We read with interest the letter by Stollberger and Finsterer [1] inresponse to our article [2] and we wish to thank the authors for givingus the opportunity to provide further considerations, based on theircomments.The possibility to correctly identify left ventricular non-compaction(LVNC) is fundamental in the context of pre-participation screening,given that cardiomyopathies are known as a primary cause for suddencardiac death in young athletes. However, at the present time, thereare uncertainties on the correct classification of LVNC, particularlywhenseeninathleteswherephysiologicalLVremodelingmaymorpho-logically mimic true myocardial disease.An interesting observation reported by Stollberg questionedwhether LV hypertrabeculation was present before training in ourcase series [2]. While 1 athlete fulfilled both the echocardiographicChin and Jenni criteria for LVNC [3,4] before the training, 3 of them ful-filled the Chin criteria and all the Jenni criteria after training. As a re-sponse to training stimulus, new trabeculae were identified and theyweremoreevidentascomparedwiththepre-trainingevaluation.Nota-bly, training was able to induce anincrease in both the non-compactedand compacted layers. The better visualization of LV trabeculae aftertraining can be explained not only by the direct stimulus related totraining, but also by the increase in LV cavity size induced by changesin hemodynamics.AssuggestedbyStollberg,thepresenceoffamilyhistoryiscrucialfortheclinicalevaluation,suchasthepresenceofsymptoms.Inourcasese-ries, none of the athletes had family history for cardiomyopathies, sud-dencardiacdeath,orheartfailure.Furthermore,nonewassymptomaticorpresentedsyncopeorarrhythmiasandnonehadsigns,symptoms,orbiochemical abnormalities related to neuromuscular disorders.Stollberg states that the intake of doping drugs is able to influencemuscular growth and could influence the pattern of LV hypertrophy.However, none of the athletes took drugs and this was confirmed byantidoping controls performed during the agonistic season, accordingto current regulation for the Italian Basketball League.Theexercise-inducedincreaseinLVtrabeculationwasaccompaniedalsobychangesat12-leadrestingECG[2].Thesechangeswerefoundin3 athletes after training, all of them of afro-Caribbean origin, and werenot interpreted as pathological, being a possible normal, race-relatedvariant,assuggestedbycurrentrecommendations[5,6].Notably,thelo-calization of negative T waves differs between patients suffering fromLVNC and athletes presenting with LV hypertrabeculation [7]: indeed,while the latter normally show anterior T-wave inversion, as found inour case series, the former have a high prevalence of T-wave inversionin the inferior and lateral leads [7]. However, we cannot negate thatthe contemporary presence of both LV hypertrabeculation and T-waveinversion in the precordial leads represents a challenge for clinicianswhen evaluating an athlete.In conclusion, our observation does not challenge the hypothesis thatLVNC is due to a disturbed compactionprocess of the embryogenic heart.Conversely,itsuggeststhatexercisecouldrepresentastimulusforthede-velopment of a LV hypertrabeculation pattern in certain subjects. Thus,according to this experience and to previous observations in athletes byother research groups [7–9], we suggest distinguishing between“hypertrabeculation” and “LVNC”. We believe that these two terms de-scribe a different phenomenon: indeed, isolated “hypertrabeculation”does potentially indicate the consequence of physiological adaptation ofthe LV to intensive training in predisposed individuals; it can be foundin the absence of pathological fidings, symptoms, or family history ofncardiomyopathies. Therefore, the optimization of echocardiographic im-aging in the last years should have at least in part in fluenced the recogni-tion of this entity. Conversely, “LVNC” represents a cardiomyopathy ableto induce life-threatening arrhythmias, LV dilatation and dysfunction,