 ]. Data of the preclinical studies demonstrate that the atrial
fibrosis is not sufficient to determine AF, but other factors are necessary. For exam-
ple, the increased vagal tone favours the excitability of myocardium creating the
substrate for a re-entry circuit [ 52 ] while the atrial ectopic beats could be the trigger
to start the arrhythmia. Therefore, the sport-related AF may occur in a middle-aged
male athlete with a history of long-term regular endurance sport practice, expecially
A. D’Andrea et al.