Author + information
- Fabian Sanchis-Gomar, MD, PhD∗ (, )
- Nuria Garatachea, PhD,
- Pilar Catalán, MD,
- Marta López-Ramón, MD, PhD,
- Alejandro Lucia, MD, PhD and
- Enrique Serrano-Ostáriz, MD, PhD
- ↵∗Department of Physiology, Faculty of Medicine, University of Valencia, Av. Blasco Ibañez, 15, Valencia 46010, Spain
A recent meta-analysis by Iskandar et al. (1) nicely showed that endurance athletes have larger left atrial (LA) diameters compared with control subjects. Yet only 9 of 54 studies included in their analysis reported LA volume values corrected for body surface area (BSA). In fact, few studies have determined LA volume in young athletes, and, to the best of our knowledge, no study has reported this variable in older athletes. This is an important question given the growing debate about the potential deleterious effects of long-term strenuous endurance exercise on the human heart, notably the higher risk of atrial fibrillation (AF), a condition for which both atrial dilation and the normal aging process are thought to be potential causative mechanisms (2). Thus, we aimed to assess the long-term consequences of endurance exercise on LA volume in athletes who were highly competitive at younger ages and are still active. To this end, we compared BSA-corrected LA volumes determined with late gadolinium enhancement magnetic resonance imaging (LGE-MRI) in former elite endurance athletes and sedentary control subjects.
After institutional review board approval, 5 healthy individuals (control subjects) and 10 former elite endurance athletes (all men; ages 57.0 ± 4.3 years and 52.4 ± 6.3 years; body mass index, 25.8 ± 2.7 kg/m2 and 22.6 ± 1.3 kg/m2, respectively) provided written informed consent and were studied. Control subjects had never participated in regular exercise, whereas the athlete group included former professional road cyclists (n = 6) and runners (n = 4, 1 of whom was a 2-time marathon world champion). Their mean experience in professional sports competition (including, for some of them, participation in the Olympic Games) was 24.3 ± 4.2 years. All but 1 of them are still training and competing regularly in Master categories. The only nonactive athlete had been retired from competition for 24 years.
Evaluations were performed with a Signa HDx 3.0-T instrument (GE Healthcare, Buckinghamshire, United Kingdom). Approximately 10 to 15 min after injection of 0.2 mmol/kg gadolinium-chelate contrast, high-resolution late gadolinium enhancement images of the left atrium were acquired in the 3 cardiac planes. LA volumes were evaluated using the software Report Card 4.3 (GE Healthcare) by a single blinded, experienced researcher.
The values of LA volumes corrected for BSA followed a normal distribution and were significantly higher in athletes compared with control subjects (58 ± 14 ml/m2 vs. 39 ± 14 ml/m2, respectively; p = 0.026). In the former, the lowest LA volume was found in the only inactive subject (individual values are shown in Figure 1).
This is the first attempt to evaluate LA volumes with LGE-MRI in former elite athletes. Although our results are preliminary and more research is needed with larger cohorts, in accordance with Iskandar et al. (1), our data suggest that long-term participation in regular endurance exercise increases LA volume. Interestingly, LA dimensions are also larger in former highly trained athletes compared with their younger peers (as shown in Figure 2 of the Iskandar et al. paper), probably due to the combined effects of long-term strenuous endurance exercise together with age-related physiological changes. It seems, however, that LA enlargement in endurance-trained athletes is an overall benign adaptation coupled with the left ventricular (LV) enlargement and volume overload induced by long-term exercise (3,4); indeed, endurance training preserves ventricular compliance, thereby preventing heart failure in later life, whereas sedentary aging is associated with decreased LV compliance and diastolic performance. Further, LA enlargement associated with sedentary aging is due to LV dilation owing to increased LV mass and eccentric hypertrophy (e.g., caused by obesity) and/or a concentric increase in LV mass (e.g., caused by essential hypertension), and eventually leads to impaired ventricular filling and diastolic dysfunction (5). However, although the association between increased LA diameter/volume and higher risk of AF is well documented, no athlete studied here has ever received a diagnosis of persistent or paroxysmal AF.
In conclusion, clinicians should be aware of the fact that highly trained endurance athletes usually have larger LA diameters compared with the general population, a phenomenon especially remarkable in veteran athletes. Future research might elucidate the clinical implications (if they exist) of such morphological changes.
Please note: The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
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