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Complete Reversion of Cardiac Functional Adaptation Induced by Exercise Training

Authors :
Attila Oláh
Mihály Ruppert
Balázs Tamás Németh
Béla Merkely
Tamás Radovits
Csaba Mátyás
Kálmán Benke
Marianna Török
Anna Meltzer
L Szabo
Árpád Lux
Alex Ali Sayour
Dalma Kellermayer
István Hartyánszky
Source :
Medicine & Science in Sports & Exercise. 49:420-429
Publication Year :
2017
Publisher :
Ovid Technologies (Wolters Kluwer Health), 2017.

Abstract

Long-term exercise training is associated with characteristic cardiac adaptation, termed athlete's heart. Our research group previously characterized in vivo left ventricular (LV) function of exercise-induced cardiac hypertrophy in detail in a rat model; however, the effect of detraining on LV function is still unclear. We aimed at evaluating the reversibility of functional alterations of athlete's heart after detraining.Rats (n = 16) were divided into detrained exercised (DEx) and detrained control (DCo) groups. Trained rats swam 200 min·d for 12 wk, and control rats were taken into water for 5 min·d. After the training period, both groups remained sedentary for 8 wk. We performed echocardiography at weeks 12 and 20 to investigate the development and regression of exercise-induced structural changes. LV pressure-volume analysis was performed to calculate cardiac functional parameters. LV samples were harvested for histological examination.Echocardiography showed robust LV hypertrophy after completing the training protocol (LV mass index = 2.61 ± 0.08 DEx vs 2.04 ± 0.04 g·kg DCo, P0.05). This adaptation regressed after detraining (LV mass index = 2.01 ± 0.03 vs 1.97 ± 0.05 g·kg, n.s.), which was confirmed by postmortem measured heart weight and histological morphometry. After the 8-wk-long detraining period, a regression of the previously described exercise-induced cardiac functional alterations was observed (DEx vs DCo): stroke volume (SV; 144.8 ± 9.0 vs 143.9 ± 9.6 μL, P = 0.949), active relaxation (τ = 11.5 ± 0.3 vs 11.3 ± 0.4 ms, P = 0.760), contractility (preload recruitable stroke work = 69.5 ± 2.7 vs 70.9 ± 2.4 mm Hg, P = 0.709), and mechanoenergetic (mechanical efficiency = 68.7 ± 1.2 vs 69.4 ± 1.8, P = 0.742) enhancement reverted completely to control values. Myocardial stiffness remained unchanged; moreover, no fibrosis was observed after the detraining period.Functional consequences of exercise-induced physiological LV hypertrophy completely regressed after 8 wk of deconditioning.

Details

ISSN :
01959131
Volume :
49
Database :
OpenAIRE
Journal :
Medicine & Science in Sports & Exercise
Accession number :
edsair.doi.dedup.....fe60756c37d8b4b7d50d900f8bc65753
Full Text :
https://doi.org/10.1249/mss.0000000000001127