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............................................................................................................................................................................. studies should also prove useful for validating current risk stratification protocols derived from a relatively sedentary population.

Exercise and atrial fibrillation. The threshold lifetime sports activity for increasing the risk of developing AF is unknown. It is also unknown whether ongoing participation in vigorous exercise at the same intensity after successful AF ablation is associated with a higher risk of AF recurrence. Benefit of invasive electrophysiological studies in adolescents with accessory pathways. The benefit/risk ratio of early invasive EP evaluation of AP conduction properties in young athletes with asymptomatic pre-excitation (<1214 years old), and prophylactic ablation, remains unclear and requires large-scale studies for clarification. Exercising with an implantable cardioverter defibrillator. Although an international registry has shown absence of sportsrelated sudden death or injury in individuals with an ICD who perform competitive, high-intensive recreational or high-risk sports, many data are sparse and have not examined specific athletic populations with reduced LV function, catecholaminergic polymorphic VT. Moreover, the long-term physical and psychological impact of appropriate and inappropriate shocks, which become more frequent with increasing sports intensity, is unknown. Arrhythmic risk of exercise in adult congenital heart disease. The relationship between intensity of exercise and risk of arrhythmias in individuals with CHD is unknown and further research is needed. Although exercise prescription is recommended in CHD patients, further studies are necessary to identify the optimal method of improving adherence to an exercise prescription.

8 Sex differences

For many years sports participation, especially at the highest echelons, has been dominated by males, but the last four decades have witnessed an increasing number of females participating in a large variety of sporting disciplines at elite level. Females constituted 45% of all athletes at the 2016 Rio Olympics and participated in 26 of the 28 different sporting disciplines including those that were traditionally considered to be ‘male sports’, such as footfall, rugby, and boxing. Although the guidelines in this document are applicable to both sexes, there are some pertinent sex-based differences relative to exercise and sport including: (i) the incidence of SCD during exercise; (ii) quantitative differences in CV adaptation to regular intensive exercise and the overlap with cardiomyopathy; (iii) the predilection of adverse events with specific CVDs in women; and (iv) the additive haemodynamic effects of exercise in pregnant women with a structurally abnormal heart. Current evidence suggests a significantly lower prevalence of exercise-related SCD in females who represent a small minority of athletes dying suddenly with a male to female ratio ranging from 3 to 10: 1.17,18,46,49,52,620 This disproportionately lower incidence of SCD among young competitive female athletes also holds true for older recreational athletes where deaths in males are 20-fold greater than in females. Apart from a lower incidence of exercise-related SCD, there appear to be sex differences related to the diseases predisposing to SCD. Unlike males, female athletes rarely succumb to SCD from HCM. In the US National Registry, females comprised only 3% of the 302 individuals who died from HCM.621 Potential determinants of this disproportionate prevalence of death in males may include a lower absolute volume and intensity of training load in females, which could make them less susceptible to ventricular tachyarrhythmias. However, it is also plausible that certain protective metabolic or hormonal mechanisms could reduce the arrhythmic risk during intense physical exertion in females with HCM. This observation is relevant to prescription of intensive exercise or competitive sports in HCM, which is relatively conservative, but could be of less concern and more liberal in affected females in the future. The diagnosis of HCM in an athlete is also relevant in this regard, because male athletes, particularly those competing in endurance sports, show quantitatively great structural changes within the heart including LV hypertrophy. Approximately 2% of white male athletes and 13% of black male athletes show a LV wall thickness of 1215 mm that overlaps with morphologically mild HCM and can pose a diagnostic dilemma. In contrast female athletes rarely reveal a LV wall thickness >12 mm or concentric LV remodelling, hence the diagnosis of HCM is clear-cut.3

In contrast, a different scenario is represented in females with MVP, where recommendation for participation in intensive exercise warrants a more detailed risk stratification. In the Italian pathology registry of 650 SCDs, 7% were attributed to MVP. Of these, the majority (60%) were female who presented a marked elongation of both leaflets due to an extensive myxomatous degeneration.332 It is also noteworthy that the majority of exercise-related SCDs in young females are associated with a structurally normal heart at autopsy. This observation from several registries suggests that genetic electrical diseases (namely, LQTS, Brugada syndrome, or catecholaminergic polymorphic VT) are likely responsible for a significant proportion of these deaths. Differences in cardiac repolarization between men and women have been reported in healthy subjects and in individuals with LQTS.622 Healthy females also have a longer QTc interval compared with males. Therefore, they are more often clinically affected by the syndrome than men, despite the equal sex distribution of the disease genotype. Females are also at a higher risk than males of developing arrhythmias in response to QT-prolonging drugs, and electrolyte disturbances compared with males. Furthermore, female sex is an independent risk factor for cardiac events in LQTS.623 Unfortunately, little is known about the influence of sex hormones on cardiac repolarization, except that androgens may shorten the QTc interval. Based on these considerations, we recommend particular caution when advising competitive sports in women with a probable or definite diagnosis of LQTS. Pregnancy is associated with a 50% increase in plasma volume and cardiac output. The stresses of exercise in pregnant women with structural heart disease have the potential to cause haemodynamic compromise. Moderate aerobic exercise is generally safe in all women and is associated with a lower prevalence of excessive weight gain, post-partum obesity, gestational diabetes, and pre-eclampsia. Female athletes may continue training intensively during pregnancy, although it is recommended that women do not exceed a heart rate of >90% of the maximum predicted for age to reduce the risk of foetal bradycardia. Pregnant women with known structural heart disease require evaluation before embarking on intensive exercise programmes. Exercise or sports involving forceful physical contact, risk of falling or abdominal trauma, heavy lifting, scuba diving, and Downloaded from academic.oup.com/eurheartj/article/42/1/17/5898937 by guest on 07 October 2026