SCIENTIFIC JOURNAL of the Hungarian Society of Cardiology

Dynamics of exercise training and detraining induced cardiac adaptations

█ Review

DOI: 10.26430/CHUNGARICA.2023.53.5.484

Oláh Attila, Sayour Alex Ali, Ruppert Mihály, Barta Bálint András, Bottlik Olívia, Merkely Béla, Kovács Attila, Radovits Tamás
Semmelweis Egyetem, Városmajori Szív- és Érgyógyászati Klinika, Budapest


The effect of intense, regular physical activity has been provided by numerous studies in sports cardiology: both its role in the cardiovascular prevention, as well as exercise-induced cardiac hypertrophy in elite athletes have already been well characterized. In this review, we would point out and summarize the rate of development and regression of the cardiac adaptations induced by long-term, regular exercise training and its cessation, focusing on three main aspects of cardiac remodeling.

While most of the cross-sectional investigations in sports cardiology compared elite athletes to healthy individuals, we focused on longitudinal follow-up investigations those also have initial data before regular exercise program and/or detraining period. Intensified exercise training induces significant improvement in functional capacity only after approximately 2 weeks, while the first marked alterations in sinus bradycardia and left ventricular hypertrophy have been observed after 2 months of regular physical activity. Comparable alterations has been observed in animal studies, with some earlier observation of morphological alterations. Both human and experimental evidences suggest rapid cardiac morphological, functional and electrical regression after the cessation of exercise training (detraining).

These data imply that regular exercise-associated cardiac functional improvement (early diastolic function, maximal oxygen uptake) develops earlier than the morphological and electrical remodeling. The improved functional capacity might be the primary alteration while the morphological and electrical adaptations might be a secondary consequence resulted by the long-term regular cardiovascular hemodynamic overload. The reversion of exercise-induced changes looks to be an accelerated, rapid regression compared to the development phase.


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