Lucas Helal1, Anderson Donelli da Silveira2. 1. Laboratório de Fisiopatologia do Exercício (LaFiEx) - Hospital de Clínicas de Porto Alegre - Programa de Pós-Graduação em Cardiologia e Ciências Cardiovasculares - Faculdade de Medicina - Universidade Federal do Rio Grande do Sul, Porto Alegre, RS - Brazil. 2. Grupo de Cardiologia do Exercício (CARDIOEX) - Hospital de Clínicas de Porto Alegre - Programa de Pós-Graduação em Cardiologia e Ciências Cardiovasculares - Faculdade de Medicina - Universidade Federal do Rio Grande do Sul, Porto Alegre, RS - Brazil.
Cardiac remodeling due to exercise training overload (the so-called "athlete's heart")
has been widely investigated since the 70's and is still acknowledged by the scientific
community. To differentiate normal adaptive responses ("benign") from abnormal ones
remains a challenge. Here we address some important issues related to the discussion on
cardiac remodeling in exercise, recently revisited by Vidaletti-Silva and
colleagues[1] in this issue.In terms of morphological adaptations, the left atrial and ventricular hypertrophy call
attention due to their potential association with the onset of supraventricular
tachyarrhythmias[2] and also of
ventricular arrhythmias,[3] which may
result in undesirable events.[4]However, mounting evidence has been suggesting that the remodeling response due to
exercise training load (e.g., length of exposure, intensity, modality etc.) may not
configure a state of disease - i.e., the "physiological but nor pathological"
remodeling.[5]"With a focus on the left chambers, it is known that the blood pressure and the volumetric
overload may result in two classical morphological characteristics, accordingly to the
Morganroth hypothesis[6] - an increase of
the left cavities' volume for those overloaded by the cardiac output (i.e., endurance
athletes); or the hypertrophy of the left ventricle (LV) septum for those overloaded by
blood pressure levels (i.e., strength-trained athletes). As a minor comment, the
Morganroth hypothesis has been recently revisited after the observation of cases of
septal hypertrophy in endurance athletes.[7]Although well-established in scientific literature, Vidaletti-Silva et al.[1] have addressed the question of
differences in cardiac remodeling due to sports modalities through a cross-sectional,
comparator-group design, comparing endurance athletes (i.e., runners) and
strength-trained athletes (i.e., powerlifters) - two classes and levels of modalities
that seem appropriate for this comparison. In their findings, no moment-differences
between groups were observed for the LV mass, when adjusted for their surface area. As
expected, septal and posterior LV thickness were different between endurance and
strength athletes, but not the LV end-diastolic volume. The vascular function (i.e.,
flow-mediated dilation and peripheral vascular resistance) was also evaluated and no
differences were found. The take-home message of this study, at least in light of our
interpretation, is that athletes in a range of 5 to 7 years of training have adaptations
no bigger than the established thresholds for normality for LV dimensions[8] and wall thickness.[9]We should acknowledge that, even within borderline values, there were no impairment of
the systolic and diastolic function of the myocardium in either groups, depicting the
normal adaptive nature of the cardiac structure findings. Even though a simple
experiment, this cross-sectional study corroborates the hypothesis of different cardiac
adaptations due to different training modalities. Finally, to detect some abnormal
morphological adaptations in athletes remains a challenge, especially for those within
borderline values. We welcome studies such as this one - that sheds a light on this gray
area.
Authors: Antonio Pelliccia; Barry J Maron; Fernando M Di Paolo; Alessandro Biffi; Filippo M Quattrini; Cataldo Pisicchio; Alessandra Roselli; Stefano Caselli; Franco Culasso Journal: J Am Coll Cardiol Date: 2005-08-16 Impact factor: 24.094
Authors: Roy M John; Usha B Tedrow; Bruce A Koplan; Christine M Albert; Laurence M Epstein; Michael O Sweeney; Amy Leigh Miller; Gregory F Michaud; William G Stevenson Journal: Lancet Date: 2012-10-27 Impact factor: 79.321