Hypertrophic cardiomyopathy (HCM) is a common cardiac genetic disorder with a prevalence of 1/500 and is caused principally by mutations in genes encoding proteins of the cardiac sarcomere (eg, β-cardiac myosin heavy chain and cardiac troponin T).1 Although of substantial scientific importance, HCM is best recognised for being the most common cause of sudden cardiac death (SCD) in the young, especially in young athletes, accounting for up to one-third of all such deaths in the US.2 HCM might be expected to impair exercise capacity, for example through left ventricular hypertrophy (LVH) and diastolic ventricular dysfunction; however, some HCM patients not only tolerate exercise well, but indeed excel athletically. This is surprising given that even HCM patients without LVH exhibit subtle systolic and diastolic abnormalities. Additionally, approximately one-third of HCM patients exhibit abnormal blood pressure (bp) responses during maximal treadmill exercise (ie, a flat blood pressure response, or a fall in blood pressure), which portends a poor prognosis.3 4 Ultimately, exercise in HCM is a matter of considerable concern, as many of the cases of SCD in HCM are associated with exertion.2 Exercise-induced SCD thus represents the rationale, albeit controversially, for preparticipation cardiac screening and exclusion of affected athletes from sporting activity.5

WHAT THEN IS THE IMPACT OF EXERCISE IN HCM?

Sakata et al address this question in this issue of (see page 1282) by proposing that exercise-induced LV systolic dysfunction (LVSD) occurs more frequently in HCM patients with cardiac troponin gene mutations than in those without troponin mutations.6 While this observation is potentially of great interest, it is not without methodological limitations. First, there are marked differences between the two patient groups other than, but potentially not independent of, …